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Elizabeth Gribaleva, MD MSc Clinical Dermatology student King's College London Inflammatory skin conditions: a brief overview Topics to be covered • Eczema: • atopic dermatitis • contact dermatitis • Psoriasis • AcneEczema: atopic dermatitis and beyond https://nationaleczema.org/eczema/ In your opinion, what eczema is?Classification of eczema Atopic (= Contact atopic (allergic, Hand Seborrhoeic dermatitis) irritant) Nummular/ Dyshidrotic Asteatotic Discoid (pompholyx) Venous Adopted from Rook's Textbook of Dermatology, 9th edition Sometimes, it can be classified into exogenous and endogenous subgroupsAtopic eczema (AE) • Atopy= predisposition to develop asthma, hay fever, AE • Loss of function mutation in filaggrin gene (FLG) is linked with the development of AE due to the impairment of skin barrier function • Complex interaction of genetic and environmental factors, leading to T-helper type 2(Th2)- driven immune signaling • Increased permeability of skin barrier makes AE patients more prone to secondary bacterial infection and overgrowth of Staphylococcus aureus, sustaining the existing inflammation Dermatology Lecture Notes 11th edition 2017 Wiley Blackwell Atopic eczema Acute: oedema, erythema, vesicles, exudation, Chronic: papulation, lichenification, fissuring https://dermnetnz.org/topics/atopic-dermatitis Atopic eczema evolution Infantile / childhood eczema Adult eczema • Frequently appears in 1st year of life • Punctated course with episodic exacerbations • Face: cheeks • Flexural areas: Antecubital fossa • Hands • Popliteal fossa • Trunk • Wrists • Generalised • Dorsa of feet • Acute characteristics: erythema, oozing, vesiculation, crusting • Chronic characteristics: lichenification, xerosis • AE often resolves in childhood • Impossible to predict the course and outcome Dermatology Lecture Notes 11th edition 2017 Wiley Blackwell Complications • Secondary bacterial infections – folliculitis, impetigo • HSV infection ! Eczema herpeticum! • Molluscum contagiosum • Viral warts Dermatology Lecture Notes 11th edition 2017 Wiley BlackwellTreatment of AE: a stepp approach • Emollients are the mainstay of treatment of eczema • Topical anti-inflammatory treatment • Topical corticosteroids (TCS): mild/ moderately potent/ potent • TCS + topical antibiotic/ systemic antibiotics • Topical calcineurin inhibitors (TCI) • Tacrolimus, pimecrolimus • Phototherapy (narrow band UVB, PUVA) • Systemic immunosuppressive agents (prednisolone, ciclosporin, methotrexate, mycophenolate mofetil, azathioprine); dupilumab (anti-IL4/13 mAb), tralokinumab (anti-IL-13 mAb), JAKi (upadacitinib, abrocitinib) • Psychological support and screening for anxiety and depression *licensed for AE treatment NICE guidance Stepped approach to treatment of AE (2007, reviewed in 2021) Contact dermatitis External agent Irritant contact dermatitis (ICD) 80% Allergic contact dermatitis (ACD) 20% • Occurs as a response to an irritant • Occurs in sensitised patients (chemical- soap, detergents, physical- • Type IV (delayed) hypersensitivity friction, trauma) in increased dose/ reaction prolonged exposure – cumulative • Common allergens: effect nickel, rubber, cosmetics, hair dyes, • Does not require sensibilisation topical medicaments, plants • Occupational ICD is common Dermatology Lecture Notes 11th edition 2017 Wiley Blackwell; Bolognia Dermatology 4th editionIrritant contact dermatitis (ICD) • Primary irritants damage the skin • Acids, alkalis, detergents, soaps—immediate effect • Weaker irritants- slower onset—cumulative effect • Xerosis, erythema, fissuring, scaling; pain • Confined to the site of contact with irritant • Periungual involvement can lead to nail dystrophy • AD patients are more susceptible to ICD • Occupational: hairdressers, healthcare professionals, cleaning and food professionals • Tx: avoid irritants; emollients Dermatology Lecture Notes 11th edition 2017 Wiley Blackwell