Update Dermatology

DERMATOLOGY

LATEST MANAGEMENT STRATEGIES FOR: Psoriasis, rosacea, acne, hidradenitis suppurativa, and wound care

SKIN

FULL COVERAGE OF THE 2022 ANNUAL MEETING

PRESCRIBING INFORMATION (PI)

SKYRIZI®▼ (risankizumab) 75 mg solution for injection in pre-filled syringe; Skyrizi 150 mg solution for injection in pre-filled pen and Skyrizi 150 mg solution for injection in prefilled syringe. Refer to Summary of Product Characteristics (SmPC) for full information before prescribing. PRESENTATION: Skyrizi 150 mg solution for injection in pre-filled pen/syringe: each prefilled pen/syringe contains 150 mg risankizumab in 1 mL solution. Skyrizi 75 mg solution for injection in pre-filled syringe: each pre-filled syringe contains 75 mg risankizumab in 0.83 ml mL solution. INDICATION: For treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy. DOSAGE AND ADMINISTRATION: Intended for use under guidance and supervision of a physician experienced in diagnosis and treatment of psoriasis. Dosage: The recommended dose of Skyrizi is 150 mg by subcutaneous injection at weeks 0, 4, and every 12 weeks thereafter. Two 75mg pre-filled syringes should be injected for the full 150 mg dose. Consider discontinuation of treatment in patients showing no response after 16 weeks of treatment. Some patients with initial partial response may subsequently improve with continued treatment beyond 16 weeks. Special Populations: Elderly: No dose adjustment required. Renal or hepatic impairment: No dose adjustment required. Paediatric Population: No data available. Overweight patients: No dose adjustment required. CONTRAINDICATIONS: Hypersensitivity to any of the active substances or excipients. Clinically important active infections (e.g. active tuberculosis). SPECIAL WARNINGS AND PRECAUTIONS: See SmPC for full details. In order to improve the traceability of biological medicinal products, the name and the batch number of the administered product should be clearly recorded. Skyrizi may increase the risk of infections. In patients with a chronic infection or history of recurrent infections, or known risk factors for infection, Skyrizi should be used with caution. Treatment with Skyrizi should not be initiated in patients with any clinically important active infection until the infection resolves or is adequately treated. Patients should be evaluated for tuberculosis infection prior to initiating treatment. Anti-TB therapy should be considered prior to initiating Skyrizi in patients with a past history of latent or active TB in whom an adequate course of treatment cannot be confirmed. Completion of all appropriate immunisations should be considered prior to initiating therapy. If a patient has received live vaccination (viral or bacterial), it is recommended to wait at least 4 weeks prior to starting treatment with Skyrizi. Patients treated with Skyrizi should not receive live vaccines during treatment and for at least 21 weeks after treatment. If a serious hypersensivity reaction occurs, administration of Skyrizi should be discontinued immediately and appropriate therapy initiated. Excipients with known effect (75 mg solution for injection only): Skyrizi contains 68.0 mg sorbitol and less than 1 mmol sodium (23 mg) per 150 mg dose. INTERACTIONS: The safety and efficacy of Skyrizi in combination with immunosuppressants, including

biologics or phototherapy have not been evaluated. PREGNANCY AND LACTATION: Women of Childbearing potential: An effective method of contraception during treatment and for at least 21 weeks after treatment should be used. Pregnancy: Limited data available. It is preferable to avoid the use of Skyrizi during pregnancy as a precautionary measure. Lactation: It is not known whether Skyrizi is excreted in breast milk. Human IgGs are known to be excreted in breast milk during the first few days after birth, which decreases to low concentrations soon afterwards; consequently, a risk to the breast-fed infant cannot be excluded during this short period. A decision should be made whether to discontinue/abstain from Skyrizi therapy, taking into account the benefit of breastfeeding to the child and the benefit of Skyrizi therapy to the woman. Fertility: The effect of Skyrizi on human fertility has not been evaluated. ADVERSE REACTIONS: See SmPC for full details on adverse reactions. Very common adverse reactions (≥1/10): Upper respiratory infections. Common adverse reactions (≥1/100 to <1/10): Tinea infections, headache, pruritus, fatigue and injection site reactions.

▼ This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions via HPRA Pharmacovigilance; Website: www.hpra.ie. Suspected adverse events should also be reported to AbbVie Limited on 01-4287900.

LEGAL CLASSIFICATION: POM (S1A). MARKETING AUTHORISATION NUMBERS/PRESENTATIONS:

Skyrizi 75 mg solution for injection in pre-filled syringe (Pack of 2 pre-filled syringes): EU/1/19/1361/001; Skyrizi 150 mg solution for injection in pre-filled pen: EU/1/19/1361/002; Skyrizi 150 mg solution for injection in pre-filled syringe: EU/1/19/1361/003. Not all presentations may be marketed. Further information is available from: AbbVie Ltd., 14 Riverwalk, Citywest Business Campus, Dublin 24. DATE OF REVISION: May 2021 PI/1361/003

HRQoL, Health-Related Quality of Life; PASI, Psoriasis Area Severity Index.

REFERENCES:

When it comes to your patients’ psoriasis treatment goals

A better model of care for Irish dermatology

In Ireland, just over half of the population is affected by skin disease annually, with up to a third of people at any one time having a skin condition that would benefit from medical care. Skin disease causes over 230 deaths each year in Ireland, including 160 deaths due to malignant melanoma and 70 from non-malignant skin cancer, as well as contributing to significant morbidity and premature mortality in many individuals. The impact of skin diseases on quality of life can be far-reaching and profound.

Timely and accurate diagnosis, especially in the case of more serious skin disease such as skin cancer, is the key to determining the most effective management strategies for patients. However, like so many other medical specialties in Ireland, a key issue in dermatology is inadequate specialist staff numbers and dedicated services against a background of ever-increasing demand and huge waiting lists following the Covid-19 pandemic.

However, the HSE launched an ambitious new Model of Care for Dermatology this time last year, and

it aims to address these issues, and — aligned with the underlying principles of Sláintecare — ensure that patients receive the right care, at the right time, in the right place. While the pandemic has impacted its roll-out, progress is being made with plans for a new national ‘hub and spoke’ model, and increased consultant dermatologist and advanced nurse practitioner posts. In this edition of Update, HSE Clinical Lead for Dermatology Prof Anne-Marie Tobin outlines the key aims of the Model of Care and gives an update on its plans.

Facilitating self-care/self-management is also a key goal of Irish dermatology healthcare policy and involves patients, pharmacists, GPs, dermatologists and nursing. An estimated 15-to-20 per cent of GP consultations relate specifically to the skin, and most skin conditions can be managed at primary care level, with huge demand for GPs with a special interest in dermatology. One such GP, Dr David Buckley of the Kerry Skin Clinic, gives a comprehensive overview of the management of acne in primary care in this edition of Update. He has also just co-written a new textbook, Textbook of Primary Care Dermatology, which is reviewed on page 46.

On the medical conference front, we have exclusive detailed coverage of the recent Primary Care Dermatology Society of Ireland (PCDSI) Annual Meeting, which featured expert updates from leading national and international speakers on eczema, psoriasis, skin lesions, cryosurgery, and many other

topical dermatology issues.

This edition of Update also contains a wide range of clinical articles offering the latest expert approaches to diagnosing and treating conditions such as psoriasis, hidradenitis suppurativa, rosacea, dry skin and dermatitis, and wound management in primary care, as well as a very informative look at gangrene and its risk factors.

There is also an article dedicated to prevention and early detection strategies for skin cancer. While there have been welcome treatment advancements in this area and immunotherapy has revolutionised the treatment of inoperable, metastasised skin cancer in the last decade, prevention and early detection remain key. Now is the time to remind patients to be sun-aware as they begin to travel abroad again in increasing numbers after the Covid-19related restrictions of the last two years.

So all-in-all, a packed edition that should hopefully prove interesting and useful to all our readers.

Thank you to all our expert contributors for taking the time to share their knowledge and advice for the betterment of patient care.

We always welcome new contributors and ideas and suggestions for future content, as well as any feedback on our content to date. Please contact me at Priscilla@mindo.ie if you wish to comment or contribute an article. ■

Editor Priscilla Lynch priscilla@mindo.ie

Sub-editor Emer Keogh emer@greenx.ie

Creative Director Laura Kenny laura@greenx.ie

Advertisements Graham Cooke graham@greenx.ie

Administration Daiva Maciunaite daiva@greenx.ie

Update is published by GreenCross Publishing Ltd, Top Floor, 111 Rathmines Road Lower, Dublin 6 Tel +353 (0)1 441 0024 greencrosspublishing.ie

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The contents of Update are protected by copyright. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form by any means – electronic, mechanical or photocopy recording or otherwise – whole or in part, in any form whatsoever for advertising or promotional purposes without the prior written permission of the editor or publisher.

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The views expressed in Update are not necessarily those of the publishers, editor or editorial advisory board. While the publishers, editor and editorial advisory board have taken every care with regard to accuracy of editorial and advertisement contributions, they cannot be held responsible for any errors or omissions contained.

GreenCross Publishing is owned by Graham Cooke graham@greenx.ie

COMPLETE

DEMONSTRABLE JOINT EFFICACY

PROVEN DURABILITY*

Most patients who started on TREMFYA® stayed on TREMFYA® long-term1,2

Durability*, also known as patient retention or drug survival is a combination of efficacy, safety, tolerability and patient satisfaction or preference. DISCOVER-2 was a Phase 3, double-blind, multi-centre, placebo-controlled study that evaluated the efficacy and safety of TREMFYA® in bio-naïve patients with active PsA.1

Tremfya▼ 100 mg solution for injection in pre-filled pen PRESCRIBING INFORMATION. ACTIVE INGREDIENT(S): Guselkumab. Please refer to Summary of Product Characteristics (SmPC) before prescribing. INDICATION(S): Treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy. Treatment of active psoriatic arthritis in adult patients, alone or in combination with methotrexate, who have had an inadequate response or have been intolerant to a prior disease-modifying antirheumatic drug (DMARD) therapy. DOSAGE & ADMINISTRATION: For use under guidance/supervision of physician experienced in diagnosis and treatment of conditions for which Tremfya is indicated. Subcutaneous injection. Avoid areas showing psoriasis. Adults: For both indications, 100 mg at weeks 0 and 4, followed by maintenance dose every 8 weeks. In the case of psoriatic arthritis, for patients at high risk for joint damage according to clinical judgement, consider a dose of 100 mg every 4 weeks. Consider discontinuation if no response after 16 weeks of treatment for plaque psoriasis and 24 weeks for psoriatic arthritis. Children: No data available in children/adolescents <18 years. Elderly: No dose adjustment required, limited information in subjects aged ≥ 65 years, very limited information > 75 years. Renal & Hepatic impairment: Not studied. CONTRAINDICATIONS: Serious hypersensitivity to active substance or excipients; clinically important, active infection. SPECIAL WARNINGS & PRECAUTIONS: Infections: Potential to increase risk. If signs/symptoms of clinically important chronic/ acute infection occur, monitor closely and discontinue Tremfya until resolved. Tuberculosis: Evaluate patients for TB pre-treatment; monitor for signs/symptoms of active TB during and after treatment. Consider anti-TB therapy prior to Tremfya if past history of latent/active TB and adequate treatment course not confirmed. Serious hypersensitivity reaction: Includes anaphylaxis. Some serious hypersensitivity reactions occurred several days after treatment and included urticaria and dyspnoea. If occurs, discontinue Tremfya immediately and initiate appropriate therapy. Hepatic Transaminase Elevations: An increased incidence of liver enzyme elevations has been observed in patients treated with Tremfya q4w compared to patients treated with Tremfya q8w or placebo. When prescribing Tremfya q4w in psoriatic arthritis, consider evaluating liver enzymes at baseline and thereafter according to routine patient management. If increases in ALT or AST are observed and drug-induced liver injury is suspected, Tremfya should be temporarily interrupted until this diagnosis is excluded. Immunisations: Consider completing all appropriate immunisations prior to Tremfya. Do not use live vaccines concurrently with Tremfya; no data available; before

live vaccination, withhold Tremfya for at least 12 weeks and resume at least 2 weeks after vaccination. SIDE EFFECTS: Very common: Respiratory tract infection. Common: headache, diarrhoea, arthralgia, injection site reactions, transaminases increased. Other side effects: hypersensitivity, anaphylaxis, rash, herpes simplex infections, neutrophil count decreased. Refer to SmPC for other side effects. LEGAL CATEGORY: Prescription Only Medicine (POM). PRESENTATIONS, PACK SIZES, MARKETING AUTHORISATION NUMBER(S): Pre-filled pen, x1, EU/1/17/1234/002. MARKETING AUTHORISATION HOLDER: Janssen-Cilag International NV, Turnhoutseweg 30, B-2340 Beerse, Belgium. FURTHER INFORMATION IS AVAILABLE

FROM: Janssen Sciences Ireland UC, Barnahely, Ringaskiddy, IRL - Co. Cork, P43 FA46. Prescribing information last revised: November 2020.

Adverse events should be reported. ▼ This medicinal product is subject to additional monitoring and it is therefore important to report any suspected adverse events related to this medicinal product. Healthcare professionals are asked to report any suspected adverse events via: HPRA Pharmacovigilance Website: www.hpra.ie.

Adverse events should also be reported to Janssen Sciences Ireland UC on 1800 709 122 or at dsafety@its.jnj.com.

1. Griffiths CEM, et al. Maintenance of Response Through 5 Years of Continuous Guselkumab Treatment: Results From the Phase 3 VOYAGE 1 Trial. Presented at the 16th Annual Coastal Dermatology Symposium. October 15-16, 2020. 2. McInnes IB, et al. Efficacy and Safety of Guselkumab, a Monoclonal Antibody Specific to the p19-Subunit of Interleukin-23, Through 2 Years: Results from a Phase 3, Randomized, Double-blind, Placebo-controlled Study Conducted in Biologic-naïve Patients with Active Psoriatic Arthritis. Presented at Innovations in Dermatology Conference, March 16-20, 2021. Online. 3. Griffiths C, et al. Achieving and maintaining long-term optimal improvements in patient-reported symptoms, signs, and quality of life among patients with moderate-to-severe psoriasis treated with guselkumab: 5-year data from VOYAGE 1. Presented at AAD VMX 2021. 4. Blauvelt A, et al. J Am Acad Dermatol 2017;76:405-417. © Janssen-Cilag Limited

References:

SKIN CLEARANCE

Sustained joint symptom relief proven for 2 years in PsA2

Fast4 and sustained complete clearance proven for 5 years in Ps01

Primary Care Dermatology Society of Ireland (PCDSI) Annual Meeting 2022 conference report

Benign skin lesions in primary care

Benign lesions are one of the most common skin presentations in primary care and can be mostly dealt with locally, but knowing when to refer for further investigation is vital, the 2022 Primary Care Dermatology Society of Ireland (PCDSI) Annual Meeting heard.

During his presentation to the meeting, Dr David Buckley, PCDSI co-founder and Medical Director of the Kerry Skin Clinic, discussed the 10 most common benign lesions in primary care, of which benign moles, viral warts, molluscum contagiosum, and seborrhoeic keratosis are the four “big ones”.

“These are the most common benign lesions that we see pretty much every day in general practice,” said Dr Buckley.

In the case of when a practitioner cannot make a complete, competent and named diagnosis, “then that lesion is by definition suspicious,” Dr Buckley said.

In this case, he advised considering referral of the patient to a colleague with more experience in dermatology as the patient may require a biopsy.

“It’s having the confidence of diagnosing the common benign skin conditions and then having the knowledge that if you can’t recognise lesions, you can’t put a name on it and you’re not quite sure, then it’s probably malignant until proven otherwise,” he continued. “Especially in adults and in the elderly.”

When a patient has symptoms that seem not severe enough to warrant a hospital referral, GPs may refer the patient to their colleagues who have a special interest in dermatology, a number of which are scattered throughout the country. This model is replicated in England, Australia, and other countries, according to Dr Buckley.

“And that model has never been formalised [in Ireland],” he added, “but perhaps it should be encouraged, supported, and funded.”

One example of this is dermatoscopy and the use of a dermatoscope (a hand-held magnifying device used to visualise features of pigmented and non-pigmented skin lesions) in primary care. While it is not available to every GP in Ireland, “hopefully in every region or town there might be one GP who has an interest and experience within dermatoscopy,” Dr Buckley commented.

Dermatoscopy is no longer optional “for anyone who has an interest in dermatology, especially in lesion recognition, and particularly if they’re going to be treating… low-risk skin cancer”, said Dr Buckley. “In my view it is compulsory.”

After conducting a dermatoscopy or taking a focused history from a patient where there has not been a change in size, shape and colour, the mole can be defined as benign.

Dr Buckley said clinicians should be “highly suspicious” of new moles developing when a patient is over the age of 40. He also recommended using a handout (Warning signs to look for in a mole) to visually show patients how to detect a change in mole size, shape, and colour, available on the Kerry Skin Clinic website (www.kerryskinclinic.ie).

For warts, treatment options included topical salicylic acid, cantharidin, cryosurgery, “traditional cures/placebos” or no treatment. “Probably the treatment of choice in children is no treatment at all because the vast majority of warts in children go away anyway,” he said.

However, in elderly patients, “the index of suspicion goes up if there’s an isolated warty-lesions or a warty lesion on an unusual location, like the face.”

Molluscum contagiosum is very common in children and “again, treatment in children is to do nothing”, as the lesion tends to clear after a few months. The lesion is associated with dry

skin, so applying a “greasy moisturiser” twice daily for about three months can help.

Seborrhoeic keratosis is more common in older patients and can be treated with cryosurgery or by scraping the skin. “Everything we scrape, we send for biopsy,” said Dr Buckley. “You have to be sure of your clinical diagnosis.”

The other most common benign skin lesions are dermatofibroma, pyogenic granuloma, sebaceous cyst, skin tags, sebaceous gland hyperplasia, and haemangiomas.

Dr Buckley also highlighted the importance of context when identifying a benign skin lesion, including age, gender, location on the body and family history.

“I think more and more GPs are left dealing with skin problems because of [issues] accessing hospital-based dermatologists, both privately and publicly,” said Dr Buckley. “The vast majority of skin problems we see in primary

care can be managed… in primary care, [if] the GP has the knowledge and the skills and the experience. And hopefully, the book will help them to build on their knowledge and skills.”

Dr Buckley published his Textbook of Primary Care Dermatology late last year, and formally launched it at the PCDSI meeting, which aims to further educate and upskill healthcare professionals in primary care and help them to become more comfortable and confident in dermatology. Dr Paula Pasquali, Consultant Dermatologist in Pius Hospital de Valls, Tarragona, Spain, aided Dr Buckley in writing the textbook.

“It’s very useful to have both the GP and the consultant dermatologist involved because you get to see it from both points of view,” Dr Buckley said. He praised Dr Pasquali as “an excellent person to work with” and “very helpful”.

A textbook written specifically for GPs, it fills

“that gap of dealing with common dermatology problems as they would present in mild and moderate fashion to GPs”, with helpful flow charts, tables, and diagrams for practitioners to refer to easily and as needed. Dr Buckley highlighted that the information in the textbook can also be useful for nurses, pharmacists, students, trainees, and allied healthcare professionals working in primary care.

“[Dermatology] makes up a large part of a GP’s workload…, yet it’s kind of grossly neglected in both undergraduate and postgraduate training,” said Dr Buckley. “So again this will hopefully address that imbalance.”

“The demand for skin, hair, and nails [care] is ever increasing but hopefully so are the skills of GPs,” Dr Buckley added, “and maybe they could manage more and more skin problems in primary care, then obviously that would free up the dermatology clinics for looking after people with very severe or refractory skin conditions that we can’t manage in primary care.”

Cryosurgery, its side-effects and how to avoid them

Although there are side-effects to cryosurgery, practitioners should not be deterred from using the technique, as it is a quick and successful treatment for a broad range of skin lesions, the 2022 PCDSI Annual Meeting heard.

Dr Paula Pasquali, Consultant Dermatologist, Pius Hospital de Valls, Tarragona, Spain, spoke about expectations in cryosurgery, possible side-effects and how to avoid them. “I think that every surgical procedure [can have] complications,” said Dr Pasquali. “And that you should be aware of them.”

Communication with patients is important, to inform them of issues with hyper- or hypo-pigmentation, and any scarring or pain that may occur.

“Depressed scars can happen especially and mostly when you do cryosurgery that are

very deep. This happens if you’re treating skin cancer,” said Dr Pasquali. The hair follicle can also be destroyed in this instance and hair will no longer grow in the area.

Cryosurgery can be painful, it should be acknowledged. “When you do cryosurgery, you have a first peak of pain and then it starts coming down. And then suddenly, you have a second peak,” Dr Pasquali said. If a patient is sent out of the office before the second peak of pain has occurred, there is a risk of a patient fainting later on.

Liquid nitrogen spattering can contribute to pain and other complications.

Performing cryosurgery around the eye may result in liquid nitrogen spraying into the conjunctiva so caution and care are needed.

“It usually heals very well,” Dr Pasquali added. She recommended protecting the eye

using a plastic or wooden piece.

There is also a risk of insufflation of the subcutaneous tissue, where liquid nitrogen spray can get under the skin tissue after a lesion has been curetted. This is harmless and can be identified by a “crunching” noise under the skin, which can alarm patients.

Dr Pasquali recommended using a probe or a rubber cone to “fix it on the area very closely so that you seal around the area, and then you can freeze”.

After curetting a lesion and performing cryosurgery, Dr Pasquali advised to let the site thaw fully before letting a patient leave, as bleeding can occur afterwards.

Other common after-effects that can occur after cryosurgery include oedema, bullae, and mummification of the lesion.

Rise in contact dermatitis in healthcare staff during the pandemic due to increased PPE use

The extensive use of personal protective equipment (PPE) by healthcare workers during the Covid-19 pandemic has contributed to a concurrent rise in contact dermatitis in this cohort in the last two years, according to Dr Johnny Bourke, Consultant Dermatologist, South Infirmary Victoria University Hospital, Cork.

“Within a few weeks of shut down, masks, gloves, and handwashing, we had a flood of staff with problems with their hands and with their face,” said Dr Bourke.

Initially, there were concerns that components of the masks were causing allergic dermatitis, with some evidence internationally of allergic dermatitis to components of masks including nickel, foam and rubber. However, from Dr Bourke’s experience and patch testing of staff, the “vast majority were not allergic dermatitis”, which was the experience nationally and internationally.

“Almost all of the dermatitis from the masks was irritant contact dermatitis,” said Dr Bourke. Staff not being used to wearing masks as often as was necessary in the pandemic, and the heavier duty FFP2 and FFP3 masks contributed to this.

Severe irritant contact dermatitis was seen in those working in ICU, where erosions occurred on the nose. However, this has lessened in recent times as people have gotten used to wearing masks, he noted.

Contact dermatitis was also seen on the hands of other workers, and while there was some allergy to gloves and fragrances and preservatives in soaps, “the vast majority” of cases were contact dermatitis from increased hand washing with soap and water, according to Dr Bourke.

The issue proved difficult to treat as increased handwashing was mandatory in healthcare settings. “We could not get them to use

emollients to wash their hands with at work,” said Dr Bourke. He was successful in getting staff to use emollients at other times, such as at night and encouraged them to use alcohol gels instead of soap and water. “It is an ongoing problem and we still are seeing a good bit of it,” he added.

