Pettersson T
Department of Medicine, University of Helsinki, Finland.
Curr Opin Rheumatol. 1997 Jan;9(1):62-7. doi: 10.1097/00002281-199701000-00012.
Our understanding of the pathogenesis of sarcoidosis has recently been improved by studies elucidating the interaction between alveolar T lymphocytes and macrophages. It is particularly the activated CD4+ T helper 1 cells that in concert with macrophages produce a cascade of cytokines and chemotactic factors, which results in lymphocytic alveolitis succeeded by the granulomatous lesions. The accumulation in the alveoli of a specific subpopulation of T lymphocytes with a restricted expression of gene segments for the variable portion of the T cell receptor suggests that the process is antigen driven. The clinical features of sarcoidosis may mimic those of many rheumatic diseases and coexistence of sarcoidosis with autoimmune diseases is reported with increasing frequency. Musculoskeletal manifestations of sarcoidosis include acute and chronic arthritis, chronic myopathy, acute polymyositis and muscle nodules, and cystic osseous lesions. Acute sarcoid arthritis represents a relatively common form of acute oligoarthritis in young adults. For patients with chronic or refractory musculoskeletal sarcoidosis, low-dose methotrexate may be a therapeutic alternative.
