Ch. 12/13-Atopic dermatitis/other eczematous processes Flashcards
Name 3 cutaneous disseminated viral infections that can occur in the setting of atopic dermatitis
Eczema herpeticum (HSV)
Eczema vaccinatum (Vaccinia)
*Eczema coxsackium (Coxsackie A16; A6; Enterovirus 71; hand-foot-mouth)
What is the atopic march
AD (often food allergy occurs around same time or after)–> Asthma–>allergic rhinitis
What is white dermatographism
Stroking the skin leads to whitening of skin due to vasoconstriction
What are 3 essential features for AD
(Previously Major criteria for Hanifin and Rafka)
Pruritus
Typical morphology in right location
Chronic/relapsing course
Fam hx atopy
Name 23 minor features of AD
White dermatographism
Mid-facial pallor
Delayed blanch response (to intradermal Ach)
Pityriasis alba
Hyperlinear palms /Itchytosis vulgaris
Keratosis pilaris
Perifollicular accentuation
Xerosis
Hertoghe sign
Allergic shiners
Recurrent conjunctivitis
Keratoconus
Anterior sub capsular cataract
Dennie Morgan lines
Anterior neck folds
Hand/foot dermatitis
Nipple eczema
Early onset
Susceptibility to skin infections
Worsened with wools/lipid solvent
Impacted by environment/emotions
Pruritus when sweating
Increased IgE
Food intolerance
Immediate Type 1 skin reactivity
What is needed to make a diagnosis of AD according to HAnifin and Raja
3 major + 3 minor
Name 3 infections that can worsten/flare eczema
Molluscum
Staph
Viral URTI
Hand/foot/mouth
What is prevalence of AD in kids and adults
10-20% kids
2-10% adults
What is early onset AD? Late onset? senile onset?
Early: first 2 years usually, sometimes before age 5
Late: Post puberty
Senil: After 60
What % of kids with AD outgrow it by age 12?
60%
3 major categories of AD pathogenesis
1- Barrier dysfunction
2- Immune dysregulaton
3- Alteration microbiome
What is strongest RF for early onset AD
Fam history-specifically parents-specifically AD > other atopic conditions
What is the strongest known genetic RF for AD
Fillagrin (FLG) loss of function mutation
What is the % of Europeans/Asians with mod-severe AD that carry mutation for FLG
20-50%
What is filagrin?
Keratin filament organizing protein
Found in stratum corneum
Breakdown products such as histidine contribute to epidermal hydration, acid mantle formation, lipid processing, and barrier function
Name 1 genetic mutations increase risk for AD that is not FLG?
SPINK5–> codes for LEKTI= lymphoepithelial Kazaa-type trypsin inhibitor (protease inhibitor, thus loss of function results in increase protease activity)
–> Excessive degradation DSG-1, degradation lipid processing enzymes, activates proinflammastory cytokines
What Th response is seen in acute AD? Chronic AD?
Acute: Th2
Chronic: Th1, Th 17, Th22
What are 2 cytokines drives Th2 response
Il-4
TSLP (thyme stromal lymphopoeitin)-produced by keratinocytes in response to viral infection, trauma, allergens, others. Highly expressed in lesions acute and chronic AD, not-non-lesional.
Describe how IL-4 and Il-13 are related
The heterodimeric receptor for IL-4 and IL-13 both share the IL4alpha receptor subunit, which activates STAT-6–> promoted th2 differentiation
Dupixent is a IL4alpha receptor blocker, thus blocks IL-13 and IL-4
What is IL-31
Th2 cytokine highly expressed in AD and pruritic skin conditions such as PN
Cutaneous exposure to staph rapidly induces Il-31 production, role for staph colonization and itch induction
It is expressed in keratinocytes, nerve fibres, dorsal root ganglion
What is the name of the IL-31 inhibitor
Nemolizumab
What % of AD patients are colonized with staph aureus? Why?
