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Among 49 patients with carcinoid tumors given long term therapy (mean, 8 months; range, 3-36) with human leukocyte-derived interferon-alpha (huLe-IFN alpha), hypothyroidism occurred in 5 and thyrotoxicosis in 2. Antibodies against thyroid microsomal antigen and/or thyroglobulin were found in 13 patients. In 7 of these, 3 of whom developed hypothyroidism, the antibodies appeared after the start of therapy. During treatment, an increase in the proportions of circulating activated surface HLA-DR-positive T-helper and T-suppressor cells occurred after 3-4 days, and the proportions remained elevated at 3 and 6 months. Incubation of T cells of normal individuals in vitro with the huLe-IFN alpha preparation induced a rise in activated T-helper and T-suppressor cells. This effect was mimicked by recombinant IFN gamma (r-IFN gamma), but not by r-IFN alpha. Further, the huLe-IFN alpha preparation employed induced HLA-DR expression on human thyroid cells in tissue culture as did r-IFN gamma, but not r-IFN alpha, suggesting the presence of bioactive IFN gamma in the huLe-IFN alpha preparation. The results demonstrate that thyroid autoimmune disease can occur as a side-effect of treatment with huLe-IFN alpha and suggest that IFNs may play important regulatory roles, at both the effector and target cell levels, in the development of human autoimmune disorders.
Burman et al. (Sat,) studied this question.