Dr Bourke has also seen an increase in occlusive acne from the wearing of masks, which was “probably caused by a combination of sweaty atmosphere, people were prone to acne anyway, and using thick, greasy emollients on their face to protect themselves from their mask”. This acne needed treatment, both with topical and systemic antibiotics and “all the way up to Roaccutane [isotretinoin] occasionally”.

Questioned on whether ‘mask-ne’ is much less common than thought by the public, Dr Bourke said mask-ne “is a real thing and it is a problem and you just have to treat it... as acne and it has to be treated traditionally and reasonably aggressively.”

Genital psoriasis often goes under-reported and under-treated

Genital psoriasis often goes under-reported and under treated in primary care, the 2022 PCDSI Annual Meeting heard.

HSE National Clinical Lead for Dermatology

Prof Anne Marie Tobin, Consultant Dermatologist, Tallaght University Hospital, spoke about diagnosis and treatment of psoriasis in primary care, including more unusual sites.

She said GPs should recognise that genital psoriasis “can have a significant impact on their [patients’] quality-of-life.” She also recommended that when a patient presents with scalp psoriasis, to “always remember to

ask: ‘do you have psoriasis anywhere else?’ And ‘do you have it in your groin?’”.

It can be treated with “mild-mid” potency steroids such as hydrocortisone or clobetasone (Eumovate), the latter of which she would start with.

Prof Tobin also covered psoriasis of the scalp and the need to descale using an emollient before applying a potent topical steroid.

She also spoke about palmo-plantar psoriasis, marked by thickening of the skin with erythema, which can cause fissuring. This should be treated with “thick, greasy

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emollients” to prevent cracking. Prof Tobin noted that palmo-plantar psoriasis “is difficult to treat with topical treatment and often patients will require treatments in secondary care”.

Nail psoriasis causes lifting of the distal nail plate, and where nail psoriasis is aggressive, a fungal infection is “very common”, Prof Tobin added. Psoriasis at the nail site can

be aided by keeping the nails clipped short and treated by a clobetasol propionate (Dermovate) or Betnovate scalp application overnight or Xamiol gel for two days a week for six months.

Dr Tobin also highlighted the importance of informing patients that “psoriasis isn’t curable, but it can be controlled and we can control it so it has minimal impact on your life”.

“All patients with psoriasis should use an emollient,” she added. “It reduces the scaling and the fissuring of the cracks. Because when the cracks fissure, they’re incredibly painful and itchy.”

In a separate presentation at the meeting, Prof Tobin spoke about rashes involving the flexures and their treatment in primary care.

‘Pearls of wisdom’ for bacterial skin infection in primary care

During the PCDSI 2022 Annual Meeting, Dr Alana Durack, Consultant Dermatologist, University Hospital Waterford, gave her “pearls of wisdom” for encountering bacterial skin infection in primary care.

“Common things are common,” said Dr Durack. “But it’s important to swab anyways so you’ve got something to back up if the antibiotics aren’t working or the patient’s not getting better.”

For example, with an impetigo, a superficial skin infection that occurs in bullous and nonbullous form, the latter of which can form a crust. “When there’s a lot of crusting it’s very easy to miss an underlying [herpes simplex

virus] HSV infection,” said Dr Durack. “With those kind of things I think it’s always sensible to think about taking a swab for HSV as well as bacterial swab.”

Her second pearl was about the importance of considering underlying viral infections, including HSV and varicella zoster virus (VZV), using the “red swabs” when conducting PCR tests.

“Give the full clinical details on the request to microbiology,” she advised. “The more information you give, the better advice that you get back.” She advised including details like where on the body the sample is from, if the wound is surgical or not, or if the wound is contaminated.

While Panton-Valentine leukocidin (PVL) staph infection is not common, it’s important to consider it, according to Dr Durack. PVL staph is a “highly pathogenic staph strain”, that’s “often recurrent and… not so easy to clear”.

“Microbiology are always available for advice if needed,” she covered in her last point. “So it’s always helpful sometimes to just pick up the phone and just get an opinion.”

“The most common infections, globally, regardless of age or geographical location are staph and strep[tococcal] infections,” said Dr Durack.

Dermatological ‘infestations love a pandemic’

There was a rise in dermatological infestations (scabies, lice, etc) during the pandemic, and also increased research around treatment, according to Dr Fiona Browne, Consultant Dermatologist, Crumlin Children’s Hospital and Children’s University Hospital, Temple Street.

“We’ve learned that infestations love a pandemic,” according to Dr Browne.

This spike in scabies and other infestations

was not anticipated, but was also seen internationally.

“It really highlights the opportunity for these infestations to take over when we are in enclosed environments, when people are not able to isolate,” said Dr Browne.

When compared to Crumlin there was also more cases recorded in Temple Street in Dublin city centre, according to Dr Browne.

Talk of “super-infestation” of scabies raised concerns that a resistance had been built up against permethrin, however, a study published in December 2021 in Dermatologic Therapy (‘Is there a really resistance to scabies treatment with permethrin?’) showed that there was no evidence for this.

“Rather then, the likelihood is that patients are just not treated appropriately,” said Dr Browne.

A study published last month in The Journal of Paediatrics (‘Comparison of permethrinbased treatment strategies against scabies in infants and young children’) showed a higher cure rate in patients treated with permethrin on their full body overnight on days one, eight, and 15 of treatment, with an added application of permethrin on the patients’ hands and feet every second day during this period. “At the moment we ask to apply and leave overnight and then repeat the treatment one week later [days one and eight],” said Dr Browne.

“We’ve always reminded patients that when you’re doing scabies treatment after handwashing and to reapply to the feet. So, clearly these are the sites particularly in children that are missed and by adding that extra treatment days to those sites alone you can achieve almost twice the cure [rate].”

Ivermectin, which is currently licensed for children “over the weight of 15 kilos and in adults”, is also suitable for children under 15 kilos, according to two large

studies referenced by Dr Browne: One published in 2021 in The Australasian Journal of Dermatology (‘A narrative review of the roles of topical permethrin and oral ivermectin in the management of infantile scabies’); and in 2019 in The British Journal of Dermatology (‘Ivermectin safety in infants and children under 15kg treated for scabies: a multicentric observational study’).

“It’s not licenced [for this indication], but it does appear to be safe,” said Dr Browne.

Most common skin issues in skin-of-colour

Dermatological issues in skin-of-colour have become more recognised in dermatology in recent years, due to recent political and social issues and acknowledgement that the area has been neglected, the 2022 PCDSI Annual Meeting heard.

Dr Daniel Creamer, Consultant Dermatologist, King’s College Hospital London, presented on the topic of dermatology in skin of colour, and said “it is a topic that is rising up the agenda”.

“It really does warrant attention, in terms of our interest and research and perhaps allocation of resources,” he added.

Dr Creamer spoke about some of the most common skin conditions suffered by people of colour including vitiligo, an

acquired depigmenting skin disorder where white patches develop on the skin, which is one of the most prominent.

“It is up until recently a disorder we’ve struggled to treat affectively,” said Dr Creamer. However, he highlighted that there have been recent developments in JAK inhibitors, like tofacitinib, which appear to be effective in treating vitiligo, both when taken orally or topically, according to some recent studies.

Tinea capitis, a fungal infection of the scalp, is also extremely common in Afro-Caribbean children, generally of primary-school age, in what Dr Creamer called an “epidemic” in south-east London. It can be treated with terbinafine, however; “you have got to treat all the friends and the schoolmates and the

siblings as well,” Dr Creamer added, as it is highly contagious.

Central centrifugal cicatricial alopecia (CCCA), a form of scarring alopecia on the scalp that results in permanent hair loss, is most common in middle-aged women, and is no longer considered self-inflicted from styling routines, Dr Creamer noted. Recent research has shown CCCA to possibly be a genetic disorder.

Dr Creamer described the condition as “tricky” to manage. “It seems to be hidden away and then middle-aged women present having suffered it a decade or so, and by that stage, very little can be done,” he added. If CCCA is recognised early, it should be treated with clobetasol propionate (Dermovate).

Primary and secondary care dermatology benefit from PCDSI education

Education on dermatology not only aids primary care practices, but also secondary care, according to Clare GP and committee member of the PCDSI, Dr Finbar Fitzpatrick.

For the second year in a row, the PCDSI’s Annual Meeting took place virtually (4-5

March) with over 200 attendees logging in to access presentations from leading national and international dermatology experts on a wide range of topics, however, the PCDSI Annual Meeting 2023 is set to go ahead in person. “At this stage in the post-Covid environment we’re missing a

little bit of the human interaction to keep the society thriving,” Dr Fitzpatrick said. “And there is an educational element that you get from meeting in person that you don’t get online. So we’re looking forward to having that in addition to the education next year.”

When asked about the importance of healthcare professionals in primary

care being able to properly diagnose and treat dermatological issues, Dr Fitzpatrick highlighted that 10 per cent of presentations in general practice involve “some dermatology or skin disease”, which rises to 20 or 30 per cent if that GP has a special interest in dermatology.

“There [are] also occasionally inappropriate referrals to secondary care for skin conditions that could be very easily managed in general practice,” he added. “There’s a lot of very common skin conditions that are most appropriately managed in general practice. We’re trying to improve education on that front.”

Similarly, the PCDSI is aiming to improve

recognition of rarer conditions so that those are referred on appropriately to secondary care with a clarification on the likely diagnosis.

“There is difficulty accessing secondary care, publicly, primarily and to an extent privately,” said Dr Fitzpatrick. He added this can cause issues regarding waiting lists for issues that do require secondary care.

“It’s really educating in dermatology and primary care improves the quality of care in general practice and also improves the rate of appropriate referrals to secondary care.”

Dr Fitzpatrick also highlighted the high standard of primary care in Ireland when compared internationally.

Eczema burden often underestimated

Eczema is a far more debilitating condition than often portrayed with multiple negative impacts on patients and caregivers, thus its burden should not be underestimated, the 2022 PCDSI Annual Meeting heard.

Dr Maeve McAleer, Consultant Dermatologist, St James’s Hospital, Dublin, and Children’s Health Ireland, and noted researcher in paediatric eczema, gave a comprehensive talk on the presentation, aetiology, impact and treatment of eczema (aka atopic dermatitis).

Atopic eczema causes a dry, red, itchy rash; it may be scaly, weep, bleed or crust over, and the condition affects one-in-five children and one-in-10 adults. The hallmarks are intense itch, associated discomfort and pain, and skin inflammation. These symptoms interfere with sleep, the ability to perform day-to-day activities, school performance, ability to work, and are associated with social stigmatisation, Dr McAleer noted. She highlighted a number of studies showing the significant impact of eczema on children and their families, and also touched upon some of the longer-term health (cardiovascular and psychiatric) risks of eczema.

One of the key building blocks of a healthy skin barrier is a protein called filaggrin, which is defective in patients with eczema, Dr McAleer explained, adding that twothirds of eczema patients have one or more filaggrin mutations.

Disease triggers in eczema include climate, irritants (wool/rough fabrics, detergents, and fabric softeners, etc), environmental and food allergens, while patients with eczema are more susceptible to superimposed cutaneous infections (staph aureus, chicken pox, warts, etc). Eczema in babies often starts on the cheeks and is associated in many cases with food allergy.

A general approach to first-line management of eczema includes (detailed) patient education, daily bathing, emollient use, appropriate strength topical corticosteroid use, and treatment of any complicating infection, she outlined.

Discussing the use of emollients, Dr McAleer said they should be used once to twice daily, be free of dyes, fragrances, and food-derived

allergens, and she advised decanting with a spoon to avoid recurrent infection risk.

She noted that aqueous cream has been shown to irritate the skin of both healthy subjects and those with eczema, yet it remains the most commonly prescribed emollient in the UK.

Discussing once-daily topical corticosteroids, Dr McAleer recommended the use of ointments over creams, as they have a higher concentration of lipids, less preservative and increased efficacy. The potency should be tailored to the individual’s eczema severity and body site, with a proactive (rather than reactive) approach taken using daily moisturising and a mild to moderate steroid intermittently, with a step-up treatment approach of seven-to-14 days for flares.

Oral JAK inhibitors are being shown to have a positive impact, with a rapid onset and high rate of efficacy, on more severe disease, but longer-term studies are needed to determine their risk benefit profile, she concluded.

Managing acne in general practice

Acne is a very common, chronic inflammatory skin disease. It occurs in 90 per cent of teenagers and half of them continue to have acne as adults. About 20 per cent of young people have moderate or severe acne.

Acne is probably the most common dermatology problem seen in general practice. The diagnosis is usually obvious and the treatment for the majority of patients is simple and straightforward. Despite this, many patients still struggle to manage their acne, which occurs on the worst part of their body (face) at the worst time of their life (teenagers and young adults). Left untreated or partially treated, acne may lead to physical and/or psychological scarring.

THERE ARE FOUR MAIN MECHANISMS IN THE AETIOLOGY OF ACNE:

A. Excessive production of sebum (under hormonal control).

B. Follicular plugging causing micro-comedones and comedones.

C. Overgrowth of micro-organisms especially C. acnes (formerly Propionibacterium acnes), which causes release of inflammatory cytokines.

D. Inflammation causes the pylosebaceous cyst wall to rupture, resulting in an intense foreign bodylike reaction, which leads to further development of inflammatory lesions (papules, pustules, nodules, cysts).

Pathophysiology

Acne is a disease of the pilosebaceous unit. There are four major contributing factors ( Table 1). It usually occurs at puberty or in early adult life when there is a surge of hormones. Patients with acne do not usually have too much or too little hormones (apart from polycystic ovary syndrome (PCOS) patients).

The problem with acne sufferers is end-organ hypersensitivity to the normal fluctuations in hormones that occur at this time of life and this may be genetically determined. This causes the pilosebaceous unit to overproduce oil-leading to blocked pores called ‘comedones’. Comedones may be almost invisible (micro-comedones), closed comedones (whiteheads) or open comedones (blackheads). These comedones become colonised by the commensal bacteria known as Cutibacterium acnes (C. acnes), which causes

inflammation in the area, resulting in the inflammatory features of acne such as papules, pustules, cysts or nodules ( Photo 1 and Figure 1).

Treating the inflammatory features of acne with oral or topical antibiotics without treating the underlying problems of excess oil and comedones will only partially help and the patient will relapse quickly once the treatment is stopped.

Topical treatments

The first-line treatment for acne sufferers should be to tackle the excess oil and comedones ( Photo 2). Acne washes containing salicylic acid, 0.5to-2 per cent, may help. However, most patients will also need a topical retinoid such as topical isotretinoin (eg, Isotrex), or a retinoid-like agent such as adapalene (eg, Differin Gel), or a combination of a retinoid-like agent such as adapalene with benzoyl peroxide (eg, Epiduo).

These topical agents can be irritating and patients need careful counselling on how to use them properly. These products should be put all over the acne-affected areas and not just onto the individual spots since they are designed to reduce oil production, prevent the build-up of comedones, and avoid the development of papules and pustules. These agents should be applied sparingly on alternate nights for the first week or two until the patient gets used to the drying effects before increasing to nightly use.

Some patients may need to use a lightweight, non-greasy, non-comedogenic moisturiser in the morning to counteract the drying effects of topical retinoids or retinoid-like agents.

Patients with sensitive skin or a history of eczema may not be able to tolerate these topical agents and may have to try a less irritating topical treatment such as azelaic acid 20 per cent (Skinoren Gel) instead.

These topical retinoids and retinoid-like agents are very slow to work. It can take weeks or months to see an improvement in the acne. Results can be enhanced by

logical combinations such as a topical retinoid or a retinoid-like agent in association with an anti-inflammatory agent such as benzoyl peroxide (BPO) or antibiotics either topically or orally ( Table 2).

BPO, like topical retinoids and retinoidlike agents, can be quite irritating and should be used sparingly and on alternate days initially before increasing to daily use. Because BPO is cheap and available without prescription it is sometimes used first-line on its own with an antiacne wash when there is primarily inflammatory acne without too much oiliness or comedones. BPO is also useful as it does not make the patient sensitive to sunlight and it can be used in pregnancy. In addition, it can be useful for treating large areas such as the back and chest as it comes in relatively large tubes (eg, Acnecide Gel 60 grams). Apart from its drying effects, the other disadvantage of BPO is that it can bleach clothing so it is best to advise patients to apply it at night and if they are putting it on their chest or back they should use a white T-shirt at night, white sheets, white pillowcases, and white towels.

B. MILD

Continue A. and add in:

 Comedonal acne: Topical retinoid or azelaic acid

 Inflammatory acne: BPO or topical antibiotics*

For mixed type acne use combinations of above

Topical retinoid = adapalene or isotretinoin

BPO = benzoyl peroxide

Oral antibacterial agents = lymecycline, doxycycline or erythromycin

A. ALL CASES

Use a salicylic acid wash; avoid oily products and no picking

C. MODERATE

Continue with A. and B. and add in oral treatments: eg, anti-bacterials x 3-6 months (+/- anti-androgens x 6-12 months in females)

D. SEVERE

Refer for Roaccutane

Anti-androgens = Dianette, OCP containing progestins with anti-androgenic properties (eg, drospirenone, chlormadinone acetate) or spironolactone

*Topical antibiotics should only be used for a maximum of 12 weeks, never with oral antibiotics

BPO does not have any anti-comedonal effects so it is best used in combination with topical retinoids or retinoid-like agents for more moderate-severity acne, especially if there are many comedones.

For most patients with acne, combining BPO with adapalene (a retinoid-like agent) such as Epiduo Gel is very convenient as it only has to be applied once at night all over the acne-affected areas of the face and neck. However, this combination of two potentially irritating agents can be drying and somewhat irritating, especially at the start of treatment. Applying it alternate nights for the first week or two can help with the irritation and most patients can then increase up

CURED

(33% may relapse)

to nightly use. One bottle (45g) should usually last two-to-three months when applying it to the face. If this combined agent causes too much irritation it might be necessary to apply a topical retinoid or retinoid-like agent such as topical isotretinoin or adapalene at night and BPO in the morning, but this involves twice-daily treatments, which may reduce compliance, especially in men.

BPO can have as good an anti-bacterial effect on acne as topical antibiotics without the risks of developing resistance. It has the advantage over topical antibiotics in that it can be used longterm for weeks, months or years without losing its effect.

Patients with more moderate to severe acne may need an antibiotic added to the above mentioned topical treatments to get the acne under control ( Table 3). While topical antibiotics offer some antibacterial effects, resistance can develop quickly and they are only licensed to be used for three months, which is a very short time in an acne sufferer’s life. Acne can lasts years, not months, so topical antibiotics have a very limited role in the overall management of acne.

Systemic treatments

Oral antibiotics used for a maximum of three-to-six months have useful antibacterial effects, but products such as lymecycline 405mg daily or doxycycline

ECZEMA,

DRY, VERY DRY, ROUGH AND CRACKED SKIN.*

OILY, BLEMISHED AND ACNE PRONE SKIN.

HYPERPIGMENTATION AND MELASMA.

100mg daily also have powerful antiinflammatory effects, which is probably their primary mechanism of action in acne. However, like BPO, antibiotics have no anti-comedonal effects, so they should never be used alone to treat acne. It is best to combine antibiotic treatments with anti-comedonal treatments such as topical retinoids or retinoid-like agents. The combination of a topical retinoid or a retinoid-like agent with an oral antibiotic for three-to-six months should clear up 90 per cent of acne in 90 per cent of patients who can tolerate this treatment. Lymecycline is usually the first-line systemic treatment as doxycycline occasionally causes photosensitivity or oesophagitis. Tetracyclines should not be used in children under the age of 12 years.

Acne is a chronic disease

Acne should be considered a chronic disease. Like many other chronic diseases such as asthma or rheumatoid arthritis, treatment should be aimed at settling the acute symptoms (papules, pustules, nodules and cysts) and preventing relapse. Once the patient’s acne is under control (90 per cent or clearer) they can stop their oral therapy, but should continue with their topical retinoids or retinoidlike agent indefinitely to prevent relapse until such time as they are convinced that they have grown out of their acne. This can be months or years if necessary. Oral tetracyclines and topical retinoids or retinoid-like agents should be avoided in pregnancy. BPO and erythromycin 500mg twice a day for three-to-six months are safe in pregnancy if required for troublesome acne.

Adapalene (a topical retinoid-like agent) combined with BPO (Epiduo Gel) is a very useful product as it can be used both to control acute flare ups of acne (with a course of oral antibiotics for three-to-six months if necessary) and it can also be used as a maintenance treatment once the acne is under control to prevent relapse. With these combinations it may be possible to explain to the patient

INDICATIONS FOR ORAL ISOTRETINOIN (ROACCUTANE)

 Severe nodulocystic acne

 Acne unresponsive to standard oral and topical treatments especially if scarring

 Acne relapsing after repeated courses of oral and topical acne therapies

 Acne associated with severe psychological upset

 Gram-negative folliculitis

 Conglobate acne

 Acne fulminans

 Pyoderma faciale

how to manage the acute phase of their moderately-severe acne (eg, Epiduo Gel and an oral anti-acne tablet for threeto-six months) and the maintenance treatment (eg, stop the tablet and use Epiduo Gel alone) in one single visit.

Lifestyle, cosmetics, and medication

Acne is primarily hormonally driven. However, poor diet, inappropriate use of cosmetics, stress and picking can all aggravate acne. There is some evidence that excessive sugar and excessive dairy in the diet may aggravate acne. When seeing a young person with acne it is a good opportunity to give them lifestyle advice about diet and exercise. Try to talk directly to the young teenager who comes with their parents. Encourage them to stay on a low-sugar diet and they should be encouraged not to consume excessive dairy products. Protein powders that are used for sports or bodybuilding should be avoided as they contain excessive amounts of whey protein and often make acne worse. While there is no hard evidence that exercise helps acne, it is a good opportunity to advise young people to take vigorous physical exercise for one hour at least five

times a week, which may help their overall health and feeling of wellness.

Young women in particular are bombarded with misinformation about skin care and cosmetics. They are encouraged to “cleanse, tone and moisturise” even if they don’t need it. Moisturising already oily, acne-prone skin is like “adding fuel to the fire”. Young people should be informed that moisturising does not prevent wrinkles or ageing of the skin. However, some acne cleansers and topical acne treatments may dry the skin, so some patients may need a light-weight, oil-free, noncomedogenic moisturiser in the mornings to control the drying effects of their acne treatments. Make up and sun blocks should be oil-free and non-comedogenic.

Underlying hormonal issues, such as women using ultra-low-dose oestrogen combined contraceptive pills, progesterone-only pills, progesterone implants or progestogen containing intrauterine devices (IUDs) (eg, Mirena or Kyleena) may aggravate acne. Women with resistant acne or acne with signs of other hormonal problems such as irregular periods, obesity or hirsutism should be investigated for PCOS. Women with PCOS and acne may do well with hormonal treatments such as the contraceptive pill Dianette for up to 12 months or spironolactone (a diuretic that has been used off-label in women with acne for over 30 years due to its antiandrogenic properties) (50-100mg daily), which can reduce oil production and comedones. These hormonal treatments are best combined with topical antiinflammatory agents such as BPO or azelaic acid. Women on spironolactone should not become pregnant, due to potential risk of birth defects.

Patients with severe nodulocystic acne, scarring acne, and acne that does not respond or relapses as quickly to six months of an oral anti-acne agent combined with appropriate topical agents

as outlined above may need a course of oral isotretinoin (Table 4). This should only be prescribed by doctors with experience of prescribing systemic retinoids (eg, GPs with a special interest in dermatology or consultant dermatologists). 

