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Long-term Effectiveness and Safety of Recombinant Human Interferon Gamma Therapy for Atopic Dermatitis Despite Unchanged Serum IgE Levels
Seth R. Stevens, MD;
Jon M. Hanifin, MD;
Ted Hamilton, MS;
Susan J. Tofte, RN;
Kevin D. Cooper, MD
Arch Dermatol. 1998;134:799-804.
Objective To assess the long-term effects of recombinant human interferon gamma treatment of atopic dermatitis (AD).
Design Case series. Patients were treated for up to 24 months.
Setting University dermatology outpatient clinics in Ann Arbor, Mich, and Portland, Ore.
Patients Twenty-four of 32 eligible patients who participated in a previously reported, 12-week, double-blind, placebo-controlled study of recombinant human interferon gamma treatment for AD were enrolled.
Intervention Patients self-administered recombinant human interferon gamma, 50 µg/m2, by daily subcutaneous injection.
Main Outcome Measures Overall response; body surface area of involvement; clinical severity scores for pruritus, erythema, edema, excoriations, dryness, scaling, and lichenification; other atopic symptoms; and laboratory parameters, including serum IgE levels, were monitored at quarterly visits. Results at 1 and 2 years were compared with baseline values.
Results All efficacy parameters improved (P<.05). For example, pruritus was reduced by 50% after both 1 (n=24, P<.001) and 2 (n=16, P=.005) years. Allergic conjunctivitis and allergic rhinitis also improved (P<.01). Eosinophil counts decreased significantly (P<.001). IgE levels increased. Clinical improvement more closely correlated with changes in eosinophil counts (r=0.3-0.5) than with changes in IgE levels (r=0.0-0.2). Only 1 patient discontinued therapy because of adverse effects (flulike symptoms).
Conclusions The initial efficacy and adverse effects reported for recombinant human interferon gamma treatment of patients with AD were maintained after 2 years of long-term use. Recombinant human interferon gamma seems to be a well-tolerated and effective agent in the long-term therapy of patients with AD. Therapies that correct cellular immune defects, but not humoral immune defects, may be effective in the treatment of patients with AD.
From the Department of Dermatology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio (Drs Stevens and Cooper); the Department of Dermatology, University of Michigan Medical Center, Ann Arbor (Drs Stevens and Cooper and Mr Hamilton); and the Department of Dermatology, The Oregon Health Sciences University, Portland (Dr Hanifin and Ms Tofte).
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