engleski

What's new in management of atopic dermatitis

Atopic dermatitis (AD) is a chronically relapsing skin disease. Complex interactions among genetic, environmental, skin barrier, pharmacologic, and immunologic factors contribute to the pathogenesis of AD. Therapy includes identification and elimination of triggering factors, topical therapy (cutaneous hydration, topical glucocorticoid treatment, topical immunomodulators) and systemic therapy. Systemic corticosteroids are most often used to control flares and should be reserved primarily for control of acute exacerbations. Cyclosporine, a macrolide agent, has shown to be an effective treatment for adult and childhood AD, prescribed on a short-term basis for recalcitrant cases of AD, with a typically rapid, 2 to 3 week response that includes marked reduction of pruritus, and with 6 to 8 weeks of therapy reduction of lichenification, extent and activity of dermatitis. Relapses usually occurred after treatment, post treatment disease often did not return to baseline levels. Long-term treatment is also possible. Azathioprine, a purine analog that rapidly converts in vivo to 6-mercaptopurine, has slow onset of action of about 4 to 6 weeks. In many reports there is evidence of a consistent, significant, and persistent reduction in disease activity and was sustained for at least 3 to 6 months. Methotrexate is safer on a long-term basis and its consideration as a steroid– sparing agent is justified. Phototherapy should be introduced to the methotrexate treatment regiment once the drug has effectively controlled the level of inflammation. Mycophenolate mofetil is useful in dermatologic inflammatory diseases, but it is not approved for the treatment of AD yet. Recent studies showed notable improvement in subjects with moderate to severe AD, but there is no informed consent. Interferon γ was supported in several open-label studies for AD and the statistically significant improvement was seen in excoriations/erosions and erythema in patients with lowest serum IgE levels and blood eosinophil percentage at the beginning of the study while other AD clinical features showed improvement but did not reach statistical significance. Intravenous immunoglobulin (IVIG), phosphodiesterase inhibitors, thalidomide, and leukotriene inhibitors have been used in AD but their effectiveness has not been confirmed. Data from experimental studies provide structure, mechanism of action, efficacy, optimal doses, safety, clinical guidelines, costs and perspective of broad use of these drugs and insight into possible future treatment methods.

Atopic dermatitis; therapy; triggering factors; systemic therapy

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