Atopic dermatitis differential diagnosis: Difference between revisions

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* Auspitz sign  (pinpoint bleeding)
* Auspitz sign  (pinpoint bleeding)
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* Epidermal hyperplasia
* Parakeratosis
* Neutrophils microabscesses (Munro microabscesses)
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* Smoking
* Smoking
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* Molluscum contagiosum  lesions on the eyelid may lead to follicular or papillary conjunctivitis
* Molluscum contagiosum  lesions on the eyelid may lead to follicular or papillary conjunctivitis
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| align="center" style="background:#DCDCDC;" | Scabies
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* Positive family history
* Positive family history
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! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Immunologic disorders
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Immunologic disorders

Revision as of 15:59, 25 October 2018

Atopic dermatitis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

Differentiating Atopic Dermatitis from other Diseases

Category Diseases Etiology Inherited Acquired Clinical manifestations Para-clinical findings Associated factors
Demography Symptoms Physical examination
Lab Findings Histopathology
Appearance Itching Fever Tenderness Other CBC Serum IgE
Single/

Multiple

Rash Involved areas Pustule WBC
Skin disorders Atopic dermatitis
  • Epidermal barrier dysfunction
  • Immune dysregulation
+ +
  • Incidence is highest during infancy and early childhood.
Multiple
  • Young children -Scalp, cheeks amd extensor surface
  • Adolescents -flexural areas and buttock-thigh creases
  • Adults - facial involvement and skin flexures
+
  • Infra-auricular and retro-auricular fissuring
  • Nipple eczema
  • White dermographism
  • Perifollicular accentuation
Nl to ↑

(Eosinophilia)

  • Epidermal psoriasiform hyperplasia
  • Marked intercellular edema with spongiotic vesiculation
Allergic contact dermatitis[1]
  • Delayed-type hypersensitivity response
  • Skin inflammation mediated by hapten-specific T cells
+ Any May be multiple after 1-2 days of exposure Erythematous well-demarcated papules Surrounding the area in contact with the offending agent + +
  • Stinging and burning
  • Localized swelling
  • Lichenified pruritic plaques
Nl to ↑

(Eosinophilia)