90%
Due to disrupted acid mantle, decreased antimicrobial peptides
Most common sites AD infantile
Cheeks, forehead, scalp, neck, extensors, trunk
Spares central face (but 90% have face involvement)
Often spares axillae/groin
What is frictional lichenoid eruption
Skin coloured flat topped papules often elbows > knees, often atopic boys in spring/summer
What is juvenile plantar dermatosis
glazed erythema, scale and fissuring of the feet
Often symmetric, forefoot on plantar surface
Most common age of onset infantile AD
2 months of life
Who gets papular eczema
African American or asian
Perifollicular flat topped papules
What are the main sites of AD in childhood? (2-12 years)
ACF, Popliteal fossa (flexures)
Wrists, ankles, hands, feet, eyelids, neck
What are the main sites of adult/adolescent AD
Flexures persist
Eyelids/hands may be only manifestation
What are the main sites of adult/adolescent AD
Flexures persist
Eyelids/hands may be only manifestation
What are the main sites of adult/adolescent AD
Flexures persist
Eyelids/hands may be only manifestation
Name 10 regional varaints of AD
Eyelid
Lip lickers dermatitis
Atopic cheilitis
Ear eczema (often retroauricular or below earlobe)
Head/neck (consider malessezia triggers)
Nipple eczema
Frictional lichenoid eruption
Nummular
Prurigo nodules
Hand dermatitis including dishydrotic
Juvenile plantar dermatosis
What % of AD patients have ichthyosis vulgaris? How does it present?
15%
Fine, whitish-brownish polygonal scaling that favours lower legs and spares flexures
KP also seen in 75%
*50% of people with IV have AD
How does KP present
Follicular hyperkeratotic papules with patchy erythema, often on arms, legs and cheeks
Grow out after puberty, especially the facial lesions
What is Keratosis Pilaris Rubra
Numerous grain like follicular papules on background confluent erythema, more widespread on face and ears >trunk
Tends to persist post puberty
Erythema >hyperpigmentation differentiates from erythromelanosis follicular facie et Colli
Lack of atrophy differentiates from keratosis pillars atrophicans
What is Hertoghe sign? Other than AD where else is it seen
Missing or thinning lateral 3rd eyebrows
AD most commonly, also hypothyroid
What is pityriasis alba
Subclinical eczematous dermatitis seen in patients with AD often.
Multiple ill defined hypo pigmented macules and patches, 0.5-2cm, fine scale, mostly on face like cheeks, sometimes shoulders and arms
Ddx Pitryriasis alba
Post inflammatory hypopigmentation from AD or other dermatides
Tinea versicolor-more sharply demarcated with smaller lesions coalescing into larger areas
vitiligo -depigmented, more sharply demarcated
Hypopigmented MF
How does eczema herpeticum present
Hemmorhogic punched out erosions
Vesicles rarely evident
Name 6 ocular complications in AD
Allergic rhinoconjuctivitis
Atopic Keratoconjuctivitis-adults
Vernal keratoconjuctivitis-kids in warm climates (arge, cobblestone-like papillae on the upper palpebral conjunctiva,)
Blepharitis
Keratoconus
Sub capsular cataracts-anterior related to AD
Name 5 path findings of Acute eczema
Spongiosis with exocytosis
Intraepidermal vesicles or bullae
Dermal edema
Perivascular lymphocytes that extend into epidermis
Variable number eosinophils
Name 3 path findings subacute eczema
Hyperkeratosis
Parakeratosis
Acanthosis
Name 3 path findings in chronic eczema
Pronounced acanthosis
Hyperkeratosis and parakeratosis
Psoriasiform hyperplasia of rate ridges, regular or irregular
Dermal fibrosis
Mast cells
Hypergranulosis, or sometimes Hypogranulosis in nummular
Name 5 immune deficiency syndromes associated with eczema
Ataxia-telangiectasia
Wiskott-Aldrich
IPEX -immune dysregulation polyendocrinopathy, enteropathy, x-linked recessive
HyperIgE syndromes:
-DOCK8 syndrome (similar to HIES but viral infections)
-STAT3 deficiency
-PGM3
STAT
Omenn syndrome
DiGeorge
Ig deficiencies
What is the triad of hyper IgE syndrome/AD-HIES
Eczematous dermatitis (staph colonization related)
Neonatal pustular dermatosis
Lung disease
Cold abscesses
Skeletal abscesses and CT diseases
“Autosomal dominant Hyper IgE syndrome”
Name 7 general categories of protein contact dermatitis (IgE-mediated)
Fruit-banana, fig, kiwi, lemon, pineapple
Vegetables-carrots, cauliflower, celery
Spices/seeds- caraway, curry, dill, garlic, paprika, parsley
Nuts-almonds, hazelnuts, peanuts
Latex
Grains
Meat-fish, poultry, seafood, beef
What diagnosis to consider in someone with chronicn eczematous in adults
MF
Treatment ladder AD
Moisturizers
Topical steroids
Topical calcineurin inhibitors
Topical crisabarole
*Topical tofactinib not yet approved
nbUVB
MTX, CsA, MMF, AZA
Prednisone
Dupixent
Omalizumab (Anti IgE)-no benefit
Nemolizumab (Anti IL-31)-pruritus
Tofacitinib
Upadacitnib
Rituxumab
INF-gamma-mixed results
Name 7 adjunctive therapies in AD
Wet wraps
Dilute sodium hypochlorite (bleach) baths
Treatment of associated bacterial, viral, or fungal infections
Oral antihistamines for antipruritic ‡ and sedative effects
Leukotriene antagonists
Sodium cromoglycate (topical or oral)
Probiotics(may have efficacy in primary prevention)
Vitamin D supplementation
What is the maintenance strategy that can be used for AD that does not result in atrophy?
