Endocrine Abstracts

Rheumatoid arthritis (RA) is a chronic inflammatory disease that results in generalized bone loss and increased fracture risk. Although glucocorticoids are frequently prescribed for the symptomatic management of inflammatory disorders such as RA, extended glucocorticoid exposure is the leading cause of osteoporosis and leaves patients at a high risk of fracture. The aim of this study is to evaluate the efficacy and safety of monthly oral minodronate for the treatment of osteoporosis induced by glucocorticoid and RA itself, and to compare minodronate with weekly or daily risedronate in glucocorticoid-induced osteoprotic RA patients. Minodronate was monthly administrated to 36 osteoporotic RA patients at a dose of 50 mg for 24 weeks. Ten RA patients were treated with no bisphosphonate (group I) before minodronate treatment. In contrast, 16 or 10 RA patients were treated with weekly or daily risedronate (groups II or III), respectively, and changed to monthly minodronate. Lumber and total hip bone mineral density were measured at 0 and 24 weeks. Serum tartrate-resistant acid phosphatase 5b (TRAP-5b) and bone-specific alkaline phosphatase (BAP), parathyroid hormone (PTH), and urinary type-I collagen cross-linked-N-telopeptide (uNTx) were measured. RA activity and a mean dose (7.3+1.1 mg/day) of oral prednisolone were not significantly changed in three groups. The percentage change from baseline (0 week) in lumber and total hip bone mineral density was increased in group I and III at 24 weeks. In contrast, bone mineral density in group II at 24 weeks was not changed compared with baseline (0 week). In addition, TRAP-5b and uNTx at 24 weeks were significantly decreased in group I and III (P<0.01) and BAP was weakly decreased in all groups at 24 weeks. Moreover, serum concentration of PTH was increased in group I, but was reduced in group II and III. In addition to those data, serum calcium was decreased in group II and III, but not group I. In conclusion, monthly administration of minodronate was effective in glucocorticoid-induced osteoporosis in RA patients. Furthermore, monthly minodronate was thought to be strong bisphosphonate, as compared with daily risedronate. Especially, the effect of minodronate on the induction of secondary hyperparathyroidism might be weak as compared to that of risedoronate.