IgG monoclonal gammopathy in four patients with polymyalgia rheumatica.

SIR, The aetiology and pathogenesis of giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are unknown. The cellular inflammation and immunoglobulin deposition in temporal artery biopsy specimens,' 2 and the dramatic clinical response to steroids suggest that an immunological abnormality might be associated with the pathogenesis of GCA or PMR. Two patients with serum monoclonal IgM and PMR have been previously reported.3 ' In the present study four patients are reported with benign monoclonal gammopathy (BMG) and PMR (with or without GCA); three of the patients had serum IgG which reacted with mouse femoral artery, raising the possibility that the IgG abnormalities may be associated with their clinical disease. All four patients had bilateral shoulder and hip arthralgias, and two also had temporal headaches. All four patients had a Westergren erythrocyte sedimentation rate (ESR) greater than 50 mm/h. The four patients were treated with prednisone 15 mg daily for PMR and 60 mg daily followed by tapering for GCA, which dramatically reduced their arthralgias and ESR within one week. Sera from these four patients were obtained when they were asymptomatic 1, 6, 7, or 13 months after starting prednisone. Sera were studied from six controls: four with IgG BMG, one with GCA, and one with PMR; the last two controls were treated with prednisone and were asymptomatic. Fresh specimens of mouse stomach and mouse femoral artery were embedded in Tissue Tek-2 (Miles) and quickly frozen in Cryokwik compound. Sections 4 pm thick