Twice weekly with mid potency TCS to active areas
What TCI’s have been approved for AD
Tacrolimus (Protopic) 0.03% and 0.1%
Pimecrolimus (Elidel) 1%
Approve ages for Protopic and elidel
Protopic 2+
Elidel 3-23 months
What % strength is crisabarole
2% ointment
What age is crisabarole approved for
2+
How does crisabarole work
PDE-4 inhibitor-prevents degradation cAMP, increase CAMP, prevents production cytokines like IL-10 and IL-4
NAme 3 types of phototherapy for AD
nbUVB
UVA1
UVA+UVB
What does dupixent target
Il-4Ralpha subunit of heterodimeric IL-4 and IL-13 receptors –> blocks Th2 inflammation
What % of patients achieved EASI 75 for dupixent at 16 weeks
50%
Dosing for dupixent
600 mg initially and then 300 mg every other week
Percentage of conjunctivitis in dupixent
10%
Typical starting dose for CsA inAd
5 mg /kg then taper
Typical dose for MTX
7.5–25 mg or 0.3–0.5 mg/kg
Typical dose for MMF
1 to 3 g/day in adults and 30–50 mg/kg/day in children
Typical dose for AZA
2 mg/kg if normal TPMT
0.5-1 mg/kg
How to decolonize superinfected AD?
Course of cephalexin
5 days monthly intranasal mupirocin x 3 months
Bleach baths twice weekly with 0.5 cup 6% sodium hypochlorite
5 most common allergens in AD
Milk
Wheat
Eggs-most often linked to AD exacerbations
Peanut
Soy
Name 2 possible preventive measures for AD
probiotics (e.g. Lactobacilli ) or prebiotics to pregnant mothers and infants was associated with significantly decreased frequencies of AD at 1 to 4 years of age
For infants with a family history of atopy, exclusive breastfeeding during the first 3–4 months of life or feeding with a formula containing hydrolyzed milk products may potentially decrease the risk of AD development compared to feeding with a formula containing intact cow’s milk protein
daily use of a moisturizing cream, oil, emulsion, or ointment beginning within the first 3 weeks of life resulted in a 30–50% reduction in the likelihood of developing AD by 6–8 months of age
What is the most common sites of seborrheic dermatitis
Nasolabial folds
Scalp
Ears
Eyebrows
Chest
Folds
Name 3 systemic associations with seborrheic dermatitis
HIV
Parkinsons
Stroke
Mood disorders
What age range for seb derm
Peak in first 3 months (up to 1 year)
Second peak 5th/6th decade
What is the most common cause seb derm
Malessezia species
-Globosa and restricta
What are the changes in skin surface lipid composition in patients with seb derm?
Increased cholesterol and triglycerides, decreased squalene and free fatty acids
What is the relationship between P.Acnes and Seb derm
P.Acnes produce bacterial lipases which convert triglycerides into free fatty acids
Seborrheic derm patients have significant less P.Acnes thus leading to decreased FFA and increased TG’s
How does infantile seb derm appear
1 week after birth, persists for months
Starts with mild greasy scales–> cradle cap
The axillae, inguinal creases, neck, and retroauricular folds acutely inflamed, oozing, sharply demarcated, and surrounded by satellite lesions.
What is a psoriasiform id reaction
Disseminated eruption of scaly papules with psoriasiform appearance on trunk, proximal extremities, often with severe seb derm or super infected seb derm (candida, strep), ESPECIALLY DIAPER area
What are the adult forms of seborrheic dermatitis
Pityriasis simplex capillitii (dandruff)
Scalp seborrheic dermatitis-inflammation, pruritus, dandruff.
