Elsevier

The Lancet

Volume 361, Issue 9352, 11 January 2003, Pages 151-160
The Lancet

Seminar
Atopic dermatitis

https://doi.org/10.1016/S0140-6736(03)12193-9Get rights and content

Summary

Atopic dermatitis is a highly pruritic chronic inflammatory skin disorder affecting 10–20% of children worldwide. Symptoms can persist or begin in adulthood. It is also the most common cause of occupational skin disease in adults. This disease results from an interaction between susceptibility genes, the host's environment, pharmacological abnormalities, skin barrier defects, and immunological factors. New management approaches have evolved from advances in our understanding of the pathobiology of this common skin disorder.

Section snippets

Epidemiology

Atopic dermatitis is a major public-health problem worldwide with a lifetime prevalence in children of 10–20%, and a prevalence of 1–3% in adults.3 Prevalence of this disease has increased by two to three-fold during the past three decades in industrialised countries, but remains much lower in agricultural regions such as China, eastern Europe, and rural Africa. Moreover, higher prevalences have been recorded in urban regions than in rural regions of developed countries, and the disease is more

Clinical diagnosis

Atopic dermatitis offers a wide clinical spectrum ranging from minor forms such as pityriasis alba (dry depigmented patches) or hand eczema to major forms with erythrodermic rash. The most common forms include the clinical features listed in panel 1.9 Of the major features, pruritus and chronic or relapsing eczematous lesions with typical shape and distribution are essential for diagnosis. Although pruritus can occur throughout the day, it is usually worse in the early evening and night.

Pathophysiology

Interactions between susceptibility genes, the host's environment, pharmacological abnormalities, and immunological factors contribute to the pathogenesis of atopic dermatitis.10 Most of the progress made in understanding the immunology of this disease is related to the IgE-mediated or extrinsic form of the disease. Clearly, atopic dermatitis has an immunological basis—as confirmed by the observation that primary T-cell immunodeficiency disorders frequently have raised concentrations of serum

Genetics

Atopic dermatitis is a genetically complex, familially transmitted disease with a strong maternal influence. Parental atopic dermatitis confers a higher risk to offspring than does parental asthma or allergic rhinitis, suggesting the existence of genes specific to atopic dermatitis. Several chromosomal regions contain pathophysiologically relevant candidate genes, especially on chromosome 5q31–33 since it contains a clustered family of Th2 cytokine genes—ie, interleukins 3, 4, 5, and 13, and

Foods

Food allergens induce skin rashes in nearly 40% of children with moderate to severe atopic dermatitis.47 Food allergies in patients with atopic dermatitis might induce dermatitis and contribute to severity of skin disease in some patients, whereas in others urticarial reactions, or non-cutaneous symptoms are elicited. Infants and young children with food allergies generally have positive immediate skin tests or serum IgE directed to various foods, especially egg, milk, wheat, soy, and peanut.48

Management

Successful management of atopic dermatitis requires a multipronged approach involving skin care, identification and elimination of flare factors, and anti-inflammatory treatment.73 Randomised controlled trials are especially important in assessing the effects of treating atopic dermatitis because of the substantial placebo effect in this disease.

Future directions

Atopic dermatitis is often the first presentation of an individual destined to a lifetime of allergy and asthma. Since the skin is a highly sensitising organ that contributes greatly to the systemic allergic response, highly effective treatments need to be developed to reduce skin inflammation in this disease. Advances are likely to need better definitions for the various clinical phenotypes of atopic dermatitis, including identification of the genes leading to the disease, a better

Search strategy and selection criteria

We did a computer-aided search of PubMed from 1990 through May, 2002, for aspects of atopic dermatitis pertinent to this review, to supplement our existing awareness of the primary published work. We searched using the keywords atopic dermatitis and eczema. Because of limitations on the number of citations, we made selections from the 2043 reports published on atopic dermatitis in the past decade to support our interpretations with criteria for assessing experimental studies and

References (100)

  • MC Mihm et al.

    The structure of normal skin and the morphology of atopic eczema

    J Invest Dermatol

    (1976)
  • LeungDY et al.

    Characterization of the mononuclear cell infiltrate in atopic dermatitis using monoclonal antibodies

    J Allergy Clin Immunol

    (1983)
  • WollenbergA et al.

    Immunomorphological and ultrastructural characterization of Langerhans cells and a novel, inflammatory dendritic epidermal cell (IDEC) population in lesional skin of atopic eczema

    J Invest Dermatol

    (1996)
  • HamidQ et al.

    In vivo expression of IL-12 and IL-13 in atopic dermatitis

    J Allergy Clin Immunol

    (1996)
  • GreweM et al.

    A role for Th1 and Th2 cells in the immunopathogenesis of atopic dermatitis

    Immunol Today

    (1998)
  • TrautmannA et al.

    Targeting keratinocyte apoptosis in the treatment of atopic dermatitis and allergic contact dermatitis

    J Allergy Clin Immunol

    (2001)
  • NovakN et al.

    IgE receptors

    Curr Opin Immunol

    (2001)
  • von BubnoffD et al.

    Antigen-presenting cells in allergy

    J Allergy Clin Immunol

    (2001)
  • Langeveld-WildschutEG et al.

    Clinical and immunologic variables in skin of patients with atopic eczema and either positive or negative atopy patch test reactions

    J Allergy Clin Immunol

    (2000)
  • LabergeS et al.

