Atopic Dermatitis Flashcards
(24 cards)
What is associated with more severe atopic dermatitis
Older children, eldest child in family, Hispanic/African American background
Genetic mutations associated with AD
Loss of function mutation in Profilaggrin (10-30% of patients)
Three main components behind pathogenesis of AD
- Immune dysregulation
- epidermal barrier dysfunction
- environmental interactions with skin
What contributes to increased amount of superinfections
Th2 cells activated to express IL4, 5, and 13 which promote eosinophilia and IgE production but also suppress antimicrobial peptides such as Beta-defensins and cathelicidin
What is presumed to mediate pruritus in AD
TSLP (thymic stromal lymphopoeitin) and IL31
Clinical criteria for AD
- Must have pruritus
- Must have 3 of the following
- hx of dry skin in past year
- personal hx of allergic rhinitis/asthma or in first degree relative if <4yo
- Onset before 2yo
- Hx of skin crease involvement
- visible flexural dermatitis
Role of ceramides
Long chain lipids that are decreased in AD (likely contribute to defective epidermal barrier)
Infantile AD
Age 0-6mo and usually on cheeks/forehead/scalp before possibly involving extensor surfaces around 8 mo as they begin to crawl
Childhood AD
From 2yo to puberty, usually less exzematous and more lichenified that in infantile form
- facial involvement changes from cheeks/chin to perioral
Adult AD
prurigo nodularis commonly seen in adolescence
- dorsal hands and feet commonly affected
Associated clinical signs
- white/regular dermatographism
- keratosis pilaris
- Lichen spinulosus (round collections of tiny flat-topped papules more common in AA children)
- atopic pleat (Dennie-Morgan fold)
- allergic shiners
- allergic salute
- hyperlinear palms
- Allergic keratoconjunctivitis (requires optho)
Bacterial Superinfections
MCC: Staph Aureus (MSSA)
- others include Strep pyogenes (classically see more facial/periorbital involvement, fever, cellulitus, +/- bacteremia)
Non-bacterial superinfections
- Molluscum
- Eczema herpeticum (punched out erosions and umbilicated vesicles)
- Eczema vaccinatum (after contact with person recently vaccinated against smallpox)
- Eczema coxsackium
- Malassezia (particularly suspect in adolescents with recalcitrant AD in head and neck region)
DDx for Ad
- Seborrheic dermatitis
- Irritant/allergic contact dermatitis
- nummular dermatitis
- psoriasis
- Scabies
- Langerhans cell histiocytosis
- Acrodermatitis enteropathica
- Scabies
- IPEX syndrome
- Wiskott-Aldrich (WAITER aka immunodeficiency, thrombocytopenia, eczema, recurrent pyogenic infections)
- Hyperimmunoglobulinemia E
Management of mild AD
bathing and barrier repair
Avoidance of irritating/allergic triggers
Intermittent short term Class VI or VII topical steroids +/- calcineurin inhibitors
Treat superinfection
Management of moderate AD
bathing and barrier repair
Avoidance of irritating/allergic triggers
Intermittent short term Class III to V topical steroids +/- calcineurin inhibitors
Treat superinfection
Oral antihistamines
Management of severe AD
bathing and barrier repair
Avoidance of irritating/allergic triggers
Intermittent short term Class III or V topical steroids +/- tacrolimus
Treat superinfection
Consider systemic anti-inflammatory agents, UV tx
When to food allergy test in AD
Test to milk/peanuts/soy/eggs/wheat if kids <5 with moderate to severe AD who wither 1) do not respond to maximum topical therapy or 2) have reliable history of flair just after ingesting certain foods
Age cut-off for Class I steroids
Typically not given in children <12yo
What to warn parents about with topical calcineurin inhibitors
Burning/pruritus on application
Practice food sun protection
Equivalency of topical calcineurin inhibitors to topical steroids
Tacrolimus 0.1% ointment comparable to mid-strength steroid. Tacrolimus 0.03% and Pomecrolimus comparable to low potency steroids
MOA of crisaborole
Phosphodiesterase 4 inhibitor
Treatment of secondary bacterial infections
Bleach baths for maintenance
Keflex for extensive involvement
Systemic Immunosuppresive therapy in AD
Narrow band UVB Cyclosporine (greatest efficacy but highest risk) Azathioprine: check TPMT levels before Methotexate CellCept Dupilumab (IL-4 antibody)
