Immunopathology, musculoskeletal features, and treatment of sarcoidosis

Sarcoidosis is a clinical expression of intricate immune events. Firm evidence exists that unchecked helper T-cell proliferation restricted to the site of disease activity is the pivotal aberration. Alveolar macrophages from patients with sarcoidosis have been observed to release high levels of tumor necrosis factor-alpha and interleukin-2 and to exhibit enhanced expression of leukocyte function antigen 1 and intercellular adhesion molecule 1. These cytokines and adhesion molecules could result in compartmentalized T-cell proliferation at certain sites of disease. A new marker, serum procollagen type III-derived peptide, is reported to correlate with disease activity. Arthrosonography revealed periarticular edema as the prime pathologic process in the acute sarcoid reaction. Magnetic resonance imaging has greater diagnostic utility than does computed tomography in sarcoid myopathy. The acute sarcoid reaction is associated with a distinct HLA type and resolves spontaneously in 1 to 6 months. Chronic sarcoid arthritis causes destructive and deforming changes that rarely can be akin to Jaccoud's type arthropathy. Muscle and osseous disease is rare and asymptomatic. Nonsteroidal anti-inflammatory drugs and corticosteroids are the mainstays of pharmacotherapy. Deflazacort is an effective and safe steroid preparation with a lesser incidence of osteoporosis when used for long periods.