Clinical improvement and immunohistochemical findings in severe atopic dermatitis treated with interferon

Background: Several clinical studies have focused on the therapeutic effect s of interferon gamma (IFN-gamma) in patients with severe atopic dermatitis (AD), although the dosage of recombinant IFN-gamma (rIFN-gamma), therapeut ic schedule, and the degree of clinical improvement were different among st udies.,Although the exact mechanism of action of IFN-gamma therapy in AD is not clear, the beneficial effects of IFN-gamma have been attributed mainly to an immunomodulating effect on the expression of certain immunologic mar kers. Objective: Our purpose was to study the therapeutic effect of two different dosages of rIFN-gamma on AD and to investigate the change of lesional expr ession of infiltrating inflammatory cell markers associated with rIFN-gamma therapeutic efficacy. Methods: Fifty-one patients with severe recalcitrant AD were treated with r IFN-gamma. Twenty patients were treated with 0.5 x 10(6) IU/m(2) of rIFN-ga mma (low-dose [LD] group); 21 patients received 1.5 x 10(6) IU/m(2) of rIFN -gamma (high-dose [HD] group); and 10 patients received placebo. The patien ts were injected subcutaneously 3 times a week for 12 weeks. Immunohistoche mical study was performed in 20 patients of the HD group in the initial vis it and after completion of rIFN-gamma therapy with a panel of 14 monoclonal antibodies as markers of inflammatory cells and cytokines. Results: The disease severity of the 2 groups treated with rIFN-gamma was r educed significantly at the end of treatment compared with that of the plac ebo group (P<.05). More rapid clinical improvement and more effective treat ment outcome were seen in the HD group than in the LD group for the initial 6-week treatment period; however, the clinical improvement in both of the treated groups was stable and maintained after week 8 of treatment. Immunoh istochemical findings showed statistically significant reduction in the les ional expression of CD25 and EG2 cells that infiltrated into skin after rIF N-gamma therapy. Conclusion: This study demonstrated that rIFN-gamma therapy for AD is safe and effective. In the early phase of therapy a higher dosage of rIFN-gamma is more effective; and for the maintenance of clinical improvement, a lower dosage of rIFN-gamma is recommended when high cost and effectiveness of rI FN-gamma are considered. The therapeutic efficacy of rIFN-gamma in AD might be in part related to the decreased number of CD25(+) and EG2(+) inflammat ory cells infiltrated into skin.