A case of atorvastatin combined toxic myopathy and inflammatory myositis.

Muscle toxicity is one adverse reaction reported with the use of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). This toxicity may include asymptomatic elevations of muscle enzymes, weakness, myalgia, and myositis. High doses of statins, or the combination of statins with other anti-cholesterol medications, increase the risk of toxicity. In addition, case reports of systemic and autoimmune reactions such as lupus, nephritis, vasculitis, and myositis, suspected to be associated with statins, have been reported. Our 76-year-old patient demonstrates a case of serologically and biopsy-proven inflammatory polymyositis, combined with a statin toxic myopathy. His symptoms and enzyme abnormalities resolved with both the removal of the statin medication and the institution of immunosuppressive therapy. Investigation of muscle enzyme elevation and weakness that do not resolve with statin removal is warranted. Certain muscle biopsy findings, including mononuclear cell infiltrate, distinguish the etiology as inflammatory/possibly autoimmune and do not suggest statin myopathy.

Analysis of CD80 and CD86 expression on peripheral blood B lymphocytes reveals increased expression of CD86 in lupus patients.

We screened peripheral blood mononuclear cells from 13 SLE patients, all having quiescent disease at the time of analysis, 12 allergy patients, and 21 normal subjects for the expression of CD80 (B7-1) and CD86 (B7-2, B70) on small (resting) and large (activated) subsets of CD19+ B cells. The percentage of CD86+ cells was significantly higher in all B cell subsets in the SLE patients compared to either normal controls or allergy patients. No differences in the mean percentage CD86+ stained B cells (CD19+) were found when comparing the allergy patients and the normal controls. The percentage of CD80+ cells in the large activated B cell (CD19+) subset of the SLE patient population was significantly higher than in the comparable subset from the normal controls and the allergy patients. Comparison of the small resting B cell subset did not reveal a significant difference in CD80 expression between the normal controls, the allergy patients, and the SLE patients. Our findings suggest that the B7 family of molecules, and CD86 in particular, may reflect immunologic dysregulation in patients with autoimmune disease and may reflect a state facilitating heightened B cell activity and hypergammaglobulinemia that occur in active SLE.