Nl NA
  • Contact with allergens in the past 1-2 days
  • Positive family history
Irritant contact dermatitis[2]
  • Activation of the innate immune system by the pro-inflammatory properties of chemicals
+ Any, more occupational exposure Usually single immediately after the exposure Well-demarcated red patch with a glazed surface Any area in contact with the irritant + +
  • Swelling, blistering and scaling of the damaged area
  • Dryness
  • Thicker skin
Nl Nl
  • Spongiosis
  • Intraepidermal vesicles or bullae
  • Necrosis of keratinocytes
  • Cumulative exposure to irritants
  • Negative hypersensitivity tests
Seborrheic dermatitis
  • Not known
+ Any, onset during the infancy and peak during 3rd-4th decades Multiple
  • Cradle cap - yellowish scales on the scalp
  • Patchy or diffuse greasy scaling with or without a yellow-red base
  • Crusts
Scalp, face, trunk, postauricular, diaper area and axilla + +
  • Infants:
    • Craddle cap (Sclap) - non-inflammatory greasy scales on the scalp
    • Asymptomatic
    • Self resolving
Nl Nl
  • Focal parakeratosis and spongiosis in epidermis
  • Psoriasiform hyperplasia
  • Neutrophils at the margins
  • Stress
  • Cold, dry weather can cause flare ups
  • Super infection with bacteria and candida
  • Generalized seborrheic erythroderma in immunodeficient patients
Psoriasis
  • Keratinocyte hyperproliferation
  • Dysregulation of the immune system
+ + Any, 2 peaks of onset 30-39 years and 50-59 years Multiple Well-circumscribed, pink papules and symmetrically distributed cutaneous plaques with silvery scales
  • Scalp
  • Trunk
  • Gluteal cleft
  • Extensor surface of elbows and knees
+ + _ +
  • Auspitz sign (pinpoint bleeding)
Nl Nl
  • Epidermal hyperplasia
  • Parakeratosis
  • Neutrophils microabscesses (Munro microabscesses)
  • Smoking
  • Skin trauma
  • Alcohol abuse
  • Stress
  • Cold weather
  • Vitamin D deficiency
  • Drugs
Lichen simplex [3]chronicus
  • Lichenified plaques and excoriations of lichen simplex chronicus develop secondary to extensive pruritus due to other conditions such as atopic dermatitis, neuropathic pruritus, etc
+ Any, peak at 30-50 years of age Multiple Lichenified and erythematous, pruritic exudative plaque, and excoriations Scalp, head, neck, hands, arms, and genitals areas +
  • Color of plaque varies fro, yellow to reddish brown
  • Plaque size can vary between 3X6 cm 6X10 cm areas.
Nl Nl
  • Markedly hyperplastic epidermis
  • Irregular hyperkeratosis and parakeratosis
  • Thick granular zone
  • Acanthosis
  • Emotional stress
  • Sleep disturbances
  • Dry weather
  • Sweating
  • Excessive dryness
  • Sexual dysfunction
  • Sleep disturbances
  • Depression
  • Dissociative disturbances
Ichthyosis vulgaris[4]
  • Loss of function mutations in the filaggrin gene (FLG)
  • Autosomal dominant inheritance with incomplete penetrance
+ + Usually in infancy Multiple
  • Xerosis and gray scaling
  • Palmar hyperlinearity
  • Keratosis pilaris
  • Extensor surfaces of the extremities
  • Scalp
  • Trunk
  • Scales can vary from mild scaling to large, plate (armor)-like scales and thickening of the skin.
Nl Nl
  • Reduced keratohyalin granules
  • Perinuclear keratin retractions in granular cells
  • Thick stratum corneum
  • Basket-weave pattern of stratum corneum
  • Dry and cold weather
  • Increased risk of atopic diseases including asthma, alllergic rhinitis and atopic dermatitis
Nummular dermatitis (discoid eczema) Unknown + Any, two peaks, 6th-7th decade of life in males and 2nd-3rd decade of life in females Multiple Nl
  • Upper extremities
  • Lower extremities
  • Lower trunk
+
  • Chronically lesions result into central clearing leading to annular lesions.
Nl Nl
  • Spongiosis
  • Perivascular lymphocytic infiltrates, with eosinophils and occasional neutrophils
  • Risk factors:
    • Temperature changes (particularly winter)
    • Emotional stress
    • Dry skin
    • Environmental irritants
    • Recent surgery
    • Medications like topical antibiotic creams and isotretinoin
  • Superinfection with staphylococcus aureus
Netherton's syndrome[5] Autosomal recessive mutations in the serine protease inhibitor of Kazal type 5 gene (SPINK5), encoding LEKTI, a serine protease inhibitor + Affects neonates Multiple
  • Classic triad
    • Congenital ichthyosiform erythroderma
    • Trichorrhexis invaginata
    • Allergic diseases with ↑ serum IgE levels
  • Ichthyosis linearis circumflexa (ILC) - serpiginous plaques with double scale at the margins
  • Diffuse pattern
  • Axillae,
  • Hair
  • Inguinal folds
  • Gluteal cleft
  • Groin
  • Lower legs
+ +
  • Trichorrhexis invaginata (hair involvement):
    • Sparse, short, spike and brittle
    • "Bamboo hair" or "ball and socket deformity" of hair and eyebrows
    • Nodes along the hair shaft
Nl to ↑

(Eosinophilia)

  • psoriasiform hyperplasia
  • Reduced granular layer
  • Dyskeratosis,
  • Dermal inflammatory infiltrate including neutrophils and eosinophils
  • Atopic diseases including asthma, atopic dermatitis and allergic rhinitis
  • Systemic and skin superinfections
  • Failure to thrive
  • Electrolyte imbalances, including hypernatremic dehydration
Diseases Etiology Inherited Acquired Demography Single/