    Association of increased CD4+ T-cell infiltration with increased IL-16 gene expression in atopic dermatitis

    J Allergy Clin Immunol

    (1998)
  • ReichK et al.

    Evidence for a role of Langerhans cell-derived IL-16 in atopic dermatitis

    J Allergy Clin Immunol

    (2002)
  • TahaRA et al.

    Evidence for increased expression of eotaxin and monocyte chemotactic protein-4 in atopic dermatitis

    J Allergy Clin Immunol

    (2000)
  • YawalkarN et al.

    Enhanced expression of eotaxin and CCR3 in atopic dermatitis

    J Invest Dermatol

    (1999)
  • KakinumaT et al.

    Thymus and activation-regulated chemokine in atopic dermatitis: serum thymus and activation-regulated chemokine level is closely related with disease activity

    J Allergy Clin Immunol

    (2001)
  • NakataniT et al.

    CCR4 memory CD4+ T lymphocytes are increased in peripheral blood and lesional skin from patients with atopic dermatitis

    J Allergy Clin Immunol

    (2001)
  • NickoloffBJ et al.

    Perturbation of epidermal barrier function correlates with initiation of cytokine cascade in human skin

    J Am Acad Dermatol

    (1994)
  • GiustizieriML et al.

    Keratinocytes from patients with atopic dermatitis and psoriasis show a distinct chemokine production profile in response to T cell-derived cytokines

    J Allergy Clin Immunol

    (2001)
  • ForrestS et al.

    Identifying genes predisposing to atopic eczema

    J Allergy Clin Immunol

    (1999)
  • ArkwrightPD et al.

    Atopic dermatitis is associated with a low-producer transforming growth factor beta(1) cytokine genotype

    J Allergy Clin Immunol

    (2001)
  • SampsonHA

    Food allergy. Part 1: immunopathogenesis and clinical disorders

    J Allergy Clin Immunol

    (1999)
  • van ReijsenFC et al.

    T-cell reactivity for a peanut-derived epitope in the skin of a young infant with atopic dermatitis

    J Allergy Clin Immunol

    (1998)
  • LiXM et al.

    Murine model of atopic dermatitis associated with food hypersensitivity

    J Allergy Clin Immunol

    (2001)
  • TupkerRA et al.

    Induction of atopic dermatitis by inhalation of house dust mite

    J Allergy Clin Immunol

    (1996)
  • TanBB et al.

    Double-blind controlled trial of effect of housedust-mite allergen avoidance on atopic dermatitis

    Lancet

    (1996)
  • ScalabrinDM et al.

    Use of specific IgE in assessing the relevance of fungal and dust mite allergens to atopic dermatitis: a comparison with asthmatic and nonasthmatic control subjects

    J Allergy Clin Immunol

    (1999)
  • ValentaR et al.

    Autoallergy: a pathogenetic factor in atopic dermatitis?

    J Allergy Clin Immunol

    (2000)
  • ValentaR et al.

    Molecular characterization of an autoallergen, Hom s 1, identified by serum IgE from atopic dermatitis patients

    J Invest Dermatol

    (1998)
  • KinaciyanT et al.

    IgE autoantibodies monitored in a patient with atopic dermatitis under cyclosporin A treatment reflect tissue damage

    J Allergy Clin Immunol

    (2002)
  • BunikowskiR et al.

    Evidence for a disease-promoting effect of Staphylococcus aureus-derived exotoxins in atopic dermatitis

    J Allergy Clin Immunol

    (2000)
  • StricklandI et al.

    Evidence for superantigen involvement in skin homing of T cells in atopic dermatitis

    J Invest Dermatol

    (1999)
  • HoferMF et al.

    Staphylococcal toxins augment specific IgE responses by atopic patients exposed to allergen

    J Invest Dermatol

    (1999)
  • HaukPJ et al.

    Induction of corticosteroid insensitivity in human PBMCs by microbial superantigens

    J Allergy Clin Immunol

    (2000)
  • SkovL et al.

    Application of Staphylococcal enterotoxin B on normal and atopic skin induces up-regulation of T cells by a superantigenmediated mechanism

    J Allergy Clin Immunol

    (2000)
  • NilssonEJ et al.

    Topical corticosteroids and Staphylococcus aureus in atopic dermatitis

    J Am Acad Dermatol

    (1992)
  • RemitzA et al.

    Tacrolimus ointment reduces staphylococcal colonization of atopic dermatitis lesions

    J Allergy Clin Immunol

    (2001)
  • ChoSH et al.

    Preferential binding of Staphylococcus aureus to skin sites of Th2-mediated inflammation in a murine model

    J Invest Dermatol

    (2001)
  • ChoSH et al.

    Fibronectin and fibrinogen contribute to the enhanced binding of Staphylococcus aureus to atopic skin

    J Allergy Clin Immunol

    (2001)
  • ImokawaG

    Lipid abnormalities in atopic dermatitis

    J Am Acad Dermatol

    (2001)
  • WoodmanseeDP et al.

    Improvement in atopic dermatitis in infants with the introduction of an elemental formula

    J Allergy Clin Immunol

    (2001)
  • WollenbergA et al.

    Topical tacrolimus (FK506) leads to profound phenotypic and functional alterations of epidermal antigen-presenting dendritic cells in atopic dermatitis

    J Allergy Clin Immunol

    (2001)
  • Cited by (1214)

    View all citing articles on Scopus
    View full text