Our new book, Textbook of Primary Care Dermatology (Buckley D, Pasquali P, 2021), has just been published by Springer and it has a number of chapters on acne including ones on oral isotretinoin and PCOS. It is currently on special offer from Springer at https://link. springer.com/book/10.1007/9783-030-29101-3 with 20 per cent off the recommended retail price until 5 April 2022 by putting the following code PrimaryCare20 when ready to pay at the ‘Place your order’ page when ordering online.

References

1. Dawson AL, Dellavalle RP  Acne vulgaris. BMJ. 2013; 346:f2634

2. Bhate K, Williams HC. Epidemiology of acne vulgaris. Br J Dermatol. 2013; 168(3):474-85

3. Mallon E, Newton JN, Klassen A, et al. The quality-of-life in acne: A comparison with general medical conditions using generic questionnaires. Br J Dermatol. 1999; 140(4):672-6

4. Teen Acne Survey; Harris Poll. Conducted between July 13 and 31, 2017 by  www.theharrispoll.com/

5. Grossi E, et al. The constellation of dietary factors in adolescent acne: A semantic connectivity map approach. J Eur Acad Dermatol Venereol. 2016 Jan; 30(1):96100. doi: 10.1111/jdv.12878

6. Nast A, et al. European evidence-based (S3) guideline for the treatment of acne

– update 2016 – short version. J Eur Acad Dermatol Venereol. 2016 Aug;30(8):1261-8.

doi: 10.1111/jdv.13776

7. Henehan M, Montuno M, De Benedetto A. Doxycycline as an anti-inflammatory a gent: Updates in dermatology. J Eur Acad Dermatol Venereol. 2017,31,1800-1808. doi: 10.1111/jdv.14345

8. Tan J, Humphrey S, Vender R, et al. A treatment for severe nodular acne: A randomised investigatorblinded, controlled, non-inferiority trial comparing fixed-dose adapalene/BPO plus doxycycline vs oral isotretinoin. Br J Dermatol. 2014;171:1508-16

9. Buckley D, Yoganathan S. Can oral isotretinoin be safely initiated and monitored in primary care? A case series. Ir J Med Sci. 2017 Jan 9. doi: 10.1007/s11845016-1540-5

10. Gollnick H, Cunliffe W, Berson D, et al. Management of acne: A report from a global alliance to improve outcomes in acne. J Am Acad Dermatol. 2003 Jul;49 (1 Suppl):S1-37

Update on the HSE Dermatology Model of Care

The Dermatology Model of Care for Ireland was launched by the HSE National Clinical Programme for Dermatology in March 2021.

Dermatology accounts for the third most numerous medical specialty in terms of outpatient appointments. The lives and care of patients diagnosed with skin cancers and inflammatory skin diseases has improved significantly due to advances in diagnosis and treatment, increases in the dermatology workforce, and structural developments like rapid access clinics for pigmented skin lesions. In addition, improvements in

diagnosis is the key to determining the most effective management procedures, particularly in relation to conditions such as skin cancer, psoriasis, and hidradenitis suppurativa (HS).

The secondary care will be provided through outreach clinics locally in peripheral hospitals, supporting the local network of GPs. New outreach clinics are planned for Midlands Regional Hospital Portlaoise, Midlands Regional Hospital Tullamore, and Mallow General Hospital. These outreach services will be

The Programme has also recommended the appointment of advanced nurse practitioners (ANPs) to dermatology departments to specifically support dermatology patients. Infrastructure is also required at key sites in South Infirmary Victoria University Hospital in Cork, and University Hospital Galway.

The Programme is also working with the ICGP to produce a practical dermatology module and recommends ongoing investment in dermatology and healthrelated research and national structures to support research delivery and impact for Irish patients. 

Log on to www.hse.ie/eng/about/who/cspd/ ncps/dermatology/resources/national-clinicalprogramme-for-dermatology-a-model-of-carefor-ireland.pdf for the full text of the Model of Care.

education, public information, technology and healthcare prevention have all helped facilitate improved care.

The Model of Care envisages close collaboration between GPs and local dermatology departments in a series of Dermatology Clinical Networks to deliver person-centred and integrated care. The Model is based on a ‘hub and spoke’ model with dermatology departments providing outreach clinics in peripheral hospitals and is both aligned to Sláintecare and international best practice.

Most dermatology conditions are managed in primary care, but for patients who require secondary care, timely and accurate

supported by dermatology department hubs in teaching hospitals with outpatient departments, patch testing, management of complex skin diseases, surgery for skin cancer, and multidisciplinary team care, which will provide care for chronic skin diseases and skin cancers.

An 11.5 additional consultant dermatologist posts recommended in the Model of Care will need to be appointed to meet a desired ratio of one-per-80,000 population, aligning towards international best practice. It is proposed that the additional consultants would be recruited over the next five years and contracts would be designed to facilitate the hub and spoke Model of Care delivery.

The Model is based on a ‘hub and spoke’ model, with dermatology departments providing outreach clinics in peripheral hospitals and is both aligned to Sláintecare and international best practice

Psoriasis: An overview

Psoriasis is a chronic immune-mediated inflammatory skin disorder, affecting at least 100 million people worldwide. A 2015 report (Burden of Psoriasis in Ireland: Epidemiology, Quality-of-Life, Co-morbidities and Treatment Goals) suggests that there are 73,000 people with psoriasis in Ireland, estimating a prevalence of close to 2 per cent of the Irish population. Within this figure it is suggested that 12.4 per cent present with a severe form of this disease.

Presentation

Psoriasis can appear at any age, but most commonly occurs with an initial peak between the ages of 18 and 35 years of age, with a subsequent peak at age 57 to 60 years. It affects males and females equally.

Plaque psoriasis (psoriasis vulgaris), affects approximately 90 per cent of people with psoriasis. Plaque psoriasis is characterised by erythematous scaly plaques with welldefined edges. The plaques can vary in number and size and affect any part of the skin surface. It most often occurs in a symmetrical pattern on extensor surfaces of the knees, elbows, scalp, and trunk.

Guttate psoriasis is the second most common form of psoriasis. The word ‘guttate’ comes from the Latin for ‘drop’ ( gutta). This type of psoriasis occurs more commonly in adolescents or young adults. Onset is sudden, with the widespread appearance of small ‘ drop-like’ patches, usually on the trunk and limbs and can be preceded by a streptococcal throat infection.

Inverse psoriasis occurs on flexural surfaces including the armpits, groin, under the breast and in skin folds. The plaques are usually smooth without scaling due to the moist nature of the area.

Painful superficial fissures sometimes occur in skin creases.

Scalp psoriasis is one of the most common sites to be affected by psoriasis, and sometimes the only area of involvement. It can extend to, or just beyond, the hairline and commonly occurs behind the ears. Almost 80 per cent of people with psoriasis will have scalp involvement at some point in their lives, and it is not unusual for the scalp to be the first site of disease involvement.

Nail psoriasis can affect the nails of both hands and feet. Changes may include thickening, onycholysis, changes in colour, and the appearance of pits. Nail changes are often associated with psoriatic arthritis.

Pustular psoriasis presents as an eruption of sterile pustules, generalised and extensive or localised to existing plaques. The diffuse variant is known as von Zumbusch variant, an uncommon severe form of psoriasis accompanied by fever, oedema, malaise and widespread pustules. Palmo-plantar pustulosis is characterised by pustules confined to the hands and feet, with scaling and pruritus. This painful and debilitating form of psoriasis can severely limit everyday activities.

Erythrodermic psoriasis describes instances where almost the entire body surface is involved, and is characterised by erythematous skin with diffuse, fine, peeling scale. Some patients may experience fever, chills, and fatigue and in some cases it can be life-threatening, requiring hospitalisation.

Pathophysiology and risk factors for the development of psoriasis

Psoriasis is a complex multifactorial condition and three central factors contribute to its development. These include abnormal immune system responses, genetic predisposition, and environmental factors.

Recent research has shown evidence that psoriasis is a cell-mediated inflammatory disease, mainly induced by pathogenic T-lymphocytes and dendritic cells. An immune response is triggered and is defined by the release of certain cytokines, including tumour necrosis factor (TNF), interleukin (IL)–12, IL–23, IL–17, and

Psoriasis can tend to run in families and in excess of 40 genetic susceptibility loci have been recognised

interferon gamma. This inflammatory reaction triggers the hyper proliferation of keratinocytes, resulting in cells being forced to the skin surface where they accumulate. This process of inflammation then attributes to erythematous plaques covered in silvery scales.

Psoriasis can tend to run in families and in excess of 40 genetic susceptibility loci have been recognised. Different types of the same gene are called allele. Psoriasis susceptible alleles, in particular one called HLA-Cw6, are thought to be associated with early-onset psoriasis and guttate lesions.

Environmental factors can also play a role in those who are susceptible. In some cases emotional stress, obesity, injury to the skin also referred to as Koebner phenomenon, infection (streptococcal), HIV infection, withdrawal of corticosteroids, and certain medications such as lithium, beta-blockers and antimalarial medication can trigger the first episode of psoriasis or exacerbate it. Certain lifestyle factors such as alcohol consumption and smoking may worsen it.

Assessment and management of psoriasis

Treatment decisions are based on disease activity, impact of the disease on the patient’s quality-of-life, co-morbidities, and the requirement for referral to specialist care.

Although there is no cure yet, there are a range of effective treatment options available depending on severity and location. The severity of psoriasis is categorized into mild, moderate or severe. The global rating scale is a tool used to evaluate the extent of the disease according to the body surface area (BSA). The categories of psoriasis are classified as mild (BSA ≤ 3 per cent), moderate (BSA 3-to-10 per cent) and severe (BSA ≥ 10 per cent) and treatment is decided by disease severity. The BSA does not assess clinical features of the disease such as erythema, scale and thickness of the plaques, therefore a common and

beneficial tool in assessing disease severity in the dermatology clinical setting is the Psoriasis Area and Severity Index (PASI).

The PASI generates a score from visual estimation, including erythema, thickness of plaques, and scaling present on head, trunk and limbs, to generate a score from one to usually >30. A PASI <10 may be considered mild, and >10 moderate-tosevere psoriasis. This tool is beneficial in assessing disease severity and is also used to monitor treatment response.

A really useful health-related quality-of-life measurement tool used in clinical practice is the Dermatology Life Quality Index (DLQI). This tool is not psoriasis specific, however it helps clinicians to assess the impact of psoriasis on the person’s life. The DLQI consists of 10 questions grading the impact psoriasis is having physically, emotionally, socially, and sexually. It also assists the clinician to measure effectiveness of treatments. DLQI scores range from 0 (no impairment of quality-oflife) to 30 (maximum impairment).

UK National Institute for Health and Care Excellence (NICE) guidelines recommend referral from a non-specialist setting for a dermatology specialist consultation if; more than 10 per cent of the BSA is affected, psoriasis cannot be controlled with topical therapy, it requires phototherapy, the patient has nail psoriasis that has a major functional impact, and in cases of psoriasis that have a major impact on a person’s physical, psychological or social wellbeing, and where there is uncertainty around diagnosis.

Topical treatments

Topical treatments are typically used when psoriasis is mild to moderate and may be prescribed alongside other therapies. When used as directed, advantages of topical treatments include that lesions are directly targeted, and it is safe, effective, and well-tolerated. However, disadvantages of topical treatments may include that application is time-consuming and inconvenient, fear

of side-effects, and some treatments can be greasy and malodorous in application and can cause staining of clothes and linen. Due to these factors, patients’ adherence to topical therapy can be suboptimal. It is important that patients are educated with verbal and written instructions to support the safe and successful use of these treatments in the long-term and to set realistic expectations.

Depending on site and type of psoriasis, topical treatments include emollients, topical corticosteroids, vitamin D analogues, coal tar, dithranol, and calcineurin inhibitors. Some of these treatments are used as monotherapy or in combination with other agents.

Phototherapy

This is the mainstay of treatment for moderate-to-severe psoriasis. Phototherapy is a form of artificial ultraviolet (UV) light treatment, comprised of either UV A (UVA) or UV B (UVB) wavelengths of light, delivered in hospital dermatology day care centres. Narrowband UVB is the most common type of phototherapy used to treat psoriasis and is usually given three times a week. Another form of phototherapy used is called PUVA. UVA must be combined with a light-sensitising medication such as psoralen to be effective, which is commonly known as PUVA and this is given twice a week.

Phototherapy can be temporarily efficacious for many patients, with remission times varying from patient to patient. However, some drawbacks of phototherapy include limited accessibility and significant time commitment by the patient. There is also a limit to the amount of UV treatments patients can receive, as there is a safety limit for skin cancer risk.

Systemic treatment

These are for people with extensive or unresponsive psoriasis where topical treatments and phototherapy have not worked or are not recommended. The

Look BETTER Move BETTER Feel BETTER

Fast and sustained long-term efficacy in skin and persistent troublesome areas3-6

Indications

Helps prevent future irreversible joint damage7 Joint relief for patients with PsA, including Axial symptoms8

Fast and significant improvement in quality of life4,9

Plaque psoriasis: Cosentyx is indicated for the treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy. Psoriatic arthritis: Cosentyx, alone or in combination with methotrexate (MTX), is indicated for the treatment of active psoriatic arthritis in adult patients when the response to previous disease-modifying anti-rheumatic drug (DMARD) therapy has been inadequate. Ankylosing spondylitis: Cosentyx is indicated for the treatment of ankylosing spondylitis in adults who have responded inadequately to conventional therapy.10

ABBREVIATED PRESCRIBING INFORMATION

Please refer to the Summary of Product Characteristics (SmPC) before prescribing.

COSENTYX (secukinumab)

Presentations: Cosentyx 150 mg solution for injection in pre-filled pen and Cosentyx 300 mg solution for injection in pre-filled pen Therapeutic Indications: The treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy; the treatment of moderate to severe plaque psoriasis in children and adolescents from the age of 6 years who are candidates for systemic therapy, the treatment of active ankylosing spondylitis in adults who have responded inadequately to conventional therapy; the treatment of active non-radiographic axial spondyloarthritis with objective signs of inflammation as indicated by elevated C-reactive protein (CRP) and/or magnetic resonance imaging (MRI) evidence in adults who have responded inadequately to non steroidal anti inflammatory drugs (NSAIDs); the treatment, alone or in combination with methotrexate (MTX), of active psoriatic arthritis in adult patients when the response to previous disease modifying anti rheumatic drug (DMARD) therapy has been inadequate. Dosage & Method of Administration: Adult Plaque Psoriasis: 300 mg given as one subcutaneous injection of 300 mg or as two subcutaneous injections of 150 mg. Dosing at Weeks 0, 1, 2, 3 and 4, followed by monthly maintenance dosing. Pediatric Plaque Psoriasis: The recommended dose is based on body weight (see Table 1 in SmPC for full details) and administered by subcutaneous injection with initial dosing at weeks 0, 1, 2, 3 and 4, followed by monthly maintenance dosing. Each 75 mg dose is given as 1 subcutaneous injection of 75 mg. Each 150 mg dose is given as 1 subcutaneous injection of 150 mg. Each 300 mg dose is given as one subcutaneous injection of 300 mg or as 2 subcutaneous injections of 150 mg. The 150 mg and 300mg solution for injection in pre-filled syringe and pre-filled pens are not indicated for administration to paediatric patients with a weight <50 kg. Ankylosing Spondylitis (AS, radiographic axial spondyloarthritis): The recommended dose is 150 mg by subcutaneous injection with initial dosing at Weeks 0, 1, 2 3 and 4, followed by monthly maintenance dosing. Based on clinical response, the dose can be increased to 300 mg. Non-radiographic axial spondyloarthritis (nr-axSpA). The recommended dose is 150 mg by subcutaneous injection with initial dosing at weeks 0, 1, 2, 3 and 4, followed by monthly maintenance dosing. Psoriatic Arthritis: For patients with concomitant moderate to severe plaque psoriasis or who are anti TNF inadequate responders, the recommended dose is 300 mg by subcutaneous injection with initial dosing at Weeks 0, 1, 2, 3 and 4, followed by monthly maintenance dosing. Each 300 mg dose is given as one subcutaneous injection of 300 mg or as two subcutaneous injections of 150 mg. For all other patients, the recommended dose is 150 mg by subcutaneous injection with initial dosing at Weeks 0, 1, 2, 3 and 4, followed by monthly maintenance dosing. Based on clinical response, the dose can be increased to 300 mg. For all of the above indications, available data suggest that a clinical response is usually achieved within 16 weeks of treatment. Consideration should be given to discontinuing treatment in patients who have shown no response up to 16 weeks of treatment. Some patients with initially partial response may subsequently improve with continued treatment beyond 16 weeks. The safety and efficacy of Cosentyx in children with plaque psoriasis below the age of 6 years have not been established.The safety and efficacy in children below the age of 18 years in other indications have not yet been established. Contraindications: Severe hypersensitivity reactions to the active substance or to any of the excipients. Clinically important, active infection (e.g. active tuberculosis). Warnings/Precautions: Infections: Secukinumab has the potential to increase the risk of infections. Serious infections have been observed in patients receiving secukinumab in the post-marketing setting. Infections observed in clinical studies are mainly mild or moderate upper respiratory tract infections such as nasopharyngitis not requiring treatment discontinuation. Non serious mucocutaneous candida infections more frequently reported for secukinumab than placebo in psoriasis clinical studies. Caution in patients with a chronic infection or a history of recurrent infection. Instruct

patients to seek medical advice if signs or symptoms suggestive of an infection occur. If a patient develops a serious infection, close monitoring and discontinue treatment until the infection resolves. Should not be given to patients with active tuberculosis. Anti tuberculosis therapy should be considered prior to initiation in patients with latent tuberculosis. Inflammatory bowel disease: Cases of new or exacerbations of inflammatory bowel disease have been reported with secukinumab. Secukinumab is not recommended in patients with inflammatory bowel disease. If a patient develops signs and symptoms of inflammatory bowel disease or experiences an exacerbation of pre-existing inflammatory bowel disease, secukinumab should be discontinued and appropriate medical management should be initiated. Hypersensitivity reactions: In clinical studies, rare cases of anaphylactic reactions have been observed in patients receiving secukinumab. If an anaphylactic or other serious allergic reactions occur, administration should be discontinued immediately and appropriate therapy initiated. Latex-sensitive individuals: The removable cap of the Cosentyx pre filled pen contains a derivative of natural rubber latex. Vaccinations: Live vaccines should not be given concurrently with secukinumab. Patients may receive concurrent inactivated or non live vaccinations. Prior to initiating therapy with Cosentyx, it is recommended that paediatric patients receive all age appropriate immunisations as per current immunisation guidelines. Concomitant immunosuppressive therapy: Use in combination with immunosuppressants, including biologics, or phototherapy have not been evaluated. Interactions: Live vaccines should not be given concurrently with secukinumab. In a study in adult subjects with plaque psoriasis, no interaction was observed between secukinumab and midazolam (CYP 3A4 substrate. No interaction seen when administered concomitantly with methotrexate (MTX) and/or corticosteroids. Caution should be exercised when considering concomitant use of other immunosuppressants and secukinumab. Fertility, Pregnancy and Lactation: Women of childbearing potential should use an effective method of contraception during treatment and for at least 20 weeks after treatment. It is preferable to avoid the use of Cosentyx in pregnancy as there are no adequate data from the use of secukinumab in pregnant women. It is not known whether secukinumab is excreted in human milk. A decision on whether to discontinue breast feeding during treatment and up to 20 weeks after treatment or to discontinue therapy with Cosentyx must be made taking into account the benefit of breast feeding to the child and the benefit of Cosentyx therapy to the woman. The effect of secukinumab on human fertility has not been evaluated. Undesirable Effects: Very common (≥1/10); Upper respiratory tract infections. Common (≥1/100 to <1/10); Oral herpes, tinea pedis rhinorrhoea, diarrhoea, fatigue, nausea and headache Uncommon (≥1/1,000 to <1/100); Oral candidiasis, otitis externa, urticaria, neutropenia, conjunctivitis, lower respiratory tract infections and inflammatory bowel disease. Rare (≥1/10,000 to <1/1,000); Anaphylactic reactions, exfoliative dermatitis and hypersensitivity vasculitis. Please see Summary of Product Characteristics for further information on undesirable effects. Legal Category: POM. Marketing Authorisation Holder: Novartis Europharm Ltd, Vista Building, Elm Park, Merrion Road, Dublin 4, Ireland. Marketing Authorisation Numbers: EU/1/14/980/004 and EU/1/14/980/010

Prescribing Information last revised: August 2021. Full prescribing information is available upon request from: Novartis Ireland Limited, Vista Building, Elm Park Business Park, Elm Park, Dublin 4. 01-2601255 or at www.medicines.ie. Detailed information on this product is also available on the website of the European Medicines Agency http://www.ema.europa.eu.

Reporting suspected adverse reactions of the medicinal product is important to Novartis and the HPRA. It allows continued monitoring of the benefit/risk profile of the medicinal product. All suspected adverse reactions should be reported via HPRA Pharmacovigilance, website www.hpra.ie. Adverse events could also be reported to Novartis preferably via www.report.novartis.com or by email: drugsafety.dublin@novartis.com or by calling 01 2080 612.

* The Complete Cosentyx Approach™ is defined as efficacy in both skin and persistent psoriasis manifestations in nails, scalp, palms,and soles, as well as psoriatic arthritis; controls irreversible structural damage (PsA) and improves quality of life. PsA = psoriatic arthritis.10

With The Complete Cosentyx Approach™, you can address the underlying cause of the disease – and decrease systemic inflammation2

individual patient profile, lifestyle factors, associated arthritis, drug cost, side-effect profile along with patient preference all influence choice of drug.

Current options include methotrexate, fumaric acid esters, acitretin, ciclosporin and apremilast. As these medications have different toxicity profiles, patients are reviewed and monitored regularly to avoid any potential side-effects.

Biologic agents

Biological drugs represent state-of-the-art treatment, and have made a profound impact on the management of moderate-tosevere psoriasis. These immunomodulators target specific molecular actions in the pathogenesis of psoriasis.

TNF- α inhibitors work by blocking the action of the protein, TNF- α, which is involved in the abnormal immune responses and inflammation that contribute to the development of psoriasis. These include adalimumab, certolizumab, etanercept, and infliximab.

IL-inhibitors block the actions of IL proteins such as IL-23 and IL-17, which are also involved in the abnormal immune response in psoriasis. These include ustekinumab, guselkumab, risankizumab and ixekizumab, secukinumab, and brodalumab. These therapies are prescribed under the guidance of specialist physicians experienced in the diagnosis and treatment of psoriasis, and patients are reviewed regularly to monitor for and reduce the risk of potential adverse effects.

Biosimilars

Recently, biosimilars have been added to the list of biological agents used to treat moderate to severe psoriasis in Ireland. Biosimilar medicines are new biological medicinal products that have demonstrated ‘similar’ efficacy to the original biological therapy (reference medicine).

It is important to mention that biosimilars are approved according to the same standards of pharmaceutical quality, safety

and efficacy that apply to all biological medicines, while offering the potential for cost-reduction in treating patients with moderate to severe psoriasis. Currently licensed biosimilars include adalimumab, etanercept and infliximab.

Co-morbidities

There are a number of other conditions that are linked to psoriasis. These include psoriatic arthritis, cardiovascular disease, Crohn’s disease, obesity, chronic obstructive pulmonary disease (OPD), kidney disorders, metabolic syndrome, sleep disorders, and non-alcoholic fatty liver disease. It is reported that people with more extensive or severe psoriasis are more likely to have co-morbidities.

