Abstract
Signals from alveolar macrophages in concert with T helper 1 cell-derived cytokines are likely to account for the development of lymphocytic alveolitis, the earliest event in pulmonary sarcoidosis. At the least, a subgroup of patients with pulmonary sarcoidosis has an oligoclonal local expansion of T cells, suggesting an ordered antigen-driven immune response. The clinical features of sarcoidosis may mimic those of many rheumatic diseases and sarcoidosis may coexist with autoimmune diseases. Patients with sarcoidosis have an abnormal regulation of 1,25-dihydroxycholecalciferol, with higher serum levels in the summer season. Although acute sarcoid arthritis does not lead to joint destruction, musculoskeletal pain may sometimes be protracted and recurrence of arthritis may occur. Corticosteroid therapy is effective in controlling symptoms in sarcoidosis, but relapse is much more common after corticosteroid-induced remission than after spontaneous remission.
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