https://dermnetnz.org/topics/irritant-contact-dermatitisMaterials from Dr Louise Cunnigham's lecture 80% of ICD cases are localised on the hands, 10% - on the face Materials from Dr Louise Cunnigham's lecture Allergic contact dermatitis (ACD) • Primary contact with allergen- period of sensitisation- re- exposure results in skin eruptions- further flares are triggered even by low concentration of the allergen • Well-demarcated pruritic acute/ chronic eczematous eruption – usually localised at the site of contact but can be diffuse depending on the nature of allergen • May co-exist with ICD • Ix: patch testing (standard series, special series, patch testing with patient's own products) • Tx: avoidance of the allergen, emollients, TCS Patch testing technique Bolognia Dermatology Textbook 4th editionMaterials from Dr Louise Cunnigham's lectureMaterials from Dr Louise Cunnigham's lectureWhich substance could potentially be responsible for the reaction? Materials from Dr Louise Cunnigham's lecture • In case of hand and neck dermatitis, always arrange patch testing! Eczema learning • Anyone can be allergic to anything points • Importance of moisturizers in management of eczema as a chronic inflammatory condition with disrupted skin barrier: compare topicals with spectacles in people with low eye acuity. • While they wear glasses, there is an improvement in eye acuity. • Once they take it off, they cannot see the world properly. • Same with eczema: as long as patient is using a product, skin has a potential to improve. • AE has one of the highest burdens of QoL among all diseases (not only skin diseases!)- 15th among all nonfatal diseases (Laughter et al, 2021) Scalp sebopsoriasis Plaque/ guttate psoriasis Plaque/ guttate psoriasis Erythrodermic psoriasis Plaque psoriasis Flexural psoriasisPsoriasis • Chronic inflammatory immune-mediated skin condition • Average prevalence worldwide: 2-3% of the population • Onset: any age; peaks: usually in early adulthood, late middle age • Genetic predisposition (HLA-C*06:02 is the major allele associated with plaque psoriasis) • In around 10-30% of patients, plaque psoriasis is accompanied by psoriatic arthritis (PsA) • Multimorbid disease: plaque psoriasis is associated with obesity (and vice versa), PsA, cardiometabolic diseases (dyslipidaemia, T2DM), inflammatory bowel diseases, psychological (anxiety, depression) Psoriasis vulgaris (plaque psoriasis) Psoriasis Guttate psoriasis Nail psoriasis Erythrodermic psoriasis Inverse psoriasis Pustular Generalised pustular psoriasis psoriasis Palmoplantar pustulosis Acrodermatitis of Hallopeau Adopted from Griffiths et al, 2021 Lancet Plaque psoriasis • Erythematous papules and plaques with superficial silvery scaling/ grey plaques in darker skin types; symmertrically distributed • Sites: • extensor aspects of the knees and elbows • lumbosacral region • scalp, rarely encroaching much beyond the hairline • !any skin surface can be involved • In active disease lesions can occur at sites of trauma or pressure on the skin (aka Koebner phenomenon). • Nails are involved in 50% of patients • nail dystrophy, pitting, onycholysis, subungual hyperkeratosis Griffiths et al, 2021 Lancet Pathogenesis and target molecules of therapeutic agents Griffiths et al, 2021 Lancet Bugault et al, 2021Management of plaque psoriasis • Managing weight and smoking cessation • Topical treatment: ointments, creams, foams, gels • keratolytics (tar-, salicylic acid- containing ointments) • moderate/ potent TCS, TCI • vitamin D derivates- calciportiol • combination of TCS +vit D • Phototherapy (PUVA, NB-UVB) • Systemic treatment: immunosuppressive agents (prednisolone, MTX, AZA, Cs, acitretin, apremilast), biologics (anti-TNFalpha, anti-IL17, anti-IL-12/23 agents) • Psychological support Griffiths et al, 2021 Lancet Psoriasis learning points • Secondary infection is psoriasis is rare as Yeung et al, 2020 its pathogenesis includes the overexpression of antimicrobial peptides (AMPs) • Always