There are significant physical and psychological morbidities associated with psoriasis. The physical impact includes itch, particularly in certain sites such as the scalp, lower legs, and groin. If psoriasis affects the hands and feet, painful fissures can develop and these can affect use of hands and walking. Psoriatic arthritis can produce pain, swelling and stiffness in one or more joints. If the nails are affected, lifting of the nail plate from the nail bed can be painful. Physical symptoms can lead to sleep disturbances, fatigue, and poor work performance.

As this can be a visible skin condition, the psychological effects are not to be underestimated. These include low self-esteem, self-consciousness, embarrassment, anger/frustration, stigmatisation, depression and influence on choice of clothing. A recent study of adolescents with psoriasis demonstrated that there was an association between psoriasis and anxiety disorders as well as impaired social adjustment skills.

A survey in Ireland in 2015 revealed that over half of the respondents believed that their psoriasis impacted on their love life, and a third reported that their condition prohibited them from dating. When

asked about applying for a job, 21 per cent acknowledged that their psoriasis had prevented them from applying for a job. Disturbingly, 56 per cent of respondents claimed that they were the subject of negative comments from other people. This highlights the lack of knowledge about psoriasis and its impact on the person with this skin condition.

Summary

In conclusion, psoriasis puts a major burden on the quality-of-life and on the mental health of patients with this skin disorder. The burden of psoriasis affects people in different ways, due to physical factors and the possible accompaniment of co-morbidities such as psoriatic arthritis and cardiovascular disease. It has been reported that disease severity also has a negative economic impact on the patient’s life, resulting in quality-oflife impairment.

In addition to controlling the symptoms of psoriasis, trigger factors should be identified and eliminated if possible. It is important to educate patients with regards to self-care in the management of their psoriasis. This includes smoking cessation, maintaining a healthy BMI, having risk factors checked such as blood pressure, cholesterol, type 2 diabetes, and psoriatic arthritis.

Although not ‘curable’, people with psoriasis should be reassured by the fact that psoriasis can be controlled as there are many excellent treatments available and new therapies in development.

The Irish Skin Foundation website offers extensive information on psoriasis, its comorbidities, and treatments to people living with psoriasis. See www.irishskin. ie for more resources on psoriasis. 

References on request

*There is also a full CPD module on psoriasis by Prof Tobin available on www.doctorCPD.ie, which can be completed to earn two free CPD points.

Diagnosing and treating psoriasis

As outlined in this module, treatments for psoriasis have advanced such that patients can expect to have clear or nearly clear skin, with a broad range of effective therapies to treat mild to moderate to severe disease.

Authors: Prof Anne-Marie Tobin, Consultant Dermatologist, Tallaght University Hospital, Clinical Associate Professor at Trinity College Dublin, and HSE Clinical Lead in Dermatology

The perioral area: A combination treatment approach using novel Definisse TM aesthetic medical treatment range

Introduction

The lip and perioral area represents one of the most common aesthetic treatments performed in cosmetic medical clinics. The ASPS in 2016 showed that 27,000+ lip procedures took place in the US, with a lip procedure being performed every 20 minutes.1 Conscientious injectors must take a multimodal approach to this complex and dynamic anatomical region to ensure the best possible aesthetic outcome. This case study will clearly demonstrate the efficacy of a novel DefinisseTM aesthetic medical range in addressing asymmetric lip volume, reshaping, and reduction in early static perioral rhytids.

Case study

A 38-year-old female mother of four with no smoking history and no other medical complaints presents to clinic for consultation. Pre-treatment assessment shows lip volume loss when compared to photographs in her 20s, asymmetric vermilion height and (Glogau) grade 3 perioral lines at rest. Of note, the patient had previously had an adverse outcome from botulinum toxin treatment for perioral lines, resulting in an asymmetric smile and discomfort when eating, and therefore wanted to try alternative approaches. After careful discussion, a treatment plan was agreed (see Table 1).

The recent introduction of new aesthetic medicine modalities under the brand name Definisse™ provides physicians with a new way and novel modalities to enhance clinical outcome and deliver greater patient satisfaction. The products used in this case report are described in Table 2

Methods

Physicians are now taking a more holistic,

multi-layered approach to the perioral region, knowing full well the impact of bone density loss, sphincter muscle overactivity, fat pad volume depletion and increasing skin laxity as we age. A combination approach to the perioral area is the approach chosen by this physician, but there is no one-size-fits-all. Table 1 outlines the anatomical deficit and this physician’s approach to this particular treatment:

Technique

A three-step approach to the vermilion was

taken. Firstly, using Definisse™ touch filler + lidocaine, using a shallow needle injection, retrograde threads along the vermilion border, including the Cupid’s bow, were used to create definition and to reduce perioral rhytid formation. The upper vermilion height was corrected by injection of retrograde threads vertically along the dry mucosa 2mm apart while the lip is elevated using manual traction. Finally, the remaining volume is distributed along the upper and lower lip to replace age-related volume loss.

The perioral lines are then addressed with two courses of DefinisseTM hydrobooster to replete HA concentration, which also stimulates native fibroblast synthesis of collagen. 5 This is complemented with the DefinisseTM Peel Programme to resurface the epidermis and further reduce unsightly perioral rhytids.

Outcome measure

Using the Glogau wrinkle scale, pre- and post-treatment photography was compared to demonstrate visible aesthetic improvement.

Day 0 Consultation, pre-treatment consent and photography

Day 1

Day 14

DefinisseTM touch filler + lidocaine 1ml for lip volume + vermilion height correction2

DefinisseTM hydrobooster for HA replacement + improved skin elasticity and tone 2ml3

Day 28 DefinisseTM lightening peel

Day 42 DefinisseTM lightening peel

Day 56

DefinisseTM hydrobooster for HA replacement + improved skin elasticity and tone 2ml3

COMMERCIAL FEATURE

PRODUCT NAME FORMULATION AND CHARACTERTISTIC

Definisse™ touch filler + lidocaine  Hyaluronic acid concentration (23mg/mL).

 Glass syringe

 Terumo™ needles (CE 0197, 2 x 27G ½” thin wall)

 G’ (G prime) 153.58

 G’’ (G second) 26.67

 Tanδ 0.174

Definisse™ lightening peel  <25% salicylic acid,

 <10% pyruvic acid,  <0.05% retinoic acid).

 <5% N-undecyl-10-enoyl-Lphenylalanine (Sepiwhite).

 <5% diacetyl boldine.

Definisse™ hydrobooster

 Hyaluronic acid (HA, 18mg/mL) non cross-linked

 Glycerol (20mg/mL)

 Glass syringe

 Terumo™ needles (CE 0197, 2 x 30G ½” thin wall)

CLINICAL BENEFIT

To create volume in order to correct wrinkles and folds, to correct moderate-to-severe nasolabial folds, and to improve lip volume to treat signs of ageing

Multi-level skin resurfacing, promote skin renewal, reduce hyperpigmentation and addresses uneven pigmentation

Improve skin hydration, skin tone, and elasticity, while being injected in the superficial dermis

preservation of the products, with the additional benefit of reducing plastic waste, a more environmentally-friendly option in the hands of the medical professional. 

* If you are interested in the Definisse™ products used in the case report please contact Fergus Gallagher at fgallagher@menarini.ie.

This case report was sponsored by RELIFE Ireland.

Please go to www.thepmfajournal.com/ events/event/relife-i-dass-internationaldermatologyaesthetic-surgery-summit to view Dr Fitzpatrick’s lip augmentation anatomical insights presentation and live procedure demonstration at i-DASS Dublin.

References

1. www.plasticsurgery.org/documents/ News/Statistics/2016/plastic-surgery-statisticsfull-report-2016.pdf

2. Definisse™ touch filler + lidocaine, Information for Use

3. Definisse™ hydrobooster, Information for Use

4. Definisse™ lightening peel, Information for Use

Subdermal dehydration due to loss of HA3

DefinisseTM hydrobooster Two courses of 2ml

Results

Using the Glogau Wrinkle Scale pre- and posttreatment photography demonstrates a clear reduction of early static perioral rhytids from type 3 to type 1. The vermilion height is made symmetrical bilaterally with subtle vermilion volume repletion, a more defined vermilion border, and a narrow, sharper Cupid’s bow to beautify the lip.

Discussion

Although a combination of anti-wrinkle injectables and dermal fillers has long been the mainstay of treatment, there is increasing evidence for the use of less-invasive procedures. This is an option for patients, or indeed, less experienced injectors who wish to avoid

complications associated with injectables in the perioral region. However, the level of studies available into combined treatments is moderateto-low and larger-scale, multi-centre, randomised and double-blinded studies are needed. There is also a paucity of histological analysis of tissues to assess response to treatments, though this process may impact on the overall aesthetic outcome. This case report publication reflects the author’s personal experiences in using novel aesthetic medicine modalities, namely the Definisse™ range. The technical features of the products are well appreciated, especially the use of glass syringes on Definisse™ touch filler + lidocaine and Definisse™ hydrobooster that provide better haptic grip, minimal risk for plastic contamination, better stability and

5. Bukhari et al (2018). Hyaluronic acid, a promising skin rejuvenating biomedicine: A review of recent updates and pre-clinical and clinical investigations on cosmetic and nutricosmetic effects. International journal of Biological Macromolecules 12 (1682-1695)

6. Salti G, Fundarò SP. Evaluation of the rheologic and physicochemical properties of a novel hyaluronic acid filler range with eXcellent three-dimensional reticulation (XTR™) Technology. Polymers (Basel). 2020;12(8):1644. Published 2020 Jul 24. doi:10.3390/polym12081644

7. Wong V (2021) Resurface, retone and reboost: A multi-modality approach for prejuvenation of millennial patients. J Clin Exp Dermatol Res. S8:549

8. Wong V, Malgapo DMH (2021)

Reharmonise: Aesthetic modalities founded on the concepts of restoring, reshaping, and resurfacing for the Comprehensive Treatment of Millennials. J Clin Exp Dermatol Res. 12:562

Definisse™

Vecchia 32, 18038 Sanremo, Italy; Definisse™ touch + lidocaine CE0123 CROMA-PHARMA GmbH; Definisse™ restore + lidocaine CE0123 CROMA-PHARMA GmbH; Definisse™ hydrobooster CE0459 CROMA GmbH

Gangrene – a blast from the past

To the average person gangrene is something that they largely associate with the past and in particular, because of injuries sustained by soldiers at war. Historically, this is true – gangrene was known as ‘the military disease’. It wasn’t until the mid-19th Century that the cause of gangrene was first linked to bacterial infection from the dirt and detritus in wounds carried from the battlefield and unwashed hands, soiled instruments, and dressings in the hospital. The work of scientist Joseph Lister in the 1870s, who first identified the need for a more ‘antiseptic’ approach to surgery and wound management practice, demonstrated to medical science the life-saving benefits of a proper hygiene regimen, replacing the largely ineffective methods that had operated for hundreds of years previously.

It was often the case, following huge military campaigns, that more men died from complications arising from infected wounds with gas gangrene (the most fatal type) than died on the battlefield. In fact, if you track campaigns from the American Civil War, where there was up to 60 per cent mortality in wounded soldiers, through the Crimean and Boer wars, it wasn’t until WW1 that this was reversed. As is often the case, innovation and development in medicine seems to evolve at a vastly increased rate during warfare. At the outbreak of WW1 in 1914, little was known regarding the treatment or prevention of gangrene or its cause, with mortality rates in the wounded from infection still high, at around 15 per cent. Standard wound practise at this time was to open the wound, irrigate, leave open to drain and then close, thus leaving the wound hugely susceptible to bacterial infection being sealed in the wound.

Often, gas gangrene would have set in, with irrevocable fatal consequences.

As WW1 progressed, the huge casualty count presented the opportunity for research analysis into the problem. Identifying the presence of anaerobic bacteria in the wounds, along with developments in hygienic wound treatment and surgical procedures, such

as debridement allied to immediate surgical intervention and evacuation to a sterile hospital facility, meant that by the time the war ended in 1918, the previously high mortality rate had fallen to about 1 per cent.

From this time forward, there was constant progress in the fight against gangrene-related death. Alexander

Gangrene remains a significant danger to high-risk groups due to the nature of certain medical conditions they have, in particular, diabetes

Fleming’s discovery of penicillin in 1928 was a major turning point in the development of an effective intervention to prevent infection. The advent of WW2 brought the discovery by Charles Pfizer of how to mass-produce penicillin, culminating in some 2.3 million doses being supplied to troops for the D-Day landings. Mortality rates in WW2 from gangrenous wound infection were exceedingly low where penicillin could be administered and removal to sterile facilities could both be achieved quickly. Such was the continued progress and development in antibiotic medicine postWW2 that an interesting statistic from the Vietnam War shows that in 1966-1967, of the almost 18,000 wounded soldiers removed quickly from conflict areas to sterile facilities for treatment, there was not a single case of gangrene reported.

Still a danger

Thankfully, today, whilst infection is still a risk if a person sustains a serious injury and wounding from perhaps a car crash or similar, with modern triage and infection control techniques, the likelihood of gangrene developing is extremely low. It would appear therefore that gangrene is no longer an issue and yes, in the case of serious injury, properly and quickly treated, this is true, however, gangrene remains a significant danger to high-risk groups due to the nature of certain medical conditions they have, in particular, diabetes.

What is gangrene?

Like so many medical conditions, if we consider the etymology of the word ‘gangrene’, we get a clue as to its nature. Gangrene is from the Latin gangraena , which means ‘putrefaction of tissues’, which aptly describes the physical action of gangrene – the necrosis of tissue caused by a loss of blood supply to the affected area. Gangrene itself is not a disease; rather, it is related to other medical conditions, particularly those that cite poor circulation and arterial damage as a symptom, ie, diabetes, or peripheral arterial disease that correlates

to the most typical sites affected by gangrene – fingers, toes, hands, and feet. This is a serious condition, which can become potentially fatal from sepsis if bacterial infection occurs.

Gangrene is usually treated by a combination of antibiotics and surgery. There are several different types of gangrene, so the success or otherwise of treatment is very much dependent on the type of gangrene present. The most successful treatment outcomes are dependent on early intervention – if the condition escalates, the treatment options decrease proportionately. In some cases, amputation becomes the only option to prevent spread.

Types of gangrene

Clinically, whilst there are many different forms, gangrene is divided into four main types:

 Dry gangrene

 Wet gangrene

 Gas gangrene

 Internal gangrene

Dry gangrene

Body tissue dies due to an inadequate or total loss of blood supply to parts of the body (most commonly limbs or digits) through arterial damage or blockage caused by another condition (ie, diabetes or atherosclerosis). Dry gangrene is characterised as ‘non-infectious’, as no anaerobic bacteria are present. Affected areas may present as red or a reddishblack colour. There may be some localised swelling, whilst feeling dry and hard to the touch. There may be a very apparent difference in colour between the affected and non-affected areas. Identification and treatment options at this stage have the best chance of success, due to lack of bacterial infection. Left untreated, the risk of secondary (bacterial) infection increases, resulting in further less manageable complications.

Wet gangrene

Here, the necrotic tissue has become infected by anaerobic bacteria, which

spread rapidly. In contrast to dry gangrene, the affected area turns soft and almost black in colour and the skin may feel thin and cold to the touch. In addition, blisters containing cloudy, opaque pus (hence ‘wet’) may form on the affected skin and may produce a foul odour. The lack of oxygen in the blood in the localised necrotic area encourages bacteria to release toxins, thereby greatly increasing the risk of potentially lifethreatening sepsis should they enter the bloodstream. Due to the high mortality rate associated with wet gangrene, emergency amputation may be the only option to save life.

Gas gangrene

Basically, the most serious form of wet gangrene caused by clostridial infection, which attacks soft muscle tissue, spreading at an alarming rate and as such presents a life-threatening emergency (as discussed earlier, gas gangrene was the cause of high mortality in wounded soldiers) and without treatment, can be fatal within 48 hours. The clostridial infection produces gas, which can produce a crackling sound when the skin is touched. The clostridium microbes also produce toxins which speed up the tissue necrosis.

Internal gangrene

The blood flow to an internal organ (ie, gall bladder, colon, appendix) becomes blocked, which if left untreated can result in serious complications, such as organ damage and/or sepsis.

Risk factors

Whilst gangrene can affect anyone, it is more likely to concern people in certain at-risk groups with different medical conditions that affect the blood flow and circulatory system, such as:

Diabetes – High blood sugar levels in people with diabetes means that their risk of developing gangrene is increased. Damage to the nerves and blood vessels can result in a loss of feeling and blood supply, particularly in the feet. Left unchecked, ulcers and sores can develop,

which can become infected and take longer to heal due to poor blood supply. It is vitally important that people with diabetes have a regular foot check to identify injury and take remedial action. Diabetes is the most important risk factor for developing both dry and wet gangrene.

Atherosclerosis – The hardening and narrowing of the arteries caused by a build-up of plaque, to the extent that a blockage may be caused.

Peripheral arterial disease – A specific example of atherosclerosis that restricts blood flow to the arms and legs and feet. This can result in numbness and similar risk of loss of feeling and wound recovery. Smokers carry a much higher risk of developing this disease.

Raynaud’s syndrome – Due to the nature of this condition, the messaging of temperature change to the peripherals causes an adverse reaction, which can cause damage to the cells in fingers and toes. This increases the risk of tissue death and gangrene.

Other groups that carry a higher risk of developing gangrene are those with weak or compromised immune systems:

 HIV/AIDS.

 Those having cancer treatment, such as chemotherapy or radiotherapy.

 Obesity.

 Renal failure.

Symptoms/signs

Gangrene can affect any part of the body, however, it is most likely to start in the fingers, toes, feet, or hands. For dry gangrene, the symptoms are usually visual, with discolouration (redness) of the skin in the affected area, accompanied by localised swelling and pain. The skin may be cool and numb to the touch.

Wet gangrene types will show more pronounced discolouration, more purple and black in the affected area, again with a stark demarcation between healthy and

affected tissue. Other symptoms include:

 Fever – temperature above 38°c.

 Swelling and pain.

 A crackling sound when the affected area is pressed.

 Liquid-filled blisters with foul-smelling pus.

With internal gangrene, feverish symptoms are accompanied by localised pain in the affected area.

Treatment options

If gangrene is diagnosed, then depending on the extent/severity of the condition, several treatment options are available. It is worth pointing out, however, that once gangrene is present, the affected tissue is dead and not recoverable.

In cases of dry gangrene, where there is no infection present, the treatment goal will be to remove the dead tissue and restore blood flow to the remaining area.

The necrotic tissue is surgically removed (debridement), allowing the remaining healthy tissue to fully heal.

Diagnosis

If someone suspects they may have gangrene or are experiencing any of the symptoms outlined above, they should act immediately and see a doctor as soon as possible.

Following a review of the current situation along with medical history, the doctor will conduct a physical examination to look for some of the obvious signs of gangrene as outlined earlier, ie, discolouration, odour, swelling.

In addition, they may request extra tests to help ascertain the correct diagnosis, which may include:

 Bloods tests to check for infection.

 To identify the most suitable antibiotic, a variety of culture tests to check for bacteria may be requested.

 Imaging tests such as MRI, CT, and x-rays to help reveal the presence of any arterial damage/blockage and infection or gangrene.

 If gangrene deep inside the body is suspected, a surgical examination may be performed, under anaesthetic.

An alternative to traditional surgery is biosurgery using maggots. Maggots have been in use for wound treatment since the 11th Century. In the UK, 40 NHS hospitals are supplied from a company in Wales with specially-bred bacteria-free Greenbottle larvae. These come in the form of ‘bio bags’, a mesh bag containing maggots that is applied tightly to the wound and left for up to 72 hours, or just loose and packed into the wound and covered. They are effective, as they consume only dead tissue and studies show that this method can achieve better results than surgery in removing just dead tissue.

In cases where surgical intervention would not be effective, amputation may be the only option to prevent the spread of gangrene to other areas. Historically, if it was just a finger or a toe, it may just have been left to ‘fall off’ or autoamputation; however, the modern view is that the potential collateral risk while waiting is not worth taking.

Where infection is also present, then treatment with strong antibiotics, either orally or intravenously in the case of severe infections, are the preferred options.

Options to restore blood flow are usually either a bypass around the blockage or, if the vein is still intact, an angioplasty.

Maggots are effective, as they consume only dead tissue and studies show that this method can achieve better results than surgery in removing just dead tissue

Check feet daily

TOP TIPS FOR BETTER DIABETIC FOOT CARE

People with diabetes may have serious foot problems, but feel no pain. Look for cuts, sores, red spots, swelling or infected toenails. Find a time (evening is best) to check feet each day. If there is trouble bending, use a mirror to help.

Wash feet daily

Wash feet in warm, not hot, water. However, do not soak feet, as this will cause the skin to get dry. Before bathing or showering, test the water to make sure it is not too hot. Use a thermometer (32-to-35o C is safe) or elbow. Dry feet well, taking care to dry between toes.

Keep feet moisturised

Rub a thin coat of skin lotion, cream, or petroleum jelly on the tops and bottoms of the feet. Do not put lotion or cream between toes, because this might cause an infection.

Do not overdo it

If using a pumice stone to smooth corns and calluses after bathing or showering, rub gently, in one direction only, to avoid tearing the skin. Do not

Hyperbaric oxygen therapy (HBOT) is indicated as an alternative form of treatment for certain types of gangrene. This therapy involves the patient entering a pressure chamber, then breathing pure oxygen through a hood placed over the head. High levels of oxygen in the bloodstream have been shown to speed-up healing. As oxygen is toxic to anaerobic bacteria, HBOT has been proven to stop or slow down the action of toxin-producing bacteria associated with gas gangrene. Its use in the effective treatment of diabetics with gangrenous foots ulcers and helping to reduce the risk of amputation has also been a success.

Whilst evidence is limited and further research is required as to HBOT

cut corns and calluses. People with diabetes should not use razor blades, corn plasters or liquid corn and callus removers, as they can damage skin.

Keep toenails trim

Cut toenails each week or when needed. Wash and dry your feet first. Trim toenails straight across and smooth them with an emery board or nail file. Do not cut into the corners of the toenail, as this can cause in-growing toenails. If eyesight is poor, if toenails are thick or yellowed, or nails curve and grow into the skin, have a chiropodist trim them.

Wear shoes and socks

Wear shoes and socks at all times. Do not walk barefoot – not even indoors –because it is easy to step on something and cause skin damage. Always wear socks, stockings, or nylons with shoes to help avoid blisters and sores. Socks that have no seams are best. Speciallydesigned socks for diabetics are ideal.

Avoid hot and cold

Always wear shoes at the beach or on hot ground and put sunscreen on the

effectiveness on other types of gangrene, initial results appear promising. There are several HBOT centres in Ireland where this treatment is available. These are currently private facilities, so prospective users would need to check with their health insurer, as availability and cover appears to vary.

Prevention of gangrene

It is forecast that by 2030, there will be just short of 300,000 people with diabetes in Ireland. If you consider these figures along with these numbers from 2017 –547 people with diabetes underwent a lower limb amputation, while a further 2,081 were hospitalised for foot ulceration treatment in the same period – it suggests that unless significant change is made,

top of feet to prevent sunburn. Keep feet away from radiators and open fires and do not put hot water bottles or heating pads on feet. Check feet often in cold weather to avoid frostbite.

Keep the blood flowing

Put feet up when sitting. Wiggle the toes for five minutes, twice or three times a day. Move ankles up and down and in and out to improve blood flow. Do not cross your legs for long. Do not wear tight socks, elastic or rubber bands, or anything restrictive around your legs. Stop smoking, as it reduces blood flow to feet.

