Atopic Dermatitis (AD) PDF

ATOPIC DERMATITIS  Atopic Dermatitis (AD) is a common inflammatory skim condition that typically begin during infancy or early childhood and often associated with other atopic disorders such as asthma, allergic rhinoconjuctivitis and foot allergies. It is a complex genetic disease with env...

ATOPIC DERMATITIS  Atopic Dermatitis (AD) is a common inflammatory skim condition that typically begin during infancy or early childhood and often associated with other atopic disorders such as asthma, allergic rhinoconjuctivitis and foot allergies. It is a complex genetic disease with environmental influences. AD is characterized by intense pruritus’ and chronic relapsing course. Acute inflammation and involvement of the cheeks, scalp and extensors aspect of extremities predominate in infants, shifting to chronic inflammation and lichenification mainly at flexors sites in children and adults.  AD maybe predisposed to skin infection with S.aureus and HSV. The treatments goals of AD are mainly : – Avoidance of triggering factors. – Regular use of emollients. – Anti-inflammetory theraties to control the subclinical as well as overt flares.  Epidemiology : The incidence of AD beaks in infancy and chronic disease is frequently seen. Three subsets of AD have been described based on age of onset into : Early-onset AD : Late-onset AD : AD in elderly : AD starts in the first AD starts after It is a subset of AD two years of life puberty that starts after 60 years of age This is the most 30% of the patients common type of AD do not develop IgE antibodies Half of Children (between two years) Most of the patients develop allergen are women specific IgE antibodies 60% of infants and young children with AD go into remission by 12 years of age Pathogenesis The pathogenesis of AD is categorized as: 1. Epidermal barrier disfunction 2. Immune dysregulation 3. Alteration of the cutaneous microbiome 1. Epidermal Barrier Disfunction Manifestation of epidermal barrier disfunction includes:  increase in transepidermal water loss (TEWL)  increase or changes in the pH  increase in permeability  alteration in the composition of the skin; this occurs in terms of changes in the protein and lipid composition:  Fillagrin is a keratin filament-aggregating protein that acts as a major structural component of the Stratum Corneum. Mutation of fillagrin leads to early onset of AD and increases the disease severity.  Stratum Corneum lipids are critical determinants of epidermal permeability barrier function. So any abnormality will lead to increases stratum corneum permeability.  Elevated levels of endogenous proteases which leads to corneocytes dysadhesions 2. Immune Dysregulation Any dysregulation of both innate and adaptive immunity leads to release of inflammatory mediators which initiate the inflammatory cascade of AD. 3. Alteration of the cutaneous microbiome The microbes present in the cutaneous microbiome represent the pathogenic and commensal homeostasis. These include: bacteria (S.aureus), fungi (Malassezia) and viruses (HSV). So any changes in their environment leads to AD. ❖ All these factors lead to an easier entry for irritants, microbes and allergens. This will trigger the immune responses, which leads to release of inflammatory mediators and cytokines. ❖ Clinical Features AD has broad clinical spectrum that varies depending upon the age of the patient. In each stage patients may develop acute, subacute and chronic eczematous lesions all of which are intensely pruritic. Infantile AD (2months - 2years) appears as edematous papules and papulovesicles which may evolve to form large plaques, mainly on: the cheeks (sparing the central face), scalp, neck, extensors and trunk (sparing the diaper area). sometimes the papules/vesicles are oozing serous fluid or covered by crustations. Childhood AD (2 years – 12 years) lesions become less exudative, xerotic (dry) and often lichenfied the classic sites are antecubital and popliteal fossae (flexural eczema) other common sites include wrists, hands, ankles, feet, neck and eyelids Adult/ Adolescent AD (> 12 years) adults usually present with hand dermatitis and involvement of the flexural folds continue others have primarily facial dermatitis with severe eyelid involvement pts who have childhood AD may have severe excoriations and chronic papular skin lesions due to continuous rubbing and scratching AD in elderly (above 60 years) there is lichenfied flexural lesions typical of AD in children with marked xerosis Pathology Histological features depend upon the clinical stage of the lesion: 1. Acute lesion; – marked spongiosis – intraepidermal vesicles/ bullae – dermal oedema – perivascular deposition of lymphocytes that extends to the epidermis with various numbers of oesinophils 2. Subacute lesion; – acanthosis with hyperkeratosis and parakeratosis – abscent vesiculation Differential Diagnosis Treatment A. General approach 1. Education of both the patients and their families about the disease cause, triggers and the appropriate use of therapies 2. Bathing: can hydrate the skin, remove scales, crusts, irritants and allergens for 5-10 mins in warm (not hot) water with fragrance-free non soap cleanser with neutral/ low pH. Then apply emollients or topical therapy immediately after bathing (soak and smear technique) 3. Moisturizers: daily use to reduce TEWL, they prevent disease flare, reduce pruritis, erythema, fissuring and lichenfication  B. Topical Therapy 1. Corticosteroids 2. Calcinurine inhibitors 3. Topical JAK inhibitors 4. Wet wrap therapy C. Systemic Therapy 1. Corticosteroids 2. JAK inhibitors (upadacitinib, abrocitinib) 3. Duplimab (IL- 4/13 inhibitor) 4. Adjunctive therapy; – antimicrobials – antiseptics – antihistamines – omalizumab – dietary manipulation  D. Phototherapy 1. NB- UVB 2. UVA