Facial/body seborrheic dermatitis-face, chest
Annular/discoid seb derm-facial lesions
Sebopsoriasis
Most common sites of scalp seb derm? How does it differ from psoriasis
Vertex/parietal
More diffuse than psoriasis but sometimes sharply demarcated at the forehead
Where does seb derm affect the face
Forehead
medial portions of the eyebrows
upper eyelids
nasolabial folds
lateral aspects of the nose
Retroauricular, non purulent otitis externa
Occiput and neck
Where does seb derm appear on the body
Central chest
Intertriginous
NAme 4 path findings of seb derm
Spongiosis
Superficial perifollicular and perivascular lymphocytic infiltrate
Older lesions:
Irregular acanthosis
Focal parakeratosis
NAme 4 path findings of seb derm
Spongiosis
Superficial perifollicular and perivascular lymphocytic infiltrate
Older lesions:
Irregular acanthosis
Focal parakeratosis
Name 4 differences between AD and seb derm in an infant
AD:
-irritable
-sleepless
-itchy
Seb derm:
-content, non irritated
-earlier onset
-intertriginous predilcietion
Name 8 things on ddx for infantile seb derm
AD
Candida-especially intertrigo
Irritant dermatitis-diaper dermatitis esp.
Psoriasis
Streptococcal intertrigo
Langerhans cell histiocytosis
Acrodermatitis enteropathica
Leiner disease (erythroderma, seb derm, diarrhea, FTT)
Ddx of adult seb derm on the scalp
Psoriasis-more silvery scale, thicker plaques, more discrete, less pruritic, less greasy
Atopic derm
Dermatomyositis
What type of organism is malessezia
Dimorphic fungi
Seb derm is reaction to the yeast form
What is sebopsoriasis
Overlap between seb derm and psoriasis
Think that maybe malessezia drives psoriasis
Yellowish, greasy scale in typical seborrhoeic dermatitis areas (scalp, nasolabial folds, eyebrows, behind the ears and over the sternum)
Deeper red, more defined margins and thicker scale than normally seen in seborrhoeic dermatitis
Less silvery scale than seen in classic psoriasis
Name 10 ddx’s for intetrigo/intetriginal dermatoses
Inverse psoriasis-well defined
Irritant dermatitis-ill defined
Tinea cruris
Candida-satellite lesions, papules, pustules
Erythrasma-re brown
Allergic contact dermatitis
Granular parakeratosis
Hailey-Hailey, Dariers
Pemphigus vegetans
SDRIFE
Toxic erythema of chemotherapy
Cutaneous chrons
Extra mammary pagets
Langerhans cell histiocytosis
Treatment for infantile seborrheic dermatitis
Emollients, bathing.
Mild shampoos
Ketoconazole 2%
Low potency topical steroids
Treatment for adult seb derm
Topical azoles-shampoo or cream (body)
-e.g. ketonconazol
Ciclopirox olamine
Adjuncts:
Emollients
low potency topical steroids
TCI’s
Shampoos containing selenium sulfide, zinc pyrthione, tar shampoo
Most common cause disseminated eczema (auto sensitization)
Allergic contact dermatitis in setting of stasis dermatitis (2/3 of patients)
Sometimes in just plain ACD, stasis dermatitis or severe tinea pedis
How does disseminated eczema present
Appears later than the primary lesions by a few days to weeks
symmetric distribution pattern
predilection for analogous body sites (e.g. extensor aspects of the lower and upper extremities, palms and soles).
How does true nummular eczema present
round (discoid) eczematous patches almost exclusively of the extremities, often the lower legs in men and the forearms and dorsal aspects of the hands in women. well demarcated and measure 1–3 cm, only occasionally being larger.
They may be acutely inflamed with vesicles and weeping, but are often lichenified and hyperkeratotic.
What is the other name for oid-oid disease, and what is it?
Sulzberger-Garbe disease or exudative discoid and lichenoid chronic dermatitis
Very therapy resistant
Name 2 variants of nummular dermatitis
Wet and dry variants
Name 4 associations with nummular dermatitis
Xerosis
ID reaction to ACD, stasis dermatitis or tinea
AD
*Staph often present, may need to treat this
What is infected dermatitis
Dermatitis associated with HTLV-1 virus, immune dysregulation leads to infection with staph and strep
What is HTLV-1? What other conditions is it associated with?