See a health professional

People with diabetes should visit a chiropodist once every six months. Chiropodists are experts in foot health and should be the first stop if foot problems occur, especially in people with diabetes, as even minor issues can turn into serious problems very rapidly. Pharmacists, general practice nurses, public health nurses, and GPs can also help with foot problems.

the numbers requiring amputation and hospitalisation by 2030 could double.

Education and early action are the key to reducing these numbers – the more people know about their condition and the potential outcomes of poor management, the better placed they will be to take control of their own outcomes.

Along with the general prevention information around exercise, smoking, alcohol, and diet, which apply to everyone at risk of gangrene, and given the significantly higher risk to those with diabetes, the above top tips for diabetic foot care are useful. 

References on request

Hidradenitis suppurativa

Hidradenitis suppurativa (HS) sometimes referred to as acne inversa, is a chronic, relapsing, inflammatory skin condition that typically occurs after puberty, with the average age of onset in the second or third decade of life.

Patients with HS present with inflammation of hair follicles in the apocrine glandbearing regions; armpits, genital area, groin, inframammary region, perianal region and buttocks, that initially manifests as painful nodules or boils and progresses to abscesses, sinus tracts and scarring.1,2 Infrequently, HS can occur in locations where apocrine glands are scant or absent and this is referred to as ectopic HS.6

The exact prevalence of HS remains unknown. Estimated prevalence is approximately 1-to-4 per cent worldwide, although these figures are thought to be underestimated because of under-reporting and misdiagnosis. HS is threetimes more common in women than men.3

The armpit and inguinofemoral regions are the most common locations for HS lesions in both sexes. Frontal lesions in the groin/ thigh and breast tend to be more common in women, whereas lesions in the buttocks, perineal/perianal regions and atypical areas tend to be more common in men.1,2

Pathophysiology

The primary defect in HS pathophysiology involves occlusion and subsequent inflammation of the hair follicle. A defective hair follicle becomes occluded and ruptures, emptying its contents, including keratin and bacteria, into the surrounding dermis. A chemotactic inflammatory response by surrounding neutrophils and lymphocytes can lead to abscess formation and subsequent destruction of the pilosebaceous unit and other adjacent structures. Other possible contributors to pathology include abnormal antimicrobial peptides, abnormal

secretion of apocrine glands, abnormal invaginations of the epidermis leading to tract formation, and deficient numbers of sebaceous glands. 2,5

Elevated levels of inflammatory cytokines including tumour necrosis factor (TNF) alpha and various interleukins have been detected in the lesions of HS and provide possible targets for emerging treatments. Bacteria do not appear to be causative, as aspirate from non-ruptured lesions typically yields a sterile culture. However, bacterial infection and colonisation that occur during the process can secondarily worsen HS.2,5

Symptoms

The presentation of HS is distinct, although the condition is not well-recognised except in dermatology clinics.3 The most troublesome symptom of HS is chronic pain, of mild-tomoderate intensity, which is reported by almost all patients. The physical symptoms of HS, which includes nodules or boils that progress to abscesses, sinus tracts, and scarring, make it a painful condition. The pain associated with HS can be intense and chronic and is reported by patients as the most significant factor contributing to impaired quality-of-life. Up to 50 per cent of patients report a burning or stinging sensation, pain, pruritus, warmth, and/or hyperhidrosis, 12-to-

48 hours before an overt nodule occurs. Mean duration of a single painful nodule is sevento-15 days. With time, the nodules may rupture, resulting in painful, deep dermal abscesses. With disease progression, draining sinus tracts, fibrosis, and scarring can be observed. After rupture, the lesions often extrude a purulent, foul-smelling discharge that stains clothing.

Unsurprisingly, HS is accompanied by embarrassment, social stigma, low self-worth and a negative impact on interpersonal relationships.2,5 With reference to psychosocial evaluation, HS can be a highly debilitating condition. The major factors influencing patients’ wellbeing are disease severity, the number of flares or affected skin areas, and the lesion location. HS not only causes skinrelated issues, but also has a profound impact on general quality-of-life measures, causing substantial deterioration of both physical and mental health. In both observational and registry studies, depression and anxiety were significantly related to HS.4

Disease staging

The Hurley Staging System is the simplest and most widely used instrument for HS classification in routine clinical practice. It classifies HS into three stages:

• Stage I: abscess formation, single or multiple, without sinus tracts and cicatrisation;

Grade I Abscess formation, single or multiple, without sinus tracts and cicatrisation

Grade II Recurrent abscesses with sinus tracts and cicatrisation; single or multiple widely separated lesions

Grade III Diffuse or almost diffuse involvment, or multiple interconnected tracts and abscess accross entire area

• Stage II: Recurrent abscesses with tract formation and cicatrisation, single or multiple, widely separated lesions; and

• Stage III: Diffuse or near-diffuse involvement, or multiple interconnected tracts and abscesses across the entire area.5 Severity is typically described according to the three Hurley categories. Most patients have Grades I (mild) or II (moderate) HS, with Grade III (severe) disease reported in 4-to-22 per cent of patients in recent studies.1

Risk factors and co-morbidities

Risk factors for HS include smoking, obesity, family history, and other patient factors. Individuals with HS are commonly overweight or obese. Obesity leads to greater intertriginous surface area and skin friction, increased sweat production and retention, and hormonal changes leading to relative androgen excess, all of which are associated with HS. Metabolic syndrome is more common in obese individuals and is also seen more commonly in HS. Smoking is prevalent among those diagnosed with HS and it is thought that nicotine may cause increased follicular plugging.

About 33-to-40 per cent of individuals with HS report an affected first-degree relative, suggesting a hereditary component with an autosomal dominant transmission pattern. In a small subset of affected families, researchers have identified a mutation of the gamma-secretase Notch signalling pathway.2

The influence of hormones can also be seen in HS. There is a greater prevalence in females than males, with the age of primary occurrence most commonly between puberty and menopause. In addition, there are fluctuations of occurrence and severity with menstrual cycles and exogenous hormones. 3

Comorbidities for HS include inflammatory bowel disease (IBD), spondyloarthropathies, tumours and pyoderma gangrenosum.1,2 Patients with HS have a higher prevalence of gastrointestinal disease. The prevalence of IBD is four-to-eight times higher in HS patients than in the general population, although there is no association with any distinct HS subtype. Compared to the general population, patients with IBD are ninetimes more likely to develop HS.5 Although the association is rare, it is speculated that pyoderma gangrenosum and HS share a common aetiology that may involve cytokine dysregulation. An increase of epithelial and non-melanoma skin cancers has also been reported in patients with HS. 3

Diagnosis

Early diagnosis is very important for patients with HS, in order to ensure the best possible disease course and prompt management. However, HS diagnosis generally occurs after an average seven-year delay, because the early stages are often mistaken for other conditions. 2,5

Diagnosis of HS is made by history and clinical observation, and a biopsy is rarely needed. However, a biopsy is beneficial to rule out squamous cell carcinoma in the presence of severe HS, if the diagnosis is uncertain. There are no blood tests to confirm HS and bacterial cultures are not beneficial unless secondary infection or an alternative diagnosis is suspected. Imaging is not typically required, however, ultrasound may be a useful tool pre-operatively to identify the extent of sinus tracts. Lesions may warrant further imaging including MRI in severe perianal disease. HS can easily be differentiated from other conditions by the age of onset and the characteristic locations of lesions.

Differential diagnosis includes common

abscess, carbuncles, furunculosis, infected Bartholin’s gland, inflamed epidermal cysts, pilonidal cyst, scrofuloderma, actinomycosis, lymphogranuloma venereum (LGV), and Crohn’s disease.2,5

Treatment

Treatment choices for HS are determined by disease severity and individual subjective impact. The degree of HS clinical involvement is usually determined according to the threestage Hurley system.2

In early uncomplicated cases, topical antibiotics are the first-line treatment. Topical clindamycin has been the most effective. Most significant effect is seen with superficial lesions while efficacy is poor with deep lesions. Intra-lesion corticosteroids can reduce local inflammation and partial de-roofing/punch debridement of individual lesions can facilitate healing.2

Systemic treatment is indicated when more severe or widely spread lesions are present. Treatment for Hurley Stage II and resistant Hurley Stage I involves oral antibiotics.5 Acute abscesses may be treated with flucloxacillin 500mgs qds for seven days. Tetracyclines, such as lymecycline 300mgs once-daily or minocycline 100mgs once daily, may be considered. The combined use of systemic clindamycin and systemic rifampicin (rifampicin 300mgs twice-daily and clindamycin 300mgs twice-daily for 10 weeks) under specialist supervision has proven beneficial, with variable results.9

For Hurley stage III and resistant lower stages, TNF-alpha inhibitors are indicated. Recent studies have shown that biologics adalimumab and infliximab, two different monoclonal antibodies against TNF- α , are effective in the treatment of moderate-to-severe HS (Hurley II–III), with improvement in the patient’s quality-of-life, with adalimumab being more tolerable.5,7 Adalimumab is licensed in Ireland for the treatment of severe HS.9

Surgery for later-stage HS is often required, and involves a wide excision to include the lesions, tracts, and scars of an entire

affected area. A combination of medical treatment and surgical excision is often the preferred approach. Other therapeutic options may include localised laser and pulsed light therapy, which can help to disrupt the inflammatory process. 2

Pain management is important. The pain of HS is both inflammatory and non-inflammatory. Sources of pain can include scarring, keloids, abscesses, open ulcerations, sinus tracts, frictional pain, lymphoedema, anal fissures, and arthritis. Depending on disease severity and type of pain, topical agents, such as lidocaine and anti-inflammatories, systemic non-steroidal anti-inflammatories, acetaminophen, atypical anticonvulsants including gabapentin or pregabalin, and serotoninnorepinephrine reuptake inhibitors (SNRIs) may be beneficial. 2

Treatment should include management of comorbidities that contribute to the development or worsening of the disease process. Individuals who are overweight or who smoke usually have more severe disease progression, therefore, help with weight loss and smoking cessation are important components of treatment. Avoidance of tight and synthetic clothing, harsh body cleaning products, and adhesive dressings can be beneficial for patients. Patient assurance that the condition is not contagious or the result of poor hygiene can be helpful.

Support

Counselling and support groups are often helpful additions to treatment plans. 2

The Irish Skin Foundation (ISF)8 provides a range of information and educational resources on HS, including a What you need to know about HS booklet, which has been prepared by people with HS, dermatology nurses, and consultant dermatologists to explain more about the condition, its causes, symptoms and self-care tips.

The ISF has also condensed a dedicated HS webinar video in to ten short, practical information videos, which explore a range of different topics related to HS, including

what it is, the causes, the impact on qualityof-life and mental health, as well as the benefits of smoking cessation and weight reduction on disease outcomes. See www.irishskin.ie for more information.

Being in touch with other people who understand what it is like to live with HS can be really helpful. Patients with HS can get in touch with the private Irish Facebook HS Support Group where they can talk to other people with HS by going to www. facebook.com/groups/359301964248883 or by emailing hsireland@outlook.com, or they can follow the Twitter account @hsireland1.

Prognosis and outlook

There is no cure for HS and prognosis is widely variable. Outcomes can worsen if there is a delay in diagnosis and treatment during the early stages of the condition, and also if comorbid conditions of smoking and obesity are not addressed and improved. The best prognosis involves early recognition and aggressive treatment at early stages of the condition

References

1. Dufour D, Emtestam L, Jemec, G. (2014). Hidradenitis suppurativa: A common and burdensome, yet underrecognised, inflammatory skin disease. Postgraduate Medical Journal 2014; 90:216-221. https://pmj.bmj.com/ content/90/1062/216

2. Ballard K, Shuman V. (2021). Hidradenitis Suppurativa. StatPearls Publishing. Available at: www.ncbi.nlm. nih.gov/books/NBK534867/

3. Miller I, McAndrew R, Hamzavi I. (2016). Prevalence, risk factors, and comorbidities of hidradenitis suppurativa. Dermatol Clin. [PubMed PMID: 26617352]

4. Matusiak, T. (2018). Profound consequences of hidradenitis suppurativa: A review. Br J Dermatol. 2018 May 9 [PubMed PMID: 29744872]

5. Napolitano M, Megna M, Timoshchuk EA, Patruno C, Balato N, Fabbrocini G, Monfrecola G. (2017). Hidradenitis suppurativa: From pathogenesis to

and psychosocial support. 2 HS is underrecognised and diagnosis is frequently delayed. Patients often attend their GP or local emergency department to have individual abscesses incised and drained, therefore the recurring patterns are not noticed at the time and often mistaken for a simple infection. 8 As the condition often goes undetected and untreated for long periods, it is important for primary care providers to recognise HS based on the morphology, location, and chronicity of lesions, and begin the correct treatment early in the disease process. An interprofessional approach is most effective in the management of the condition. HS can cause significant psychosocial distress for patients and mental health supports from psychiatrists, psychologists, or counsellors should be provided as necessary. Therapeutic options for HS are gradually expanding, however, further research studies are necessary to ascertain whether certain genetic, clinical, or phenotypic factors may predict or guide more effective treatments and outcomes.

diagnosis and treatment. Clin Cosmet Investig Dermatol. 10, 105-115. doi:. org/10.2147/CCID.S111019

6. Gutierrez N, Cohen P. (2021) Ectopic hidradenitis suppurativa: Case report and review of literature. Cureus 13(1): e12966. doi:10.7759/cureus.12966

7. van Straalen K, Schneider-Burrus S, Prens E. (2018). Current and future treatment of hidradenitis suppurativa. Br J Dermatol 2020 Dec; 183 (6):e178-e187. doi: 10.1111/bjd.16768. Epub 2018 Jul 7. PMID: 29981245

8. Irish Skin Foundation. (2022). What is Hidradenitis Suppurativa (HS)? Available at: https://irishskin.ie/ hidradenitis-suppurativa/

9. HSE (2017). Hidradenitis Ssuppurativaantibiotic prescribing. Available at:

www.hse.ie/eng/services/list/2/gp/antibioticprescribing/conditions-and-treatments/skinsoft-tissue/hidradenitis-suppurativa/

10. Images: Creative Commons. https://creativecommons.org/

Skin cancer prevention in Ireland

In Ireland, the incidence of melanoma has increased in both sexes since 1994, with melanoma accounting for 3 per cent of all invasive cancers. The incidence in people aged over 60 years old is approximately five times higher than those under 60 years, according to the latest skin cancer trend report by the National Cancer Registry Ireland (NCRI). Melanoma is now the fourth-most common cancer in both sexes, with more than 1,200 cases reported annually.

Melanoma accounts for 1.7 per cent of cancer deaths in Ireland (154 deaths per year). Survival for melanoma in Ireland is generally high. However, early diagnosis can significantly improve survival rates. Nine-out-of-10 (90 per cent) patients that are diagnosed with stage I and II melanoma are alive at 10 years post-diagnosis. This compares to just one-in-two (48 per cent) of those diagnosed with stage IV disease.

Non-melanoma skin cancer (NMSC) is even more common — basal cell carcinomas (BCC) account for approximately 12,000 cases annually in Ireland, or more than all other cancers combined. The other form of skin cancer, squamous cell carcinoma (SCC), accounts for approximately 1,200 cases. Once diagnosed early, most cases of NMSC are successfully treated by surgery alone. SCC can, however, be lethal, with approximately 20 per cent of patients developing metastatic disease.

Risk factors for the development of skin cancer: Ultraviolet light

The main risk factor for the development of melanoma is ultraviolet (UV) light and the pattern of exposure is one of intense, periodic sun exposure during childhood and adolescence. It is estimated that one blistering sunburn in childhood doubles the chances of developing melanoma in later life. This intense exposure with sunburn acting as a surrogate marker also results in intermittently exposed sites having the highest rates — trunk in men, and legs in

women. Similarly, exposure to UV light through the use of sunbeds increases risk.

Certain genetic factors also increase risk of melanoma, such as having fair skin type; 75 per cent of Irish people have Fitzpatrick skin type I/II, which burns easily in the sun. Patients can check their Fitzpatrick skin type (a numerical classification schema for human skin colour) on the Irish Cancer Society website, www.cancer.ie/ cancer-information-and-support/cancer-types/skincancer/quiz-what-type-of-skin-do-you-have.

Patients who also have a large number of moles — >100 naevi in an adults and >50 in a child, or atypical naevi or dysplastic naevi — have double the risk of developing a melanoma.

These moles act as a marker of genetic risk; 70 per cent of melanomas arise de novo and not from an existing mole, however.

A family history of a first-degree relative also doubles the risk for melanoma and if patients have a personal history of a melanoma, 5-to-15 per cent of these will develop a second melanoma.

Risk factors for the development of NMSC

Fair skin type and UV exposure are the most important contributors to the development of NMSC, both BCC and SCC. The pattern of exposure to UV light is different, with chronic sun exposure such as on the face and hands of outdoor workers, while the incidence of SCC doubles every 8-to-10° closer to the Equator. Use of sunbeds also increases the risk of SCC development.

Immunosuppressant medication and skin cancer risk

Certain immunosuppressive medications also increase the risk of developing skin cancer, in particular thiopurines such as azathioprine. This risk was first recognised in organ transplant recipients, where SCC is the third-leading cause of death. In recognition of this, in 2019 the HSE reimbursed the cost of SPF for organ transplant recipients who hold a medical card. It had been known since the 1990s that azathioprine acts synergistically with UV light to cause DNA damage but in 2008, it was also shown that azathioprine makes skin photosensitive. This can induce the field change of multiple actinic keratoses, ie, on the scalp, and the risk of skin cancer here is greatest for the development of SCC.

In a large systematic review of the use of biologics in inflammatory bowel disease (IBD), rheumatoid arthritis (RA) and psoriasis, researchers found that although biologic treatment was positively associated with melanoma in patients with IBD (pRR,

1.20; 95% CI, 0.60-2.40), RA (pRR, 1.20; 95% CI, 0.83-1.74), or psoriasis (HR 1.57; 95% CI, 0.61-4.09) when compared with those who received conventional systemic therapy, the differences were not statistically significant.1 In another systematic review of 7,054 patients with IBD on biologics such as infliximab, adalimumab, certolizumab and golimumab, there was no excess risk of NMSC.2

In research work from St Vincent’s University Hospital, Dublin, the combination of thiopurines and biologics in 2,054 patients with IBD increased the risk of NMSC compared to that in the normal population recorded by the NCRI.3

Relevant history in patients with a suspected skin cancer

 Skin type: Do they tan/burn in the sun?

 Recreational sun exposure: Sun holidays/ use of sunbeds, history of blistering sunburn.

 Occupational sun exposure: Outdoor work.

 Family history of skin cancer.

 Immunosuppressive medications: Thiopurines.

Protection against skin cancer: Advice for patients

From April to September, UV radiation in Ireland is sufficiently high at ground level to cause sunburn and damage to keratinocytes. Patients should be advised to cover up with clothing, a hat and sunglasses, and use at least SPF 30 (for children this should be SPF 50) applied to exposed sites such as face, neck and back of hands. Shade should also be sought between noon and 3pm, when

PROTECT YOURSELF IN FIVE WAYS FROM SKIN CANCER

the sun is at its highest point in the sky. In 2019, the Department of Health launched the Healthy Ireland National Skin Cancer Prevention Plan, and skin cancer prevention is a key goal in the Healthy Ireland strategy.

Patients should also be aware of choosing a broad-spectrum sun factor that blocks both UVA wavelengths: 315-400nm, and UVB wavelengths: 290-315nm. The number of SPF, such as 30 or 50, refers to the UVB protection. SPF should also have a high star rating (Figure 2).

Early detection of skin cancer

The other key to reducing morbidity from skin cancer is its early detection. Patients should be able to recognise the signs of skin cancer, including the ABCDE scale of melanoma (Figure 3).

The early signs of NMSC are those of a lump or spot that is tender to touch, an ulcer that will not heal, or a lump with a scaly horn or top.

All healthcare professionals and patients have a part to play in reducing Ireland’s rising number of skin cancers. 

References

1. Esse S, et al. Melanoma Risk in Patients Treated With Biologic Therapy for Common Inflammatory Diseases: A Systematic Review and Meta-analysis. JAMA Dermatol. 2020 Jul 1;156(7):787-794.

2. Huang SZ, et al. Risk of skin cancers in thiopurines-treated and thiopurinesuntreated patients with inflammatory bowel disease: A systematic review and meta-analysis. J Gastroenterol Hepatol. 2019 Mar;34(3):507-516.

3. Clowry J et al. Increased nonmelanoma skin cancer risk in young patients with inflammatory bowel disease on immunomodulatory therapy: A retrospective single-centre cohort study. J Eur Acad Dermatol Venereol 2017 Jun;31(6):978-985.

Rosacea in focus

Rosacea is an inflammatory skin disease causing facial flushing, redness, papules, pustules and in some cases permanent dilation of small blood vessels (known as telangiectasia). The cheeks, chin, forehead, and nose are usually the worst affected, with the rest of the face mainly unaffected. Rosacea can be temporary in some cases, but is often recurrent or persistent. There are four subtypes of rosacea. It is sometimes referred to as acne rosacea; however, this can cause confusion, as rosacea is unrelated to acne vulgaris. Rosacea is mostly diagnosed in people aged 40-to-59 years and is rare in people aged under 30.

Prevalence

Worldwide estimates of prevalence vary widely from 1-to-22 per cent. It is often referred to as the ‘Curse of the Celts’, as it is especially prevalent in people of Celtic and Irish decent. For example, in a study in the US, 33 per cent of those with rosacea reported at least one parent of Irish ancestry, despite only 15 per cent of the US population being of Irish decent. Despite its association with Celtic people, rosacea also occurs in populations with darker skin tone. Its estimated prevalence in the UK is 10 per cent and an estimated 15 per cent of the population in Ireland.

Causes

The pathophysiology of rosacea is complex and multifactorial; and causes are a mix of genetic and environmental influences. A genetic cause has not been found; despite this, studies suggest that people with rosacea are four times more likely to have a family history of the disorder than people without the condition.

The immune system also has an influence in causing rosacea. High levels of cathelicidins are present in people with rosacea. Cathelicidins are antimicrobial peptides that are part of the innate immune system that cause neutrophilic infiltration of the dermis and dilation of blood vessels, causing oedema and inflammation.

Ultraviolet (UV) radiation from sunlight has a pro-inflammatory effect, which explains why sunlight exacerbates symptoms of rosacea. UVA light causes collagen denaturation and activates an inflammatory response. UVB light promotes release of fibroblast and vascular growth factors, which increase blood vascularity. Higher levels of matrix metalloproteinases (MMPs), including collagenase and elastase, increase inflammation and are seen in patients with rosacea, which may be a factor in causing the thicker and harder skin.

Other factors, including heat or capsaicin in foods, can increase flushing and burning. Increased water loss in the epithelium results in decreased epidermal hydration for rosacea patients, which worsens symptoms as it reduces the skin’s barrier function.

Influence of skin bacteria

Patients with rosacea have been shown to have higher counts of Staphylococcus epidermidis and

the hair follicle mite Demodex folliculorum, which promote inflammation.

Noted Irish rosacea expert dermatologist and researcher Prof Frank C Powell, UCD Charles Institute of Dermatology, has noted that the Dermodex mites are most plentiful in the same regions of the face that are most commonly affected by rosacea — the cheeks, nose, chin and forehead — and that large quantities of mites have been found in biopsies of rosacea papules and pustules.

Bacillus oleronius has also been linked to rosacea, probably due to increased inflammatory cytokine production.

