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Arch Dermatol. 1998 Jul;134(7):799-804.

Long-term effectiveness and safety of recombinant human interferon gamma therapy for atopic dermatitis despite unchanged serum IgE levels.

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  • 1Department of Dermatology, Case Western Reserve University and University Hospitals of Cleveland, Ohio 44106-5028, USA. srs@po.cwru.edu



To assess the long-term effects of recombinant human interferon gamma treatment of atopic dermatitis (AD).


Case series. Patients were treated for up to 24 months.


University dermatology outpatient clinics in Ann Arbor, Mich, and Portland, Ore.


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.


Patients self-administered recombinant human interferon gamma, 50 microg/m2, by daily subcutaneous injection.


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.


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).


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.

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