Atopic dermatitis differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shalinder Singh, M.B.B.S.[2]

Overview

Atopic dermatitis is a chronic inflammatory skin disorder, which is indistinguishable from other causes of dermatitis. Atopic dermatitis is usually associated with personal or family history of atopic diseases including asthma, allergic rhinitis and food allergy. The most common clinically similar dermatitis in infancy is seborrheic dermatitis which includes hyperkeratosis of the scalp, also found in atopic dermatitis.

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 Eosinophils Serum IgE
Single/

Multiple

Rash Involved areas Pustule
Skin disorders Atopic dermatitis
  • Epidermal barrier dysfunction
  • Immune dysregulation
+ + 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] + Any May be multiple after 1-2 days of exposure Erythematous well-demarcated papules Surrounding the area in contact with the offending agent + + Nl to ↑

(Eosinophilia)

Nl
Irritant contact dermatitis[2] + Any, more with occupational exposure Usually single immediately after the exposure Well-demarcated red patch with a glazed surface Any area in contact with the irritant + + Nl Nl
  • 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:
    • Cradle cap (Sclap) - non-inflammatory greasy scales on the scalp
    • Asymptomatic
    • Self resolving
Nl Nl Risk factors include

Generalized seborrheic erythroderma in immunodeficient patients

Psoriasis + + 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
+ + _ + Nl Nl Risk factors include
Lichen simplex [3]chronicus + 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 from yellow to reddish brown
  • Plaque size can vary between 3X6 cm 6X10 cm areas.
Nl Nl Risk factors include
Ichthyosis vulgaris[4] + + Usually in infancy Multiple
  • 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
Nummular dermatitis (discoid eczema) Unknown + Any, two peaks, 6th-7th decade of life in males and 2nd-3rd decade of life in females Multiple
  • Symmetrical coin-shaped erythematous plaques
  • Erosions and excoriations
  • Chronic lesions- central clearing leading to annular lesions
  • Upper and lower extremities
  • Lower trunk
+
  • Chronically lesions result into central clearing leading to annular lesions.
Nl Nl
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)

Diseases Etiology Inherited Acquired Demography Single/

Multiple

Rash Involved areas Pustule Itching Fever Tenderness Other WBC Serum IgE 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
+ If molluscum contagiosum is acquired as sexually transmitted disease, it involves, groin and genital region. Nl Nl
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, 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
Immune deficiency Wiskott-Aldrich syndrome[7] + Seen almost exclusively in males in infancy Multiple 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
Hyper-IgE syndrome[8] + Rare, begin in infancy Multiple
  • 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
Malignancy Mycosis fungoides Clonal expansion of CD4+ memory T cells (CD45RO+) + Mean age is 55- 60 years Multiple
  • Asymmetrical
  • Hips, groin and trunk
+ Nl Nl
Category Diseases Etiology Inherited Acquired Demography Single/

Multiple

Rash Involved areas Pustule Itching Fever Tenderness Other WBC Serum IgE 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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