Current management of atopic dermatitis and interruption of the atopic march

Boguniewicz, Mark; Eichenfield, Lawrence F.; Hultsch, T.

doi:10.1016/j.jaci.2003.09.031

Cited by 70 publications

(48 citation statements)

References 113 publications

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“…These would include treatment of patients who are poorly responsive to topical steroids or have steroid phobia, and treatment of face and neck dermatitis where ineffective, low-potency topical corticosteroids are usually used due to fears of steroid-induced skin atrophy. The potential use of topical calcineurin inhibitors as maintenance therapy is also intriguing for prevention of AD flares and progression of the atopic march (28,29). However, although systemic absorption of these compounds is low, there is a need for careful surveillance to rule out the possibility that skin cancers and increased viral skin infections will appear when such agents are used long-term.…”

Section: Factors Contributing To Flares Of Admentioning

confidence: 99%

New insights into atopic dermatitis

Leung¹,

Boguniewicz²,

Howell³

et al. 2004

J. Clin. Invest.

482

574

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Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often the first step in the atopic march that results in asthma and allergic rhinitis. The clinical phenotype that characterizes atopic dermatitis is the product of interactions between susceptibility genes, the environment, defective skin barrier function, and immunologic responses. This review summarizes recent progress in our understanding of the pathophysiology of atopic dermatitis and the implications for new management strategies. Historical perspectiveAtopic dermatitis (AD) is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers that are innocuous to normal nonatopic individuals (1). Although written descriptions of AD date back to the early 1800s, an objective laboratory test does not exist for AD. The diagnosis of AD is based on the following constellation of clinical findings: pruritus, facial and extensor eczema in infants and children, flexural eczema in adults, and chronicity of the dermatitis.AD usually presents during early infancy and childhood, but it can persist into or start in adulthood (2). The lifetime prevalence of AD is 10-20% in children and 1-3% in adults. Its prevalence has increased two-to threefold during the past three decades in industrialized countries but remains much lower in countries with predominantly rural or agricultural areas. Wide variations in prevalence have been observed within countries inhabited by groups with similar genetic backgrounds, suggesting that environmental factors play a critical role in determining expression of AD.A precise understanding of the mechanisms underlying AD is critical for development of more effective management strategies (Table 1). Various studies indicate that AD has a complex etiology, with activation of multiple immunologic and inflammatory pathways (3). The clinical phenotype that characterizes AD is the product of complex interactions among susceptibility genes, the host's environment, defects in skin barrier function, and systemic and local immunologic responses. An understanding of the relative role of these factors in the pathogenesis of AD has been made possible by a variety of approaches, including the analysis of cellular and cytokine gene expression in AD skin lesions in humans as well as gene knockout and transgenic mouse models of candidate genes in AD. The current review will summarize progress in our understanding of the pathophysiology of AD and implications for therapy. Atopy as a systemic diseaseSeveral observations suggest that AD is the cutaneous manifestation of a systemic disorder that also gives rise to asthma, food allergy, and allergic rhinitis (1, 2). These conditions are all characterized by elevated serum IgE levels and peripheral eosinophilia. AD is often the initial step in the so-called "atopic march," which leads to asthma and allergic rhinitis in the majority of afflicted patients. In experimental models of AD, the induction...

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Section: Factors Contributing To Flares Of Admentioning

confidence: 99%

New insights into atopic dermatitis

Leung¹,

Boguniewicz²,

Howell³

et al. 2004

J. Clin. Invest.

482

574

View full text Add to dashboard Cite

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“…In several short-term studies, tacrolimus ointment has been shown to be an effective treatment for AD in adults and children [30, 31, 33, 34, 84]. Patients treated with tacrolimus ointment, 0.03 and 0.1% applied twice daily for up to 6 weeks showed improvement in outcomes such as modified EASI and Investigator Global AD Assessment.…”

Section: Clinical Experience With Topical Calcineurin Inhibitorsmentioning

confidence: 99%

Immunomodulation and Safety of Topical Calcineurin Inhibitors for the Treatment of Atopic Dermatitis