Multiple

Rash Involved areas Pustule Itching Fever Tenderness Other WBC ESR/CRP Histopathology Associated factors
Infection Molluscum contagiosum Molluscum contagiosum virus inoculation through direct skin contact + Any, peak among children >5 years of age and young adults Multiple
  • Flesh-colored, dome-shaped papules with a central umbilication
  • Lesions are 2-5mm in diameter
  • Face, trunk, antecubital, popliteal fossae and groin
+ If molluscum contagiosum is acquired as sexually transmitted disease, it involves, groin and genital region. Nl Nl
  • Keratinocytes containing eosinophilic inclusion bodies (Henderson-Paterson bodies)
  • H&E stain - inwards indentation of the epidermis
  • Often asymptomatic
  • Tender or pruritic skin lesions
  • Self resolve within 2 months
  • Immunocompetent patients present with extensive and severe infections
  • Molluscum contagiosum lesions on the eyelid may lead to follicular or papillary conjunctivitis
Scabies Multiple Erythematous papular lesions Flexor wrists, finger webs and genitalia +++
  • Positive family history
Immunologic disorders Dermatitis herpetiformis[6] Autoimmune disorder as a result of gluten sensitivity leading to the formation of IgA antibodies + Any, mean age of disease onset is 2nd-4th decade Multiple
  • Excoriated papules or plaques and vesicles arranged in a clustered fashion
  • Symmetrical
  • Erosions and excoriations
  • Extensor surfaces including arms, knees, and buttocks.
+
  • Oral manifestation such as vesicles and erosion may be present
Nl Nl
  • Papillary micro-abscesses
  • Sub-epidermal blisters containing neutrophils, eosinophils, and fibrin
  • Sub-epidermal vacuolization
  • Intermittent pruritic papules and vesicles
  • Associated small intestine celiac disease with villous atrophy and crypt hyperplasia
  • Abdominal bloating, pain, diarrhea, or constipation
Immune deficiency Wiskott-Aldrich syndrome[7]
  • Mutation in the gene encoding for Wiskott-Aldrich syndrome protein (WASp) on the short arm of the X chromosome
  • X-linked disorder
+ Seen almost exclusively in males in infancy Multiple
  • Rash is clinically similar to atopic dermatitis
  • Erythematous and pruritic lesions
  • Lesions can bleed due to thrombocytopenia
  • Cutaneous manifestations includes petechiae and ecchymosis
Rash can involve lesions located at the same areas of classical atopic dermatitis:

extensor surfaces of extremities and cheeks or scalp

+ Infants can present with petechiae, prolonged bleeding from umbilicus or circumcision, purpura, hematemesis, melena, epistaxis, hematuria or unusal bruising Nl to ↑

(Eosinophilia)

  • Epidermal psoriasiform hyperplasia
  • Marked intercellular edema with spongiotic vesiculation
  • ↑ serum IgA levels
  • ↑ serum IgE levels
  • Bleeding: severe thrombocytopenia,
  • Eczema - similar to atopic dermatitis
  • Recurrent sino-pulmonary infections
  • Opportunistic infections.
  • Autoimmune diseases
  • Malignancies
Hyper-IgE syndrome[8]
  • Defects in the JAK-STAT signaling pathway leading to dysfunctional T helper cell type 17 (Th17) differentiation
+ Rare, begin in infancy Multiple
  • Papulopustular
  • Severely pruritic eczematous rash
  • Pustular and may impetiginized
  • Lichenification may occur
  • Face and scalp
  • Upper trunk and shoulders
  • Buttocks
  • Area behind the ears and around the hairline
+ +
  • Characteristic coarse facies
  • Increased alar width and broad nasal bridge
  • High-arched oral palate
  • Hyperextensible joints
Nl to ↑

(Eosinophilia)