Helicobacter pylori (H.pylori), a common bacteria found in the gastrointestinal tract, has been shown to have a higher prevalence in the gastrointestinal tract of rosacea patients. H.pylori increases levels of nitrous oxide in the blood and tissues, which is the reason it seems to increase erythema (red inflamed skin) in rosacea.

Presentation

Facial redness is the most obvious symptom of rosacea, as well as dry, flaky, sensitive skin that burns or stings when facial creams like sunscreen or make-up are applied. Rosacea increases the risk of blepharitis, sore and inflamed eyes, swelling of facial areas, and can risk development of an enlarged nose (rhinophyma) with prominent pores (sebaceous hyperplasia). The area around the eyes is unaffected, though the eyelids are often affected.

It is more common in women but tends to be more severe and peaks later in men. Rosacea tends to affect women more on the cheeks and chin, while men are more likely to have rhinophyma. Rosacea can result in self-consciousness and embarrassment that can lead to social anxiety and depression. Therefore, it is important that rosacea is not dismissed as either trivial or a simple cosmetic issue.

Primary symptoms: Erythema, pustules, and telangiectasia

Temporary facial flushing similar to blushing or sunburn in the centre of the face is often the first sign of rosacea. This is due to vasodilation. This erythema (flushing) generally becomes more permanent and noticeable with time, with swelling often developing.

Blood tests or skin biopsies are not needed to diagnose; diagnosis is based on physical signs and symptoms. Identifying triggers to be avoided should be part of the diagnosis process.

Rosacea diagnosis requires one or more of the primary symptoms, which are:

 Transient erythema, ie, flushing.

 Non-transient erythema.

 Telangiectasia: Image 1

 Papules or pustules: Image 2

Secondary symptoms

Secondary features can include a burning or stinging sensation, dry skin, oedema, phymatous changes, ie, thickened skin, lumplike nodules and enlarged, red and bumpy nose, known as rhinophyma (Image 3).

Ocular rosacea

Approximately half of people with rosacea

have symptoms affecting the eyelids or eyeball (Image 4). Symptoms include watery or bloodshot eyes, dry eyes, burning, stinging or itchy eyes, blurred vision, sensitivity to light, and recurrent styes. Ocular rosacea is also associated with conjunctivitis, anterior blepharitis, including irritation of eyelash bases and eyelid margin, and posterior blepharitis, which affects ducts and eye secretions, and meibomian cysts (small swellings on either the upper or lower eyelid, or on both). Symptoms of more severe ocular rosacea include keratitis, iritis, episcleritis and scleritis.

Conditions with similar symptoms

Skin conditions with similar symptoms to rosacea include:

 Acne vulgaris: New-onset acne vulgaris is uncommon in older populations. If open and closed comedones (blackheads and whiteheads) occur, then acne vulgaris is more likely, as they do not occur with rosacea. People with acne tend to have more greasiness of the skin. Involvement of the chest and back is often a feature of acne, but this is not the case in rosacea.

 Contact dermatitis: Irregular distribution and recurrent episodes of blistering with swelling, or red, dry plaques may indicate contact dermatitis.

 Seborrhoeic dermatitis: Presents as erythema and scaling, with some itch. Seborrhoeic dermatitis most commonly affects the lateral sides of the nose and the nasolabial folds (skin folds that run from each side of nose to corner of mouth), eyebrows and glabella (area of the forehead above and between the eyebrows).

 Rosacea fulminans: Rosacea fulminans occurs more in young women after puberty and resembles rosacea or severe acne, but flushing does not occur.

 Steroid rosacea: Due to overuse of topical steroid creams. The symptoms are similar to conventional rosacea, making it difficult to distinguish.

Subtypes of rosacea

The four subtypes are not an indication

the condition is worsening, and patients can have more than one subtype at any one time. They are:

● Erythematotelangiectatic rosacea (Image 1): Frequent episodes of transient facial erythema (flushing) and nontransient, or persistent erythema. Associated with facial oedema, burning, or stinging and rough or scaly skin.

● Papulopustular rosacea (Image 2): Includes ‘whitehead’ pustules and red, swollen bumps, which typically occurs on the cheeks, chin, and forehead and can be mistaken for acne. Facial redness and flushing may appear too, but people with papulopustular rosacea tend to have less flushing.

● Phymatous rosacea: Thickening of the skin and uneven surface nodularities on the nose, forehead, chin, ears and eyelids.

● Ocular rosacea (Image 4): Described above.

Treatment

Non-pharmacological options

There are triggers which may not be the primary cause of rosacea, but may exacerbate symptoms. They should be identified and avoided. Triggers can include sunlight, temperature extremes, wind, stress, spicy foods, hot drinks, alcohol, and some drugs such as topical corticosteroids, vasodilators such as nicotinic acid.

General advice

 Moisturise regularly, especially if skin is dry, ie, non-greasy emollients that reduce moisture loss and reduce roughness.

 Wear sunscreen. Some patients benefit by use of a high-factor sunblock (factor 30+) all-year-round.

 Placing ice between cheek and gum can reduce erythema short-term.

 Reduce spicy foods, alcohol, and hot showers.

 Ease blepharitis from ocular rosacea with:

 Warm compression and gentle massage of the eyelid margin.

 Cleaning the eyelid with a cotton bud or along the eyelid margin with diluted baby shampoo.

 Avoiding cosmetics around the eye, especially eye-liner.

 Preservative-free ocular tear substitutes are best to treat dry eyes.

Pharmacological treatment

Topical treatments are first choice for mild rosacea and oral treatments should be reserved for moderate-to-severe rosacea. The UK’s Primary Care Dermatology Society (PCDS) published Rosacea: A primary care treatment pathway in 2016. It identified that patients with rosacea often end up on prescribed antibiotics for many years; however, now that very effective non-antibiotic alternatives are available, the PCDS were keen to endorse the use of nonantibiotic treatments to help reduce risk of antibiotic resistance. For example, in the UK, it is estimated that 8 per cent of all antibiotics prescribed are for dermatology indications.

There are many topical rosacea treatments, which include:

● Metronidazole cream: Topical metronidazole’s ability to treat rosacea is due to its anti-inflammatory properties instead of its antimicrobial effects. It can be used short-term for a flare-up or longer term for more persistent cases, or combined with oral medication in persistent or severe rosacea.

Topical metronidazole should be applied to affected areas twice daily for three-to-four months to experience maximum benefit. This benefit can last for three-to-six weeks after treatment, but in some cases can give remission for up to six months after treatment. Side-effects of topical metronidazole can include dry and irritated skin, but side-effects are generally mild.

● Azelaic acid: A topical anti-inflammatory used as an alternative to topical metronidazole. It is licenced for the relief of mild-to-moderate papulopustular acne of the face and the treatment of papulopustular rosacea.

Some evidence suggests topical azelaic acid may have the benefit of not contributing to antimicrobial resistance when compared to topical metronidazole. Apply azelaic acid once or twice daily, for three-to-four months for maximum benefit. Some 70-to-80 per cent of cases see symptom improvement to some degree

within three-to-six weeks of commencement.

Side-effects of topical azelaic acid can include mild skin burning, stinging, and irritation, especially on initial use. Tolerance to sideeffects usually develops with ongoing use. Wash hands after each application to avoid irritating hands or inadvertently rubbing in the eyes. Avoid alcoholic cleansers, tinctures and astringents, abrasives, and peeling agents when using azelaic acid to minimise irritation.

Comparing topical metronidazole to topical azelaic acid

No major differences in efficacy of topical metronidazole and topical azelaic acid have been noted in studies over the years. When comparing metronidazole to azelaic acid, metronidazole 0.75 per cent gel was less effective than azelaic acid 15 per cent gel (Skinoren) in reducing inflammatory lesions and erythema. Metronidazole 0.75 per cent cream and azelaic acid 20 per cent cream (Skinoren 20 per cent cream, which is licenced in the UK, but not in Ireland) induced significant and near-equal reduction in papules and pustules. Additionally, more satisfaction was reported with azelaic acid.

Topical corticosteroids

Topical corticosteroids should not be used to treat rosacea. While topical corticosteroids can give short-term relief due to vasoconstrictive and anti-inflammatory action, they will aggravate symptoms over the following weeks. This is why topical corticosteroids are known as the ‘Great Impostor’ when it comes to rosacea; as while they reduce inflammation and redness short-term, long-term use of topical corticosteroids actually causes rosacealike symptoms.

Other topical treatments

Brimonidine gel 0.33 per cent (Mirvaso) is relatively new to the market and aims to reduce redness short-term in erythematous rosacea. It is more effective in treating flushing, but does not appear to be any more effective than metronidazole or azelaic acid for other rosacea symptoms. The possibility of rebound flushing can limit use of brimonidine gel.

The European Medicine Agency’s (EMA)

public assessment report in 2019 for Mirvaso stated that it “has not been systematically investigated” when compared to metronidazole or azelaic acid gel. While it does give relief, its effectiveness compared to more traditional treatments like metronidazole or azelaic acid is less proven, but more studies will help prove its effectiveness.

Ivermectin cream (Soolantra) can improve papulopustular rosacea. Studies show ivermectin cream will produce partial to full clearance of rosacea lesions in 40-to-80 per cent of those with moderate-to-severe symptoms after three months of treatment. Studies indicated ivermectin is more effective than metronidazole cream and gave improved quality-of-life, reduced lesion counts, and less disease severity compared to metronidazole.

Oral rosacea treatments NSAIDs

Oral medicines are reserved for rosacea that is resistant to topical treatments and for more with severe rosacea. Non-steroidal antiinflammatory drugs (NSAIDs) will not cure the condition, but may relieve discomfort (or ‘soreness’) caused by rosacea and moderately ease erythema. However, NSAIDs should in no circumstance be a first-line treatment or a longterm treatment to ease symptoms.

Oral antibiotics

Tetracycline antibiotics interfere with the inflammatory process that causes both acne and rosacea. They reduce rosacea-associated erythema, papules, pustules, and eye symptoms.

Tetracycline is effective at doses lower than required for antimicrobial treatment, meaning the clinical benefit is not due to its antimicrobial effect, but through the still unproven theory of its inhibition of MMPs. MMPs, also called matrixins, are enzymes which function in the extracellular environment of skin cells and degrade both matrix and non-matrix proteins, such as collagen and elastin.

Doxycycline and minocycline are two tetracyclines effective against rosacea. Tetracyclines in lower doses, ie, 50mg daily, are considered as effective as higher doses. Repeated

courses of tetracyclines may be required, but at low doses antimicrobial resistance is not deemed an issue.

Recommended initial treatment regimens are:

 Doxycycline 50mg, once daily, for six-to-12 weeks.

 Minocycline 50mg, once daily, for six-to-12 weeks.

Gastrointestinal side-effects of tetracyclines can include heartburn, nausea, vomiting, and diarrhoea. Photosensitivity, including photoonycholysis, can occur when taking doxycycline. Photo-onycholysis is a rare phototoxic reaction, which causes the separation of the nail plate from the nail bed. Avoid prolonged exposure to UV light from the likes of sunlight when taking doxycycline; sunscreen is advised.

Gastrointestinal adverse effects and photosensitivity are less likely with minocycline compared to doxycycline, though there is an increased risk of hepatitis and drug-induced lupus erythematosus.

Tetracycline antibiotics are teratogenic, so are contraindicated in women who are pregnant or breast-feeding. Oral contraceptives are advised in women of childbearing age.

Doxycycline MR 40mg (Efracea MR 40mg) is licenced in Ireland and the UK for rosacea with papulopustular lesions; it has fewer side-effects without being less effective than doxycycline 100mg.

Oral erythromycin may be prescribed for rosacea as an alternative to oral tetracyclines. Erythromycin is unlicensed for rosacea, but is an effective antibiotic for papulopustular rosacea. Its use can be limited by gastrointestinal disturbance. Erythromycin at a dose of 250mg/ day is effective for rosacea when intolerant to tetracyclines or those where tetracyclines are contraindicated, including pregnant women. Clarithromycin is also sometimes used for rosacea where tetracyclines are contraindicated.

Isotretinoin

Low-dose oral isotretinoin is licensed for acne, not rosacea, but it is prescribed in an unlicensed manner by dermatologists as an alternative

if oral antibiotics have been ineffective or not tolerated. The dose used for rosacea is approximately a quarter that used to treat acne, meaning side-effects are minimised; however, the course needs to continue for many months or even longer. There is good evidence to support its use with severe and persistent rosacea and in those with papulopustular and phymatous subtypes of rosacea. It is teratogenic, so female patients should use at least one effective form of contraception for one month before, during, and one month after treatment has ceased. Isotretinoin and tetracyclines are contraindicated due to a higher risk of benign intracranial hypertension.

Recommended isotretinoin regimen for rosacea is:

 Isotretinoin, 0.1-0.3mg/kg/day for 12 weeks; followed by twice-weekly long-term dosing, if required.

Side-effects of isotretinoin are numerous, but in low doses it is well tolerated. Side-effects include dry skin, lips, and eyes. Rarely, isotretinoin causes hepatic impairment, elevated serum lipid levels, pancreatitis and psychiatric events, including depression and suicide.

Drugs to reduce flushing in an unlicensed capacity

Carvedilol, a non-selective beta-blocker with some alpha-blocking activity, may be prescribed to reduce flushing as an unlicensed indication. Carvedilol 6.25mg twice-daily is thought to be the effective dose for flushing in rosacea. As with all beta blockers, carvedilol is contraindicated with asthma, hypotension, or bradycardia.

Clonidine, an alpha2-receptor agonist, is sometimes prescribed in an unlicensed indication for rosacea to reduce flushing. Its effect on facial flushing is questioned by some experts. Low-dose regimes of clonidine are advised, ie, clonidine, 25-to-50mcg daily.Clonidine is contraindicated with s evere bradyarrhythmia. It is advised to withdraw clonidine slowly to prevent rebound hypertension.

Calcineurin inhibitors such as tacrolimus ointment and pimecrolimus cream are

again unlicensed, but are only thought to give a small reduction in inflammation in severe rosacea.

These unlicensed drugs should only be prescribed as a last resort when traditional licenced treatments have failed and symptoms are so severe that they are affecting the patient’s quality-of-life. They should only be prescribed under specialist dermatologist supervision.

Pharmacological treatment for ocular rosacea

Practice good eyelid hygiene and use ocular lubricants. Pharmacological treatment for ocular rosacea should only be considered after non-pharmacological treatments have been used without success.

Evidence suggests oral tetracyclines (ie, doxycycline) and macrolides (ie, erythromycin) for one-to-three months improves tear film stability and increases meibomian secretions where ocular rosacea is severe.

Topical corticosteroids are best avoided and should only be used for the short-term treatment of very severe inflammation or rosacea keratitis (best under supervision of an ophthalmologist); as the long-term use of topical corticosteroids increases risk of glaucoma and cataracts.

Specialised treatments for rosacea

Persistent telangiectasia that is not improved by conventional topical or oral therapies for rosacea may be treated with vascular laser or intense pulsed light (IPL) treatment, with varying degrees of success in terms of reducing erythema and flushing. If these techniques are unavailable, cautery (use of mild electric current), diathermy (electrosurgery) or sclerotherapy (saline injections) may be beneficial. Where rosacea causes severe nose deformity (ie, rhinophyma), surgery or carbon dioxide laser may be used by dermatologists or plastic surgeons to reshape the nose. 

References available upon request

Disclaimer: Brands mentioned in this article are meant as examples only and not meant as preference to other brands.

PRESCRIBING INFORMATION (PI)

RINVOQ® (upadacitinib) 15 mg and 30mg prolonged-release tablets. Refer to Summary of Product Characteristics (SmPC) for full prescribing information. PRESENTATION: Each 15 mg prolonged-release tablet contains upadacitinib hemihydrate, equivalent to 15mg of upadacitinib. Each 30mg prolonged-release tablet contains upadacitinib hemihydrate, equivalent to 30 mg of upadacitinib. INDICATION: Treatment of moderate to severe active rheumatoid arthritis (RA) and active psoriatic arthritis (PsA) in adult patients who have responded inadequately to, or who are intolerant to one or more disease-modifying anti-rheumatic drugs (DMARDs). RINVOQ may be used as monotherapy or in combination with methotrexate. Treatment of active ankylosing spondylitis (AS) in adult patients who have responded inadequately to conventional therapy. Treatment of moderate to severe atopic dermatitis (AD) in adults and adolescents 12 years and older who are candidates for systemic therapy. DOSAGE AND ADMINISTRATION: Intended for use under guidance and supervision of a physician experienced in diagnosis and treatment of conditions for which upadacitinib is indicated. Dosage: RA, PsA and AS: The recommended oral dose is 15mg once daily. Consideration should be given to discontinuing treatment in patients with AS who have shown no clinical response after 16 weeks of treatment. Some patients with initial partial response may subsequently improve with continued treatment beyond 16 weeks. AD (adults): The recommended oral dose is 15 mg or 30 mg once daily based on individual patient presentation. 30 mg once daily dose may be appropriate for patients with high disease burden and for patients with an inadequate response to 15 mg once daily. The lowest effective dose for maintenance should be considered. For patients ≥ 65 years of age, the recommended dose is 15mg once daily. AD (adolescents from 12 to 17 years): The recommended oral dose is 15mg once daily for adolescents weighing at least 30 kg. Adults and adolescents 12 years and older: Upadacitinib can be used with or without topical corticosteroids. Topical calcineurin inhibitors may be used for sensitive areas such as the face, neck, and intertriginous and genital areas. Consideration should be given to discontinuing upadacitinib treatment in any patient who shows no evidence of therapeutic benefit after 12 weeks of treatment. Special Populations: Elderly: For AD, doses higher than 15mg once daily not recommended in patients aged 65 years and older. Limited data for patients aged 75 and older. Renal: No dose adjustment required in mild-moderate renal impairment. Upadacitinib 15mg once daily should be used with caution in patients with severe renal impairment. Upadacitinib 30 mg once daily is not recommended for patients with severe renal impairment. Upadacitinib has not been studied in subjects with end stage renal disease. Hepatic impairment: No dose adjustment is required in patients with mild (Child Pugh A) or moderate (Child Pugh B) hepatic impairment. Should not be used in patients with severe (Child Pugh C) hepatic impairment. Paediatric Population: No data available in the following paediatric patient populations: children with AD below the age of 12 years; children and adolescents with RA, PsA and AS aged 0 to less than 18 years. CONTRAINDICATIONS: Hypersensitivity to active substance or excipients. Active tuberculosis (TB) or active serious infections. Severe hepatic impairment. Pregnancy. SPECIAL WARNINGS AND PRECAUTIONS: See SmPC for full details. Immunosuppression: Combination use, with immunosuppressants e.g. azathioprine, ciclosporin, tacrolimus, and biologic DMARDs or other JAK inhibitors has not been evaluated in clinical studies and is not recommended as the risk of additive immunosuppression cannot be excluded. Serious infections: Serious and fatal infections have been reported. Caution when treating patients ≥65 years. Frequently reported – pneumonia and cellulitis. Bacterial meningitis has been reported. Opportunistic infections reported –TB, multidermatomal herpes zoster, oral/oesophageal candidiasis, and cryptococcosis. Do not initiate treatment in patients with active, serious infection, including localised infections. Consider the risk/benefit of treatment in patients with: chronic or recurrent infection, history of serious or opportunistic infection, those exposed to TB, those who have resided or travelled in areas of endemic TB or endemic mycoses, those with underlying conditions that may pre-dispose patients to infection. Closely monitor patients and interrupt treatment if there are signs and symptoms of infection pre and post treatment. Tuberculosis: Pre-screen patients for active or latent TB. RINVOQ should not be given to patients with active TB. Consider anti-TB therapy in patients with previously untreated latent TB or in patients with risk factors for TB infection. Consult with a physician with experience in TB therapy to assess whether initiating anti-TB therapy is appropriate for an individual patient. Monitor patients for the development of signs and symptoms of TB, including patients who tested negative for latent TB infection prior to initiating therapy. Viral reactivation: Cases of herpes virus reactivation have been reported e.g. herpes zoster. If herpes zoster is reactivated, consider interruption of upadacitinib therapy until the episode resolves. Screen for viral hepatitis and monitor regularly for reactivation before starting and during therapy with upadacitinib. Patients, positive for hepatitis C antibody/hepatitis C virus RNA and hepatitis B surface antigen/hepatitis B virus DNA were excluded from clinical studies. If hepatitis B virus DNA is detected while receiving RINVOQ, a liver specialist should be consulted. Vaccination: Use of live, attenuated vaccines during or immediately prior to therapy is not recommended. It is recommended that patients be brought up to date with all immunisations, including

THE ITCH & RASH OF MODERATE TO SEVERE ATOPIC DERMATITIS 1

RINVOQ demonstrated in an integrated analysis of the MEASURE UP 1 & 2 monotherapy studies at Week 16:

• EASI 75 skin clearance rates of 76% and 65% for patients treated with RINVOQ 30 mg QD and 15 mg QD, respectively, vs 15% with placebo (p<0.001 for both comparisons)2

• Itch reduction (mean percent change from baseline in Worst Pruritus NRS) of –70% and –58% for RINVOQ 30 mg QD and 15 mg QD, respectively, vs –24% with placebo (p<0.001 for both comparisons)2

prophylactic zoster vaccinations prior to starting therapy, in agreement with current immunisation guidelines. Malignancy: Immunomodulatory therapies may increase the risk of malignancies including lymphoma and nonmelanoma skin cancer in RA patients. Malignancies were observed in clinical studies. Periodic skin examination recommended for patients who are at increased risk for skin cancer. See SmPC for full details. Haematological abnormalities: Do not start therapy if Absolute Neutrophil Count <1 x 109 cells/L, Absolute Lymphocyte Count <0.5 x 109 cells/L and Hb <8 g/dL. Monitor patients and temporarily stop therapy if abnormal haematological parameters as specified are detected during routine patient management. Diverticulitis: Events of diverticulitis have been reported in clinical trials and post-marketing. Upadacitinib should be used with caution in patients with diverticular disease and especially in patients chronically treated with concomitant medications associated with an increased risk of diverticulitis. Patients presenting with new onset abdominal signs and symptoms should be evaluated promptly for early identification of diverticulitis to prevent gastrointestinal perforation. Cardiovascular Risk: RA patients have an increased risk for cardiovascular disorders. Manage patient’s risk factors for e.g. hypertension, hyperlipidaemia as per usual standard of care. Lipids: Monitor total cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) at 12 weeks and thereafter according to international guidelines. Elevated LDL in clinical trials decreased to pre-treatment levels in response to statin therapy, although evidence is limited. The effect of these lipid parameter elevations on cardiovascular morbidity and mortality has not been determined. Hepatic transaminase elevations: Monitor liver enzymes at baseline and thereafter according to routine patient management. Prompt investigation of the cause of liver enzyme elevation is recommended to identify potential cases of drug-induced liver injury. In such cases therapy should be interrupted until this diagnosis is excluded. Venous thromboembolism: Deep vein thrombosis (DVT) and pulmonary embolism (PE) have been reported in patients receiving JAKi, including upadacitinib. Use therapy with caution in patients at high risk for DVT/PE. Risk factors should be determined by patients age, obesity and medical history of DVT/PE, patients undergoing major surgery and prolonged immobilisation. If clinical features of DVT/PE occur discontinue therapy, evaluate and treat promptly. INTERACTIONS: Upadacitinib is metabolised mainly by CYP3A4 and plasma exposures may be affected by CYP3A4 inhibitors or inducers. Upadacitinib 15 mg once daily should be used with caution in patients receiving chronic treatment with strong CYP3A4 inhibitors. Upadacitinib 30 mg once daily dose is not recommended for patients receiving chronic treatment with strong CYP3A4 inhibitors. See SmPC for full details. FERTILITY, PREGNANCY AND LACTATION: Upadacitinib is contraindicated during pregnancy. Women of childbearing potential should be advised to use effective contraception during treatment and for 4 weeks following the final dose of upadacitinib. Female paediatric patients and/or their parents/caregivers should be informed about the need to contact the treating physician once the patient experiences menarche while taking upadacitinib. Upadacitinib should not be used during breast-feeding. The effect of upadacitinib on human fertility has not been evaluated. ADVERSE REACTIONS: Refer to SmPC for full details on adverse reactions. Very common adverse reactions (≥1/10): upper respiratory tract infections, acne. Common adverse reactions (≥1/100 to <1/10): bronchitis, herpes zoster, herpes simplex, folliculitis, influenza, anaemia, neutropaenia, hypercholesterolaemia, cough, abdominal pain, nausea, urticaria, fatigue, pyrexia, increased blood CPK/ALT/AST, increased weight and headache. This medicinal product is subject to additional monitoring. This will allow quick identification of new safety information. Healthcare professionals are asked to report any suspected adverse reactions via HPRA Pharmacovigilance; website: www.hpra.ie.