2005

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Atopic dermatitis (AD) is a chronic or chronically relapsing inflammatory skin condition that primarily affects children. Topical corticosteroids have been the mainstay of treatment since the late 1950s. While providing excellent short-term efficacy, topical corticosteroid usage is limited by potential adverse effects, including impairment of the function and viability of Langerhans cells/dendritic cells. The recently introduced topical calcineurin inhibitors pimecrolimus cream 1% (Elidel^®) and tacrolimus ointment 0.03 and 0.1% (Protopic^®) exhibit a more selective mechanism of action and do not affect Langerhans cells/dendritic cells. For the immune system of young children ‘learning’ to mount a balanced Th1/Th2 response, this selective effect has particular benefits. In clinical experience, topical calcineurin inhibitors have been shown to be a safe and effective alternative to topical corticosteroids in almost 7 million patients (>5 million on pimecrolimus; >1.7 million on tacrolimus). Topical pimecrolimus is primarily used in children with mild and moderate AD, whereas tacrolimus is used preferentially in more severe cases. None of the topical calcineurin inhibitors have been associated with systemic immunosuppression-related malignancies known to occur following long-term sustained systemic immunosuppression with oral immunosuppressants (e.g., tacrolimus, cyclosporine A, and corticosteroids) in transplant patients. Preclinical and clinical data suggest a greater skin selectivity and larger safety margin for topical pimecrolimus.

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“…Neonates with infantile eczema had a significantly higher number and ratio of eosinophils in the cord blood (eosinophil count: 670. 8 tions develop atopic dermatitis, an initial manifestation of atopic march [8,9] . However, it is still obscure what types of skin eruptions are associated with the subsequent development of atopic dermatitis and why [8,[10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Infantile Eczema at One Month of Age Is Associated with Cord Blood Eosinophilia and Subsequent Development of Atopic Dermatitis and Wheezing Illness until Two Years of Age

Matsumoto

Shimanouchi

Kawakubo

et al. 2005

Int Arch Allergy Immunol

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Background: Physiological and pathological skin eruptions are commonly encountered in neonates in our clinical practice. However, the types of skin eruptions that are associated with the subsequent development of atopic dermatitis and the mechanisms of these associations remain uncertain. Methods: A total of 105 newborn babies with normal delivery were enrolled in this prospective cohort study. The cord blood eosinophil count was measured and the neonates were examined at 1 month of age and followed until 8 years of age. Results: At 1 month of age, infantile eczema, seborrheic dermatitis, intertrigo and diaper dermatitis were diagnosed in a total of 29, 7, 14 and 24 neonates, respectively. No association was found among the prevalences of these eruptions. Neonates with infantile eczema had a significantly higher number and ratio of eosinophils in the cord blood (eosinophil count: 670.8 ± 67.8 vs. 349.0 ± 30.3/µl, p < 0.0001; eosinophil ratio: 5.12 ± 0.53 vs. 2.61 ± 0.22%, p < 0.0001, for the presence and the absence of infantile eczema, respectively). In contrast, no such tendency was found for any other skin eruptions. In neonates with infantile eczema at 1 month of age, the diagnosis of atopic dermatitis had been made significantly earlier and the prevalence of wheezing illness was significantly higher than in those without infantile eczema until 2 years of age. Conclusion: Infantile eczema, but not other skin eruptions, precedes the development of atopic dermatitis and wheezing illness during early infancy, presumably because of the activation of eosinophils before birth.

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Current management of atopic dermatitis and interruption of the atopic march

Cited by 70 publications

References 113 publications

New insights into atopic dermatitis

New insights into atopic dermatitis

Immunomodulation and Safety of Topical Calcineurin Inhibitors for the Treatment of Atopic Dermatitis

Infantile Eczema at One Month of Age Is Associated with Cord Blood Eosinophilia and Subsequent Development of Atopic Dermatitis and Wheezing Illness until Two Years of Age

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