keep comorbidities in mind, especially joint involvement • Facial and genital areas are more resistant to treatment and can take longer to improve Psoriasis, as other inflammatory conditions, can leave • Psoriasis on the legs is also improving prominent postinflammatory hyperpigmentation which can slower take up to a year to resolve Acne vulgaris • Chronic inflammatory condition of pilosebaceous unit • Prevalence in the UK: 80%; 3.5 million consultations occur annually of acne (Dawson, 2013) • Can occur at any age: infantile/ children/ adolescent/ adult acne • Clinical presentation: open/closed comedones; papules, pustules; nodules, pseudocysts • Can be accompanied by scars, pigmented macules (postinflammatory erythema/ hyperpigmentation) • Majority of patients have oily skin • Face, back and chest areas can be involved (seborrhoeic sites)https://dermnetnz.org/topics/acne-face-imagesDescribe what you see https://dermnetnz.org/topics/acne-face-imagesDescribe what you see https://dermnetnz.org/topics/acne-face-images Acne vulgaris • Pathogenesis: chronic inflammation of pilosebaceous unit • Sebaceous hyperplasia and hypersecretion of sebum driven by androgen activity • Altered follicular growth and differentiation, • Follicular colonization by the bacteria Cutibacterium acnes (formerly Propionibacterium acnes) • Ix: if treatment-resistant, consider checking hormonal profiles- r/o PCOS, androgenic diseases ( it may be accompanied by signs of androgen excess such as hirsutism or menstrual irregularities) Eichenfield et al, 2021 JAMA Dréno B, 2017 JEADVAcne-associated syndromes • Beware of rare autoinflammatory syndromes such as: • SAPHO- synovitis- acne-pustulosis- hyperostosis- osteitis • PAPA- pyogenic arthritis- pyoderma gangrenosum- acne • PAPASH- pyogenic arthritis- pyoderma gangrenosum- acne- hidradenitis suppurativa Cugno et al, 2017 Am J Clin DermatolDegree of severity Clinical presentation Mild acne • <20 comedones • <15 inflammatory Management of lesions • Or, total lesion count acne vulgaris <30 Moderate acne • 20–100 comedones • Disease severity evaluation usually guides the • 15–50 inflammatory lesions treatment options • Or, total lesion count • Truncal acne is a criteria for escalating strength of 30–125 treatment and consider systemic options (esp isotretinoin) Severe acne • >5 pseudocysts • ! Set treatment goals and discuss expectations with • Total comedo count >100 patient- clinical severity sometimes does not correlate with the disease burden and impact on • Total inflammatory QoL count >50 • Or, total lesion count >125 Eichenfield et al, 2021 JAMATreatment options for acne vulgaris Eichenfield et al, 2021 JAMA Diet should not be used as monotherapy in acne management Identification of triggers is important: stress/ menstruation/ diet/ topical products- Practical tips in some patients the use of thick products for hair styling can block the pores and contribute to acne development on acne Daily skincare routine: daily cleansing in the evening, daily moisturizing (use of cosmeceuticals can be a great option); avoid skin picking. Sunscreen is important when using BP/ topical or systemic retinoids; tetracycline antibiotics can cause photosensitivity reactions When using topical BP/ retinoids/ combination, take a gradual approach: introduce once weekly at night, then increase number of applications each week depending on tolerability In some patients, topical and systemic retinoids can cause exacerbation of acne in first week of treatment which will improve if continuing the treatment- make sure patient is aware of that When commencing retinoids, always (!) talk with patient about the importance of double contraception in women of childbearing potential- retinoids are teratogenic! Systemic retinoids are better be taken with fatty food/ milk as vitamin A is fat- solubleThank you for your attention! I will be happy to take any questions Please also use the QR-code for the feedback elizaveta.gribaleva@kcl.ac.uk