LEGAL CLASSIFICATION: POM (S1A). MARKETING AUTHORISATION NUMBER/ PRESENTATION: EU/1/19/1404/001 and EU/1/19/1404/006 – Calendar blister packs containing 28 prolonged-release tablets. MARKETING AUTHORISATION HOLDER: AbbVie Deutschland GmbH & Co. KG, Knollstrasse, 67061 Ludwigshafen, Germany. Further information is available from AbbVie Limited, 14 Riverwalk, Citywest Business Campus, Dublin 24, Ireland.

DATE OF REVISION: December 2021. PI-1404-005

Abbreviations: EASI – eczema activity and severity index; NRS – numerical rating scale; QD – once daily; EU – European Union.

* The recommended dose of RINVOQ is 15mg once daily for adolescents weighing at least 30kg. The safety and efficacy of RINVOQ in children with atopic dermatitis below the age of 12 years have not been established. No data are available. No clinical exposure data are available in adolescents <40kg. The posology in adolescent patients 30kg to <40kg was determined using population pharmacokinetic modelling and simulation.2

Reference: 1. Langan S. et al. Atopic dermatitis. The Lancet. 2020;396(10247):345-360. DOI: https://doi.org/10.1016/ S0140-6736(20)31286-1. 2. RINVOQ Summary of Product Characteristics, available on www.medicines.ie

3. Baricitinib Summary of Product Characteristics, available on www.medicines.ie 4. Abrocitinib Summary of

Product Characteristics, available on www.medicines.ie

RINVOQ, the first and only oral JAK inhibitor indicated for the treatment of both adults and adolescents ≥12 years* with moderate to severe Atopic Dermatitis in the EU2-4

Tackling dry skin and dermatitis

There are many causes of dry skin, among the most common are conditions like dermatitis, eczema, psoriasis, and seborrheic dermatitis.

Dermatitis

The simple definition of dermatitis is inflammation of the skin. Different types of dermatitis include contact dermatitis, seborrheic dermatitis (dandruff) and atopic dermatitis (eczema). Symptoms include swollen, reddened and itchy skin. About 80 per cent of dermatitis cases are ‘contact dermatitis’, caused by an allergic response to a substance with which skin has been in contact. This can include latex, detergents or jewellery, such as nickel. Symptoms are often mild. Treatment involves avoiding contact with the offending substance. Skin hydration with an emollient is important (more details below). A topical steroid such as hydrocortisone 1 per cent cream may be required.

Eczema

Eczema, a type of dermatitis called atopic dermatitis, is a chronic inflammatory skin condition that involves a complex interaction between environmental and genetic factors. It generally starts in childhood, with many growing out of it. Eczema affects over 20 per cent of children and one-in-10 adults in Ireland. It is often hereditary and there is an association with asthma and hay fever. Eczema has become more common in recent years; the cause of this is uncertain. There are theories such as the ‘hygiene theory’, which is discussed in more detail later in this article. Skin hydration can control eczema and in more severe cases, steroid creams may be temporarily required.

Psoriasis

Psoriasis affects between one-and-100 to three-in-100 of the population. It is caused by inflammation of the skin. It typically develops as patches of red, scaly skin. Plaque psoriasis is the most common type of psoriasis (about 80

per cent of cases). Symptoms are dry, red skin lesions, known as plaques, that are covered in silver scales. They normally appear on the elbows, knees, scalp, and lower back, but can appear anywhere on the body. The plaques are normally itchy, sore, or both. In severe cases, the skin around the joints may crack and bleed. Appropriate treatment will keep psoriasis under control, but there is not a definitive cure. Skin hydration is important; other treatment options for more severe psoriasis include topical steroids, topical vitamin D analogues (ie, Calcipotriol), and coal tar preparations.

Seborrhoeic dermatitis

Seborrhoeic dermatitis is characterised by red, scaly patches that develop on the scalp, face, and upper trunk. It is more likely to affect men than women. It is often aggravated by changes in humidity, changes in seasons, trauma (ie, scratching), or emotional stress. The usual onset occurs with puberty. It peaks at age 40 years and is less severe in older people. Approximately 1-to-3 per cent of adults suffer from seborrhoeic dermatitis. Dandruff is a mild form of seborrhoeic dermatitis and is estimated to affect 15-to-20 per cent of the population.

The cause of seborrhoeic dermatitis is unknown. There is evidence that a type of fungus called malassezia has an influence. Seborrhoeic dermatitis most commonly affects the sides of the nose and the nasolabial folds (skin folds that run from each side of nose to corner of mouth), eyebrows, glabella (space between eyebrows and above the nose), and scalp. There are many treatment options for seborrhoeic dermatitis. Shampoos containing anti-fungal agents like ketoconazole or ciclopirox appear to be the most effective in the control of scalp seborrhoeic dermatitis, including dandruff.

The ‘hygiene hypothesis’ and autoimmune conditions like eczema The ‘hygiene hypothesis’ is a theory that lack of exposure in early childhood to infectious

agents means that the child’s immune system has not been activated sufficiently during childhood. This lack of exposure is down to our super-clean world of modern living, including antibacterial washes, vaccinations, and general sterility where children are not exposed to germs in a similar manner to previous generations of children. The theory hypotheses that because the immune system is ‘not activated’ during childhood, this leads to the immune system becoming over-sensitive to common substances such as pollen, dust-mite, and animal fur, leading to the higher incidence of autoimmune conditions like asthma, hay fever, and eczema in recent years.

One of the first scientific explanations of this theory was by a lecturer in epidemiology from the London School of Hygiene and Tropical Medicine, David P Strachan, who published a paper on the theory in the British Medical Journal in 1989. He noticed that children from larger families were less likely to suffer from autoimmune conditions like asthma and eczema. Families have become smaller in the Western world over the last 40 years, meaning less exposure to germs and infections; it is over the same period that health authorities have seen an explosion in autoimmune conditions such as asthma and eczema. Further studies have been conducted since then, supporting the theory. For example, studies show that autoimmune diseases are less common in developing countries, however, when immigrants from developing countries come to live in developed countries where living environments are more sterile, these immigrants suffer from increased levels of autoimmune conditions like asthma, and the rate of autoimmune conditions increases the longer immigrants live in developed countries.

Treatment options Diet

In adults, food allergies or food intolerance

do not appear to be a factor in dry skin conditions such as eczema and psoriasis, so avoiding certain foods is not of any benefit. In infants, avoidance of certain foods can be helpful, but healthcare professional advice is important. Common food triggers include eggs, nuts, peanut butter, chocolate, milk, seafood, and soya.

Maintaining adequate skin hydration

Evaporation of water on the skin leads to dry skin, especially in people suffering from dry skin conditions, such as dermatitis, eczema or psoriasis; skin hydration is a key component of their overall management. Thick creams (ie, Diprobase), which have a low water content, or ointments (ie, petroleum jelly, emulsifying ointment), which have zero water content, will better protect against dry skin than lotions. Hydration is best applied immediately after bathing, when skin is hydrated. Improve hydration by soaking in a bath containing a bath additive such as Oilatum for 10-to-20 minutes. Moisturisers and emollients are discussed in more detail below.

Use of steroids

Topical corticosteroid such as hydrocortisone 1 per cent cream may be prescribed by a GP (or OTC from pharmacy) for many dry-skin conditions. The face and skin folds are areas that are at high risk of thinning and marking with corticosteroids, so care and moderation are important.

The GP may prescribe more potent corticosteroid creams, such as Clobetasone

0.05 per cent (ie, Eumovate), betamethasone

0.01 per cent (ie, Betnovate), or clobetasol

0.05 per cent (ie, Dermovate) for short periods during bad flare-ups.

In relation to potency, topical corticosteroids are classed as follows:

 Mildly potent: Hydrocortisone 1 per cent.

 Moderately potent: (two-to-25 times as potent as hydrocortisone): Clobetasone (ie, Eumovate), alclometasone (ie, Modrasone).

 Potent (100-to-150 times as potent as hydrocortisone): Betamethasone (ie, Betnovate), Mometasone (ie, Elocon).

 Very potent (up to 600 times as potent as hydrocortisone): Clobetasol (ie, Dermovate).

Corticosteroids, especially the more potent versions, should be used for the shortest period possible and use of the most potent ones should be under strict medical supervision. The patient may need to be referred to a dermatologist in more severe cases.

When using a corticosteroid and a moisturiser, it is good practice to use the corticosteroid first and to put on the moisturiser after half an hour to allow the skin time to absorb the corticosteroid. In more severe cases, treatment may include tacrolimus (Protopic ointment) for eczema or UVB phototherapy and psoralen plus ultraviolet A (PUVA) therapy for psoriasis.

Therapies with no evidence-base

Supplementation with essential fatty acids, pyridoxine, vitamin E, multivitamins, and zinc salts has no proven value. Reactions to washing powders are rare and avoidance of biological washing powders is of no benefit.

Moisturiser and emollient therapy (more detail)

No matter what type of dry skin condition, keeping the skin well moisturised is key to managing the condition. Using moisturisers and emollients is key.

Emollient therapy

 Always use soap substitutes for washing the skin at all times, ie, Silcock’s base, aqueous cream, emulsifying ointment or any brand name soap substitute.

 Do not let soap, shower gel, bath foam or shampoo contact the skin.

 Avoid perfumed products – spray on clothes if necessary.

 If possible, wash hair over the bath or sink.

Drying

Pat-dry the skin gently. Avoid scrubbing skin with a towel.

How and how often to use moisturisers

Moisturise skin immediately after washing while it is still damp; it is more effective when applied at this stage. The more often one moisturises their skin, the more

effective moisturisers are. There is no limit to the number of times that one can apply a moisturiser. Always apply moisturisers in a downward motion, in the direction of hair growth. Gently massage it into the skin. Apply enough to moisten the skin without leaving it greasy. To help remember to apply it, keep samples in various locations at home, at work and in a bag or pocket. Choose one that feels comfortable. Always avoid perfumed products.

Emulsifying ointment

Run a lukewarm water bath. Put two tablespoons of emulsifying ointment into a jug of almost-boiling water. Whisk into creamy froth and add to bath water. Emulsifying ointment makes the bath slippery, so caution is needed when getting in and out of the bath. Emulsifying ointment can be kept soft by storing it in the hot press. Stay no longer than 10 minutes in the bath. Pat skin dry afterwards and if prescribed steroidal skin cream, apply to affected area then wait 10-to-15 minutes and apply moisturiser in a downward motion.

Practical advice to manage dry skin conditions

 Nails should be kept short and well-filed to reduce damage from scratching.

 Avoid strong detergent for washing clothes; use liquid detergent.

 Double-rinse after washing; do not use a fabric softener.

 Keep the skin cool, use 100 per cent cotton, keep wool away from skin.

 Keep dust down; the house dust mite causes a problem for some people with eczema.

 Adults should wear protective gloves when doing housework.

 Avoid pets and animals if possible or at best, keep pets out of a sufferer’s bedroom. 

References available upon request

Disclaimer: Brands mentioned in this article are meant as examples only and not meant as preference to other brands.

Improving care of lower limb wounds in general practice

Lower limb ulcers are a common presentation in general practice. They are defined as a defect in the dermis located on the lower limb (HSE National Wound Management Guidelines 2018). Many of these patients present with symptoms such as leaking legs, advanced oedema, ulceration pain, and malodour. It is estimated that the population of over-65s in Ireland will triple over the next few decades, which will likely increase the prevalence and incidence of wounds and have a major impact on healthcare finances. The cost associated with management in Ireland is poorly appreciated; however Gillespie et al (2016) estimated costs of €788.5 million per annum were spent on wound care in the Irish healthcare service. Guest et al (2015) found that the management of wounds and associated co-morbidities costs the NHS in the UK £5.3 billion per annum and estimated that 1.5 per cent of the adult population in the UK is affected by active leg and foot ulceration. Within the study, Guest et al (2015) reported significant variation in care provision and the authors suggest that similar variations in care exist in the Irish healthcare service. The UK has implemented a national wound care strategy to address these anomalies with a specific strategy for the management of lower limb ulcers (2020).

Whilst we are uncertain of the true extent of lower limb ulcers in the Irish healthcare setting, the majority of these wounds are caused by chronic venous insufficiency. Arterial disease is prevalent in 15-to-20 per cent of presentations and other diseases, such as dermatological, immunological, skin tumours, and trauma, account for the remainder (HSE 2018). Leg ulcers can be time consuming and difficult to

manage in general practice. This is further compounded by varied or poor access to specialised services and the advanced wound care products required to safely and effectively manage these wounds. The purpose of this article is to inform staff working in general practice in Ireland of the current guidelines on the assessment and management of lower limb wound presentations. The information provided is based on the HSE National Wound Management Guidelines (2018) and the clinical practice recommendations therein.

When undertaking a lower limb assessment the following factors should be assessed:

 Medical and surgical history i ncluding assessment of comorbidities and medications.

 Previous or current DVT.

 History of phlebitis.

 Surgery or trauma of the affected leg.

 Prolonged standing or sitting.

 Physical examination including detailed examination of both lower limbs, the wound itself, and the surrounding skin.

 Leg wound history to include duration, size, previous wounds and treatments used.

 Vascular assessment (see Table 1 for indicators of aetiology), ABPI, pulse palpation.

 Previous venous disease, presence of varicose veins or chronic skin changes.

 Mobility and functional status.

 Pain history.

 Biochemical investigations where appropriate.

Ankle brachial pressure index (ABPI) and its interpretation

Basic assessment of lower limb wounds

One of the key questions in the guidelines asks who should assess patients who present with lower limb ulcerations. In general practice settings this can either be the GP or the general practice nurse (GPN). The HSE National Wound Management Guidelines (2018) recommends that a clinician should possess post basic education and training in the assessment and management of wounds in order to comprehensively assess and put in place an evidence-based treatment plan to manage these patients.

The ABPI is an investigation that compares ankle systolic pressure to central systolic pressure and the calculated index or result signifies the absence or presence of arterial disease, which will directly impact how the wound is managed. It is important to note that most general practices do not undertake this assessment, however, many public health centres have trained nurses who can provide this assessment. The ABPI result must be interpreted (See Table 2) in conjunction with pulse palpation and overall clinical assessment. If pulses are palpable and there is no history of diabetes or peripheral arterial disease, lower limb wounds should be placed in compression therapy (HSE National Wound

Whilst we are uncertain of the true extent of lower limb ulcers in the Irish healthcare setting, the majority of these wounds are caused by chronic venous insufficiency

Management Guidelines 2018). Application of compression therapy must be undertaken by a competent practitioner.

General lower limb wound care –back to basics

The importance of making a positive impact from the first consultation with a patient presenting with a wound cannot be underestimated. Engaging in a positive relationship is underpinned by providing the patient with the assurance that we as clinicians know what we are doing or can refer on to the appropriate specialist for further assessment. If a patient needs to be referred on for specialist opinion it is important to do so at the first contact and a plan put in place that will address the main issue that the patient is presenting with in the interim; for example, malodour, exudate

management, or pain. Once a treatment plan is adhered to, ongoing evaluation is required to determine whether this has made a positive impact on the wound and the patient.

Much has been written pertaining to variation in wound assessment and treatment in clinical practice (Guest et al, 2015). An expert group was formed and the World Union of Wound Healing Societies (WUWHS) published a consensus document (Strategies to reduce practice variation in wound assessment and management: The TIME Clinical Decision Support Tool 2020). The tool is widely used in wound care assessment and management. It was first developed by Schultz et al (2003) and has been updated to address changes in wound care practice (Moore et al

2019). The premises of the tool are to provide a structured approach to wound assessment, including holistic assessment of the patient and their wound. The tool was updated to assist clinicians who do not have specialist training in wound care management to assess patients and their wounds in a manner that provides a structured approach with clear rationale for treatment decisions. The TIME Tool assists in aiding the clinician to assess the tissue type in the wound bed, presence of inflammation or infection, moisture balance, and the status of the wound edge. It gives a pictorial guide to descriptors and dressing types suitable to each descriptor and provides a structured wound management approach that enables consistency, which then contributes to better patient outcomes.

Wound hygiene

Wound hygiene has become an important concept in wound care (International Consensus Document Wound Hygiene, 2020). The concept was devised to address the growing burden of hard-to-heal wounds, particularly in relation to biofilm and wound infection identification and management. The consensus document promotes the application of a wound cleansing strategy to improve the management of hard-to-heal wounds through disruption of biofilm present in the wound bed, and prevention of its reformation. It consists of two stages with overlapping strategies:

 Cleansing the wound and peri-wound skin.

 Debridement as necessary, which may be more aggressive initially, but reverts to maintenance debridement when clinically indicated.

 Refashioning the wound edge.

 Dressing the wound.

The document proposes that all hard-to-heal wounds contain biofilm (International Consensus Document Wound Hygiene, 2020) and in the absence of good wound hygiene, progression to failure to heal becomes a real threat despite the use of dressings. Whilst it may seem strange that a strategy needs

The following should be considered by clinicians when assessing lower limb wounds to differentiate between venous and arterial aetiology

ABPI

ABPI

ABPI

ABPI < 0.5 Critical ischaemia

ABPI > 1.3 Refer to vascular/ diabetic specialist

Table 2 : ABPI interpretation (Adapted from Andriessen et al, 2017)

to be employed to promote wound cleansing, let us as practitioners reflect back on our practice and last dressing change. When cleansing the wound did you simply gently swipe moistened gauze over the wound bed itself and proceed to dressing or did you cleanse the wound bed aggressively enough to remove devitalised tissue, debris, and biofilm? Moreover, did you cleanse the peri-wound tissue to remove skin scales or callus or built-up dressing debris? This is perhaps a major failing in wound care practice today and failure to do so encourages growth of biofilm and transitioning of a wound to the hard-toheal stage.

Debridement is also a vital part of wound hygiene and whilst the term itself may lend one to think of a scalpel, there are many forms of wound debridement that result in removal of necrotic tissue, slough, debris and wound biofilm (HSE National Wound Management Guidelines, 2018).

Wound edges can provide a sanctuary for biofilm to form and refashioning the edges in the aforementioned strategy alludes to simply removing necrotic or crusty

material from the overhanging wound edges. It is also important to ensure the skin edges are aligned to facilitate the advancement of epithelial cells and in turn promote wound contraction or closure (International Consensus Document Wound Hygiene, 2020).

References

1. Gillespie P, Carter L, McIntosh C, and Gethin G, (2016). Estimating the healthcare costs of wound care in Ireland. Unpublished poster presentation at EWMA 2016, May 10-13 2016, Bremen, Germany

2. HSE National Wound Management Guidelines 2018. Available at: www.hse.ie/ eng/about/who/onmsd

3. Moore Z, Dowsett C, Smith G, et al (2019). TIME CDST: An updated tool to address the current challenges in wound care. Journal of Wound Care 28(3): 154-61

4. Murphy C, Atkin L, Swanson T, et al (2020). International consensus document. Defying hard to heal wounds with an early antibiofilm intervention strategy: Wound hygiene. Journal of Wound Care 29(Suppl 3b): S1-28

Finally, in order to address the remaining biofilm or prevent overt formation or delay growth of biofilm it is important to use appropriate dressings (HSE National Wound Management Guidelines 2018). These dressings may contain antimicrobial or anti-biofilm properties (Schultz et al 2017). Further consideration must be given to patient choice and engagement and to availability. Dressings available can be prescribed for patients and dispensed in their local pharmacy. The pharmacy will have a list of what products are available on the medical card scheme. Referral to the local primary care centre with access to a dressing clinic can also be arranged, particularly for patients with wounds that are likely to become hard to heal.

As previously stated, the number of people living with complex conditions is increasing, which directly impacts on the increasing number of hard-toheal wounds with both financial and social implications in a health service that has finite resources. Tackling these wounds in the early stages of onset may circumvent later complications and promote better patient outcomes. 

5. National Wound Care Strategy Programme (2020). Recommendations for lower limb ulcers

6. Schultz GS, Bjarnsholt T, James GA, et al (2017). Consensus guidelines for the identification and treatment of biofilms in chronic non-healing wounds. Wound Repair and Regeneration, 25: 744-757

7. Schultz GS, Sibbald RG, Falanga V, et al (2003). Wound bed preparation: A systematic approach to wound management. Wound Repair and Regeneration, 11:1-28

8. World Union of Wound Healing Societies (2020). Strategies to reduce practice variation in wound assessment and management: The TIME Clinical Decision Support Tool. London: Wounds International. Available at: www.woundsinternational.com

Book review: Textbook of Primary Care Dermatology

BOOK TITLE: Textbook of Primary Care Dermatology

AUTHORS: Dr David Buckley and Dr Paola Pasquali

PUBLISHER: Springer

REVIEWER: Dr Karen Enright

As a GP with more than a little interest in dermatology, this book by the guru of primary care dermatology Dr David Buckley, and Dr Paolo Pasquali, was my favourite Christmas present.

Dr Buckley is a leader in Irish community dermatology with the Kerry Skin Clinic, which treats all manner of medical, surgical, and allergic skin disease and is an outstanding example of what can be achieved in primary care with training, expertise and passion.

I cannot recommend this textbook enough. All GPs, general practice nurses and other healthcare professionals with (or without) an interest in dermatology would benefit from having a copy of this book on their shelf.

It is written from the perspective of a GP, focusing on the practical management of common, and some uncommon, skin conditions, what we can safely manage ourselves, and how and when to phone a friend.

Skin complaints represent at least 15 per cent of GP consultations, and often times they are an ‘add on’ at the end of the consultation – “oh, while I am here doc, can you check this mole/rash/lump for me”.

As Dr Buckley points out, skin disease should be considered as relevant and prioritised the same way as any other medical complaint and we need to remind ourselves and patients of this, because a life-threatening skin cancer could be missed at a treatable stage.

Dr Buckley makes a great point in the chapter on ageing skin; the burden of skin disease is much higher in the elderly and with life expectancy increasing year on year – based on trends predicted by the Central Statistics Office (CSO) in Ireland – the number of people aged over 65 years is likely to double or even triple over the next 35 years. Therefore, there will be an

ever-increasing demand for skin care in the elderly in the community going forward.

Dermatology tends to be a marmite subject among GPs; you either love it or hate it. Undergraduate training is significantly lacking in dermatology and so unless they are lucky enough to get a postgraduate dermatology post, skin disease can be much of a mystery to many GPs.