  • Eosinophil-rich infiltration around the hair follicles
  • Cold abscesses
  • Pruritic eczema
  • Allergic diseases
  • Noneruption of permanent teeth
  • Multiple bone fractures and scoliosisis
  • Peripheral T-cell lymphoma
  • Coronary artery aneurysms
Malignancy Mycosis fungoides Clonal expansion of CD4+ memory T cells (CD45RO+) + Mean age is 55- 60 years Multiple
  • Non pruritic patches and intensely pruritic plaques
  • Comedones, cysts
  • Tumors of skin
  • Erythematous macules
  • Hypopigmented patches
  • Asymmetrical
  • Hips, groin and trunk
+
  • Alopecia
  • Acneiform lesions
  • Plaques size can vary between 2-20 cm
  • Lymphadenopathy
  • Children- hypopigmented patches most common
Nl Nl
  • Perifollicular infiltrates around the infundibulum
  • Epidermis is spared or has minimal spongiosis
  • Band-like dermal infiltrate of lymphocytes and and histiocytes
  • Increased risk of :
    • Severe viral and bacterial infections
    • Secondary malignancies, especially lymphomas
  • Staging of Mycosis fungoides is based upon:
    • Patches
    • Plaques
    • Skin tumors
    • Lymphadenopathy
    • Erythroderma
    • Histology
Category Diseases Etiology Inherited Acquired Demography Single/

Multiple

Rash Involved areas Pustule Itching Fever Tenderness Other WBC ESR/CRP Histopathology Associated factors

References

  1. Nosbaum A, Vocanson M, Rozieres A, Hennino A, Nicolas JF (2009). "Allergic and irritant contact dermatitis". Eur J Dermatol. 19 (4): 325–32. doi:10.1684/ejd.2009.0686. PMID 19447733.
  2. Bains SN, Nash P, Fonacier L (October 2018). "Irritant Contact Dermatitis". Clin Rev Allergy Immunol. doi:10.1007/s12016-018-8713-0. PMID 30293200.
  3. Voicu C, Tebeica T, Zanardelli M, Mangarov H, Lotti T, Wollina U, Lotti J, França K, Batashki A, Tchernev G (July 2017). "Lichen Simplex Chronicus as an Essential Part of the Dermatologic Masquerade". Open Access Maced J Med Sci. 5 (4): 556–557. doi:10.3889/oamjms.2017.133. PMC 5535688. PMID 28785363.
  4. Thyssen JP, Godoy-Gijon E, Elias PM (June 2013). "Ichthyosis vulgaris: the filaggrin mutation disease". Br. J. Dermatol. 168 (6): 1155–66. doi:10.1111/bjd.12219. PMID 23301728.
  5. Chavanas S, Bodemer C, Rochat A, Hamel-Teillac D, Ali M, Irvine AD, Bonafé JL, Wilkinson J, Taïeb A, Barrandon Y, Harper JI, de Prost Y, Hovnanian A (June 2000). "Mutations in SPINK5, encoding a serine protease inhibitor, cause Netherton syndrome". Nat. Genet. 25 (2): 141–2. doi:10.1038/75977. PMID 10835624.
  6. Kárpáti S (2012). "Dermatitis herpetiformis". Clin. Dermatol. 30 (1): 56–9. doi:10.1016/j.clindermatol.2011.03.010. PMID 22137227.
  7. Buchbinder D, Nugent DJ, Fillipovich AH (2014). "Wiskott-Aldrich syndrome: diagnosis, current management, and emerging treatments". Appl Clin Genet. 7: 55–66. doi:10.2147/TACG.S58444. PMC 4012343. PMID 24817816.
  8. Mogensen TH (April 2013). "STAT3 and the Hyper-IgE syndrome: Clinical presentation, genetic origin, pathogenesis, novel findings and remaining uncertainties". JAKSTAT. 2 (2): e23435. doi:10.4161/jkst.23435. PMC 3710320. PMID 24058807.


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