Human T-cell lymphotropic virus Type I
Human T cell leukemia/lymphoma
Tropical spastic paresis
Increased susceptibility to parasitosis/strongy
Infective dermatitis
How does infective dermatitis present
Crusted oozing dermatitis to scalp, ears, eyelids, neck, paranasal, axillae, groin
Generalized fine papular rash
Secondly infection most often seen
What are the 4 major criteria for HTLV-1 associated infective dermatitis
Eczema of the head and neck region, including the scalp, ears, eyelid margins and paranasal skin, as well as the axillae and groin (at least 2 sites)
Chronic watery nasal discharge or crusting anterior nares
Chronic relapsing dermatitis that responds to antibiotics but recurs on withdrawal
Onset early childhood (after done breastfeeding and ab’s wean)
HTLV-1 SEROPOSITIVY (must occur)
5 minor criteria of infective dermatitis
Hyperimmunoglobulinemia
Fine papular rash
Postive cultures: staph or strep, from lesions or nares
Anemia, ESR
Elevated CD4 and CD8 T cell counts, elevated CD4:CD8 ratio
Name 8 findings of chronic venous hypertension
Hemosiderin deposits/purpura
Edema
Varicose veins
Petechiae overlying yellow-brown discoloration (stasis purpura)
Stasis dermatitis
Lipodermatosclerosis
Stasis ulcerations
Acroangiodermatitis/psuedo KS
Livedoid vasculopathy/atrophie blanche-porcelain white scars surrounded by punctate telangiectasis and ulcerations
Describe the progression of stasis dermatitis
Pitting edema at medial shin and calf proximal to the ankle –> stasis purpura with hemosiderin deposition–> dry/itchy skin–> edema extends to the distal third of the calf and subfascial edema arises = psuedoerysipelas/acute lipodermatosclerosis–> chronic LDS (inverted wine bottle)–> ulcers and atrophic blanche
Name 3 biopsy findings of venous HTN
- Dilated capillaries surrounded by cuffs of fibrin
- hemosiderin deposits
- hyperplastic (and at times thrombotic) venules
What is one procedural treatment that can be used for dishydrotic eczema
Botox if hyperhidrosis
What conditions can you see dishydrotic eczema in
AD
ID
ACD
What is the name for larger bullae in dishydrotic eczema
Pompholyx
What is Dyshidrosis lamellosa sicca
variant dishydrotic eczema with no bullae or vesicles but annular collates of white scale
Name 4 treatments for dishydrotic eczema
TCS
TCIs
Phototherapy
Systemic steroids
Treatment for plantar juvenile plantar dermatosis
impermeable socks and shoes
emollients
keratolytics
paraffin-type ointments
Dry socks
Name 6 ddx for plantar foot dermatosis
Juvenile plantar dermatosis (young males)
Acquired plantar keratoderma
Tylosis
ACD
Tinea pedis
Psoriasis
Dishydrotic eczema and recurrent focal plantar and palmar peeling (likely mild form of the former)
Pustulosis palms and soles
Others:
PRP
Keratoderma blenorrhagicum
Crusted scabies
What is the main cause of diaper dermatitis? What is the pathophysiology
Irritant contact dermatitis from the alkaline diaper environment due to
1)alkaline pH of urine
2) fecal bacteria (esp. cows milk fed babies) have urease enzymes
How does diaper dermatitis secondary to irritation present
Spares the folds, favours convex surface areas
Glazed erythema, punched out erosions, scaling
Psuedoverrucous papules can develop
Name the ddx for diaper dermatitis
SCAMP:
Seb derm
Candida, contact (allergic, irritant)
AD, acrodermatitis enteropathica
Milaria
Perianal strep and bullous impetigo, psoriasis
Others:
Extramammary pagets
LCH
Granuloma gluteal infantum
How does candida present in diaper area
Bright red intense erythema, involvement of skin folds (+/- scrotum), and satellite papules and pustules at the periphery of dermatitis
Recent abx use, thrush
How does candida present in diaper area
Bright red intense erythema, involvement of skin folds (+/- scrotum), and satellite papules and pustules at the periphery of dermatitis
Recent abx use, thrush
How does seb derm present in diaper area
Well demarcated salmon-red coloured patches
Look for involvement other intertriginous zones
How does perianal strep present
Brith red eyrhtme perianal and folds, no satellite lesions, foul odour
Family member with history sore throat
How does perianal strep present
Brith red eyrhtme perianal and folds, no satellite lesions, foul odour
Family member with history sore throat
