Fenbufen induced pure red cell aplasia in rheumatoid arthritis.
Pure red cell aplasia occurred after fenbufen administration in a patient with severe rheumatoid arthritis. In vitro studies were performed to determine the pathogenesis of the selective red cell aplasia. No cellular or humoral inhibitory mechanisms were demonstrated on growth of erythroid and multipotent bone marrow progenitors. Also, no direct effect of fenbufen alone or in combination with IgG and/or patient serum was found. It is possible that a metabolite of the drug formed from its metabolism was responsible for the aplasia and that the target marrow cell precursor affected is later than both erythroid bone marrow progenitors (BFU-E and CFU-E) and therefore not apparent in our studies. Recovery upon cessation of fenbufen suggests its implication in the pure red cell aplasia.
D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy*; D001853:Bone Marrow / Q000473:pathology; D006801:Humans; D008297:Male; D010654:Phenylbutyrates / Q000009:adverse effects*; D012010:Red-Cell Aplasia, Pure / Q000139:chemically induced* / Q000473:pathology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D010654:Phenylbutyrates; C010725:fenbufen