Dr Buckley makes the reassuring statement that when it comes to undiagnosed skin eruptions, it is much more likely to be an unusual presentation of a common problem than a rarity in the subtext of a dermatology textbook. So a broad knowledge of the basics of medical dermatological presentations with a fundamental plan for each is likely to get the majority of presentations managed.

Skin lesions

When it comes to surgical dermatological presentations of pigmented and nonpigmented skin lesions in Dr Buckley’s words: “There is only one rule when assessing suspicious pigmented (or nonpigmented) lesions – if in doubt cut it out or refer to a colleague with more experience in skin recognition.”

The chapter on lesion recognition is a great resource with a flowchart from the Primary Care Surgical Association (PCSA) describing management of new or changing lesions.

Dr Buckley’s four-point warning signs for skin cancer ‘new cancers do show’ is a very useful and memorable acronym to alert doctors and patients to lesions that should be viewed with suspicion:

 New – a new growth sore, freckle or mole that has appeared in the past sixto-12 weeks.

A strap line for all primary care surgical-trained GPs is, ‘If in doubt, cut it out’

 Changing – a growth, sore, freckle or mole that is changing in size, shape or colour.

 Different – a growth, sore, freckle or mole that looks different from any other, ‘ugly duckling’ sign.

 Sore – a growth, sore, freckle or mole that is sore, tender, bleeding or itchy.

Acne

Acne is one of the most common dermatological presentations in general practice, with 90 per cent of teenagers developing it at some stage and around half of these continuing to suffer as an adult. Dr Buckley describes a stepwise approach to management with flow charts, rationale behind each treatment, and what to do if not responding.

Included is a prescribing guide, courtesy of Dr Deirdre Lundy; one of Ireland’s leading experts in women’s health, describing acne as generally mediated through progesterone, which can be a likely side-effect of secondgeneration oral contraceptive pills (OCP). Therefore, it is recommended to switch to a fourth-generation OCP initially and if not improving increase to a higher oestrogen dose OCP. The examples of each of these with trade names are listed, making this a most useful and practical reference flowchart.

Dr Buckley also describes how to safely treat acne in pregnancy, which can be challenging.

Eczema

Included in the chapter on eczema is something I have never read before; a table listing over-the-counter (OTC) emollients from most oily to least. This is incredibly helpful when suggesting the most appropriate emollient or soap substitute for a patient, when invariably they have already tried a few, and this gives the expertise to explain why their eczema/ dermatosis/xerosis has not responded and what might be a better choice.

Allergic skin disease

Included in the allergic skin diseases chapter is a table describing how to distinguish various forms of dermatitis; atopic, irritant contact dermatitis, and allergic contact dermatitis from clinical features. Then most helpfully when and what allergy test is required to confirm the diagnosis; from IgE blood tests, skin patch or skin prick testing – which speaking for myself has always been a subject of confusion. Following is a list of common allergens tested on a patch test (type 4 allergy, eg, allergic contact dermatitis) and aeroallergens and ingested allergens on skin prick testing (type 1 hypersensitivity, eg, urticaria). Although any type of drug can cause any type of dermatological eruption, a list of the most common suspects is provided to give some clarity when trying to eliminate iatrogenic aetiology in those difficult to treat chronic urticaria presentations.

Warts

Warts are a very common and often frustrating presentation in primary care for the doctor and the patient. Although they are harmless (aside from anogenital warts, which are associated with increased risk of cancer) and will inevitably resolve within two years, they can cause distress and embarrassment especially in children and young adults when on the face or hands. A list of treatment options when the first-line OTC topical ointments have not been successful is provided. This includes the obvious cryosurgery, but also the less obvious 5 per cent imiquimod, topical podophyllotoxin, topical glutaraldehyde, and a very effective treatment used in Canada, cantharidin, which may become available in Ireland in the future. Equally practical information is a list of the salicylic acid-based topical treatments with the percentage of salicylic acid present in the preparation from ‘Vericaps plasters’ at 12 per cent to ‘Verrugon ointment’ at 50 per cent, meaning if patients want to stick with topical therapy, an evidence-based suggestion can be given with stepwise increase in concentration of salicylic acid. About 75 per cent of warts will resolve with

topical salicylic acid when used properly.

Skin surgery

Now for a subject close to my heart, skin surgery. A strap line for all primary care surgical-trained GPs is, “If in doubt, cut it out.” As Dr Buckley describes, training in dermoscopy can often help with diagnosis of pigmented and non-pigmented skin lesions, but if an accurate diagnosis cannot be made, the safest option is to gain histology with an incisional or excisional skin biopsy. In Dr Buckley’s words, “any changing or new mole over the age of 40 should be viewed with suspicion and referred to a colleague with more experience in skin lesion recognition.” Equally, although most melanomas are pigmented, amelanotic melanomas can present as a non-pigmented macule or nodule and “any new or changing lesion, regardless of colour, should be viewed with suspicion and biopsied unless a confident, clinical, named diagnosis can be made based on history, examination, and dermoscopy”.

Dr Buckley outlines best practice for simple skin surgery with pathways for biopsy and safeguarding tips including: “most skin surgery errors are made with the pen not the knife”. Other tips include stretching the skin perpendicular to Langer lines when doing a punch biopsy to enable easy closure, wound healing, and reduced scar formation.

Something very useful as a quick reference for any GP performing skin surgery is the outline of the PCSA guidelines for patients taking anticoagulants and skin surgery, for patients taking antiplatelets, DOACs or warfarin.

There is also a great tip on local anaesthetic and adrenaline use when performing skin surgery.

Photoageing

The chapter on photoageing was most interesting. Dr Buckley makes an interesting point that most ageing of

the face and hands is likely to be due to accumulation of photodamage from UV exposure. Actinic keratosis, solar lentigos, elastosis, skin thinning, wrinkling, telangiectasia, purpura, and of course NMSA all increase with age, but if you compare the skin on the face to that of the buttocks – it is evident there is a vast influence from UVR.

There are various treatments including topical tretinoin, hydroquinone, vitamin C and E, chemical peels, and aesthetic injectables, such as botulinum toxin and intradermal fillers, which can address some of the ageing effects of the skin. However, the most basic and effective is prevention rather than cure by the application daily of SPF factor 30 or greater all year round.

Dr Buckley debunks some of the myths surrounding SPFs. Anything over SPF 50 does not confer any additional benefit and adds an additional chemical load as the higher the SPF in chemical sunscreens, the higher the concentration of sun-filtering chemicals. For this reason physical sunscreens may be more suitable for people with sensitive or allergy prone skin. Chemical sunscreens may be poorly tolerated by patients with rosacea, lupus or photodermatosis. Of course, here in not-so-sunny Ireland the majority of us are vitamin D deficient in the winter months. The use of high-factor SPF may interfere with the skin’s ability to metabolise vitamin D in the summer, therefore Dr Buckley suggests considering a vitamin D supplement, especially in those aged over 50 years.

Leg ulcers

The chapter on leg ulcers gives a really straightforward approach when addressing a leg ulcer. Dr Buckley recommends that basic advice to the patient should not be underestimated, which includes encouraging walking and avoiding standing, elevating the feet and ankles for two hours in the morning and evening, and maintaining a healthy weight, diet, and level of hydration.

In clinic the next practical step is to perform a pedal pulse check and ankle brachial pressure index (ABPI) if these are weak, impalpable or difficult to assess. Based on the ABPI index, the recommendation of grades of compression or referral to a vascular surgeon is described.

He then gives a visual step-by-step demonstration of how to apply compression bandages. And beyond that a description of what type of dressing is suitable for each type of ulcer whether it be infected, complicated/resistant, non-infected exudative or simply weeping eczema. I will admit the world of dressings has always been a mystery to me, leaving that rather sheepishly in the hands of my esteemed nursing colleagues!

and melanocytic naevi in children is very useful. Dr Buckley describes the different vascular tumours: Capillary haemangioma (strawberry naevus), capillary malformations (port wine stain), and nevus flammeus (stork mark and angel kisses). He describes the clinical features, the natural history and when to refer to dermatology and why. Of interest the advice is to refer infants with over five capillary haemangiomas for a liver ultrasound, because of increased risk of liver haemangiomas. Also, presence of capillary haemangiomas in the midline increases risk of airway haemangiomas.

Melanocytic naevus acquired before the age of two are deemed congenital and over the age of two, acquired. He describes the appearance and histological features of the different types of melanocytic naevus; junctional, compound, and intradermal.

There is also a chapter on Covid-19 skin disease and the merits of telemedicine in dermatology, which is very topical.

Dr Buckley outlines timeframes where ulcers less than 1cm should heal over six-to-12 weeks with compression bandages, with advice on when to change the dressings.

Practical tips

A tip I will most definitely use to aid diagnosis of pityriasis versicolour is to place sellotape over a small plaque. This common patchy scaly hyper- or hypo-pigmented eruption is caused by a proliferation of a normal skin commensal Malassezia. Using the sellotape will reveal an area of scales in the exact shape as the skin lesion. Once treated with oral or topical anti-fungals the infection is no longer present, but the pigmentary changes can persist for six-to-12 weeks.

Vascular tumours and naevi

The chapter on vascular tumours

A special mention also needs to be given to the patient information leaflets. These are so practical, useful, and timesaving for GPs to have to hand. There is everything from consent forms for minor surgery, hand-care tips for dermatitis, how to safely use topical steroids with fingertip units, to managing scabies and head lice. With Dr Buckley’s permission I will have a copy of all these sitting to hand in my clinic!

I have read my fair share of dermatology textbooks and this is the best; most comprehensive, practical and GP-focused guide I have come across. Thank you Dr Buckley and Dr Pasquali for sharing your wealth of experience and information. The GPs and GPNs who read it, and their dermatology patients, will be all the better for it. 

To order a copy of this book go to: https://link.springer.com/book/10.1007/978-3030-29101-3.

... and this is the best; most comprehensive, practical and GP-focused guide I have come across

DEMONSTRABLE JOINT EFFICACY

PROVEN DURABILITY*

Most patients who started on TREMFYA® stayed on TREMFYA® long-term1,2

Durability*, also known as patient retention or drug survival is a combination of efficacy, safety, tolerability and patient satisfaction or preference. DISCOVER-2 was a Phase 3, double-blind, multi-centre, placebo-controlled study that evaluated the efficacy and safety of TREMFYA® in bio-naïve patients with active PsA.1

Tremfya▼ 100 mg solution for injection in pre-filled pen PRESCRIBING INFORMATION. ACTIVE INGREDIENT(S): Guselkumab. Please refer to Summary of Product Characteristics (SmPC) before prescribing. INDICATION(S): Treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy. Treatment of active psoriatic arthritis in adult patients, alone or in combination with methotrexate, who have had an inadequate response or have been intolerant to a prior disease-modifying antirheumatic drug (DMARD) therapy. DOSAGE & ADMINISTRATION: For use under guidance/supervision of physician experienced in diagnosis and treatment of conditions for which Tremfya is indicated. Subcutaneous injection. Avoid areas showing psoriasis. Adults: For both indications, 100 mg at weeks 0 and 4, followed by maintenance dose every 8 weeks. In the case of psoriatic arthritis, for patients at high risk for joint damage according to clinical judgement, consider a dose of 100 mg every 4 weeks. Consider discontinuation if no response after 16 weeks of treatment for plaque psoriasis and 24 weeks for psoriatic arthritis. Children: No data available in children/adolescents <18 years. Elderly: No dose adjustment required, limited information in subjects aged ≥ 65 years, very limited information > 75 years. Renal & Hepatic impairment: Not studied. CONTRAINDICATIONS: Serious hypersensitivity to active substance or excipients; clinically important, active infection. SPECIAL WARNINGS & PRECAUTIONS: Infections: Potential to increase risk. If signs/symptoms of clinically important chronic/ acute infection occur, monitor closely and discontinue Tremfya until resolved. Tuberculosis: Evaluate patients for TB pre-treatment; monitor for signs/symptoms of active TB during and after treatment. Consider anti-TB therapy prior to Tremfya if past history of latent/active TB and adequate treatment course not confirmed. Serious hypersensitivity reaction: Includes anaphylaxis. Some serious hypersensitivity reactions occurred several days after treatment and included urticaria and dyspnoea. If occurs, discontinue Tremfya immediately and initiate appropriate therapy. Hepatic Transaminase Elevations: An increased incidence of liver enzyme elevations has been observed in patients treated with Tremfya q4w compared to patients treated with Tremfya q8w or placebo. When prescribing Tremfya q4w in psoriatic arthritis, consider evaluating liver enzymes at baseline and thereafter according to routine patient management. If increases in ALT or AST are observed and drug-induced liver injury is suspected, Tremfya should be temporarily interrupted until this diagnosis is excluded. Immunisations: Consider completing all appropriate immunisations prior to Tremfya. Do not use live vaccines concurrently with Tremfya; no data available; before

live vaccination, withhold Tremfya for at least 12 weeks and resume at least 2 weeks after vaccination. SIDE EFFECTS: Very common: Respiratory tract infection. Common: headache, diarrhoea, arthralgia, injection site reactions, transaminases increased. Other side effects: hypersensitivity, anaphylaxis, rash, herpes simplex infections, neutrophil count decreased. Refer to SmPC for other side effects. LEGAL CATEGORY: Prescription Only Medicine (POM). PRESENTATIONS, PACK SIZES, MARKETING AUTHORISATION NUMBER(S): Pre-filled pen, x1, EU/1/17/1234/002. MARKETING AUTHORISATION HOLDER: Janssen-Cilag International NV, Turnhoutseweg 30, B-2340 Beerse, Belgium. FURTHER INFORMATION IS AVAILABLE FROM: Janssen Sciences Ireland UC, Barnahely, Ringaskiddy, IRL - Co. Cork, P43 FA46. Prescribing information last revised: November 2020.

Adverse events should be reported. ▼ This medicinal product is subject to additional monitoring and it is therefore important to report any suspected adverse events related to this medicinal product. Healthcare professionals are asked to report any suspected adverse events via: HPRA Pharmacovigilance Website: www.hpra.ie.

Adverse events should also be reported to Janssen Sciences Ireland UC on 1800 709 122 or at dsafety@its.jnj.com.

References:

1. Griffiths CEM, et al. Maintenance of Response Through 5 Years of Continuous Guselkumab Treatment: Results From the Phase 3 VOYAGE 1 Trial. Presented at the 16th Annual Coastal Dermatology Symposium. October 15-16, 2020. 2. McInnes IB, et al. Efficacy and Safety of Guselkumab, a Monoclonal Antibody Specific to the p19-Subunit of Interleukin-23, Through 2 Years: Results from a Phase 3, Randomized, Double-blind, Placebo-controlled Study Conducted in Biologic-naïve Patients with Active Psoriatic Arthritis. Presented at Innovations in Dermatology Conference, March 16-20, 2021. Online. 3. Griffiths C, et al. Achieving and maintaining long-term optimal improvements in patient-reported symptoms, signs, and quality of life among patients with moderate-to-severe psoriasis treated with guselkumab: 5-year data from VOYAGE 1. Presented at AAD VMX 2021. 4. Blauvelt A, et al. J Am Acad Dermatol 2017;76:405-417.

© Janssen-Cilag Limited

COMPLETE SKIN CLEARANCE

Sustained joint symptom relief proven for 2 years in PsA2

Fast4 and sustained complete clearance proven for 5 years in Ps01

OTEZLA® has an established efficacy and safety profile for up to 5 years†1,2

No contraindications for concurrent use with live vaccination

2

Minimise frequency of clinical appointments

No warnings regarding risk of serious infection

2

A short half-life of 9 hours

Means that OTEZLA® is rapidly cleared from the body if administration needs to be stopped2

Immunomodulatory mode of action

2

No laboratory pre-screening, and no drug specific blood monitoring required

2

Make OTEZLA® the positive choice for your psoriasis and psoriatic arthritis patients

OTEZLA® (apremilast) 10mg, 20mg and 30mg film coated-tablets Brief Prescribing Information. Refer to the Summary of Product Characteristics (SPC) before prescribing. Further information is available upon request. Presentation: 10mg, 20mg and 30mg film coated-tablets. Indications: Psoriatic arthritis: OTEZLA, alone or in combination with Disease Modifying Antirheumatic Drugs (DMARDs), is indicated for the treatment of active psoriatic arthritis (PsA) in adult patients who have had an inadequate response or who have been intolerant to a prior DMARD therapy. Psoriasis: OTEZLA is indicated for the treatment of moderate to severe chronic plaque psoriasis in adult patients who failed to respond to or who have a contraindication to, or are intolerant to other systemic therapy including ciclosporine, methotrexate or psoralen and ultraviolet-A light (PUVA). Dosage and administration: Treatment with OTEZLA should be initiated by specialists experienced in the diagnosis and treatment of psoriasis or psoriatic arthritis. The recommended dose of OTEZLA is 30mg twice daily taken orally in the AM and PM, approximately 12 hours apart, with no food restrictions. The film-coated tablets should be swallowed whole. An initial dose titration is required per the following schedule: Day 1: 10mg in the AM; Day 2: 10mg in the AM and 10 mg in the PM; Day 3: 10mg in the AM and 20mg in the PM; Day 4: 20mg in the AM and 20mg in the PM; Day 5: 20mg in the AM and 30mg in the PM; Day 6 and thereafter: 30mg twice daily in the AM and PM. No re-titration is required after initial titration. If patients miss a dose, the next dose should be taken as soon as possible. If it is close to the time for their next dose, the missed dose should not be taken and the next dose should be taken at the regular time. Patients with severe renal impairment: The dose of OTEZLA should be reduced to 30mg once daily in patients with severe renal impairment (creatinine clearance of less than 30mL per minute estimated by the Cockcroft-Gault equation). For initial dose titration in this group, it is recommended that OTEZLA is titrated using only the AM doses and the PM doses be skipped. Paediatric population: The safety and efficacy of OTEZLA in children aged 0 to 17 years have not been established. No data is available. Contraindications: Hypersensitivity to the active substance(s) or to any of the excipients. OTEZLA is contraindicated in pregnancy. Pregnancy should be excluded before treatment can be initiated. Special warnings and precautions: Diarrhoea, nausea and vomiting: Severe diarrhoea, nausea, and vomiting associated with the use of OTEZLA have been reported. Most events occurred within the first few weeks of treatment. In some cases, patients were hospitalized. Patients 65 years of age or older may be at a higher risk of complications. Discontinuation of treatment may be necessary. Psychiatric disorders: OTEZLA is associated with an increased risk of psychiatric disorders such as insomnia and depression. Instances of suicidal ideation and behaviour, including suicide, have been observed in patients with or without history of depression. The risks and benefits of starting or continuing treatment with OTEZLA should be carefully assessed if patients report previous or existing psychiatric symptoms or if concomitant treatment with other medicinal products likely to cause psychiatric events is intended. Patients and caregivers should be instructed to notify the prescriber of any changes in behaviour or mood and of any suicidal ideation. If patients suffered from new or worsening psychiatric symptoms, or suicidal ideation or suicidal attempt is identified, it is recommended to discontinue treatment with OTEZLA. Severe renal impairment: See dosage and administration section. Underweight patients: OTEZLA may cause weight loss. Patients who are underweight at the start of treatment should have their body weight monitored regularly. In the event of unexplained and clinically significant weight loss, these patients should be evaluated by a medical practitioner and discontinuation of treatment should be considered.

Lactose content: Patients with rare hereditary problems of galactose intolerance, total lactase deficiency or glucose-galactose malabsorption should not take this medicinal product. Interactions: Co-administration of strong cytochrome P450 3A4 (CYP3A4) enzyme inducer, rifampicin, resulted in a reduction of systemic exposure of OTEZLA, which may result in a loss of efficacy of OTEZLA. Therefore, the use of strong CYP3A4 enzyme inducers (e.g. rifampicin, phenobarbital, carbamazepine,

Confidence not compromise in immune response, down-regulation of proinflammatory cytokines and up-regulation of anti-inflammatory cytokines

phenytoin and St. John’s Wort) with OTEZLA is not recommended. In clinical studies, OTEZLA has been administered concomitantly with topical therapy (including corticosteroids, coal tar shampoo and salicylic acid scalp preparations) and UVB phototherapy. OTEZLA can be co-administered with a potent CYP3A4 inhibitor such as ketoconazole, as well as with methotrexate in psoriatic arthritis patients and with oral contraceptives. Pregnancy, lactation and fertility: Women of childbearing potential should use an effective method of contraception to prevent pregnancy during treatment. OTEZLA should not be used during breast-feeding. No fertility data is available in humans. Undesirable effects: Psychiatric disorders: In clinical studies and post-marketing experience, uncommon cases of suicidal ideation and behaviour, were reported, while completed suicide was reported post-marketing. The most commonly reported adverse reactions with OTEZLA in these indications are gastrointestinal (GI) disorders including diarrhoea (15.7%) and nausea (13.9%). These GI adverse reactions generally occurred within the first 2 weeks of treatment and usually resolved within 4 weeks. Adverse reactions reported in the psoriatic arthritis and/or psoriasis clinical trial programme and post marketing experience include: very common (≥ 1/10) diarrhoea*, nausea*; common (≥1/100 to <1/10) bronchitis, upper respiratory tract infection, nasopharyngitis*, decreased appetite*, insomnia, depression, migraine*, tension headache*, headache*, cough, vomiting*, dyspepsia, frequent bowel movements, upper abdominal pain*, gastroesophageal reflux disease, back pain*, fatigue; uncommon (≥1/1,000 to <1/100) hypersensitivity, suicidal ideation and behaviour, gastrointestinal haemorrhage, rash, urticaria, weight loss; not known (cannot be estimated from the available data) angioedema. *At least one of these adverse reactions was reported as serious. Please consult the SPC for a full description of undesirable events. Pharmaceutical Precautions: Do not store above 30°C. Legal category: POM. Presentation and Marketing Authorisation Numbers: Initiation pack containing 27 film coated tablets (4 x 10mg, 4 x 20mg, 19 x 30mg) - EU/1/14/981/001; 30mg film coated tablets in a pack size of 56 tablets - EU/1/14/981/002. Marketing Authorisation Holder: Amgen Europe B.V. Minervum 7061, 4817 ZK Breda, The Netherlands. Further information is available from Amgen Ireland Limited, 21 Northwood Court, Santry, Dublin D09 TX31. OTEZLA is a trademark owned or licensed by Amgen Inc., its subsidiaries, or affiliates. Date of preparation: April 2020 (Ref: IE-OTZ-2000019).

Adverse reactions/events should be reported to the Health Products Regulatory Authority (HPRA) using the available methods via www.hpra.ie. Adverse events should also be reported to Amgen Limited on +44 (0)1223 436441.

† Otezla met the primary endpoint of the pivotal trials in psoriasis: PASI-75 response vs placebo at 16 weeks. ESTEEM 1: 33.1% (N=562) vs 5.3% (N=282); ESTEEM 2: 28.8% (N=274) vs 5.8% (N=137), P<0.0001. OTEZLA met the primary endpoint of the pivotal trials in Psoriatic Arthritis: ACR 20 response vs placebo at 16 weeks. PALACE 1: 38% (N=168) vs 19% (N=168), P≤0.001. PALACE 2: 32% (N=162) vs 19% (N=159) P≤0.01; PALACE 3: 41% (N=167) vs 18% (N=169) P≤0.001.2

References: 1. Kavanaugh et al. Arthritis Research & Therapy 2019: 21;118. 2. OTEZLA (apremilast). Summary of Product Characteristics.

OTEZLA® can offer solutions to the challenges in this new environment