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Osteoporosis is a common complication of Crohn's disease (CD). Glucocorticoid use and detrimental effects of inflammatory cytokines including tumor necrosis factor-alpha (TNF-α) can lead to osteoporosis. The aim of this study was to assess the ability of treatment with the TNF-α antagonist infliximab to increase bone formation as measured by surrogate markers of bone turnover in patients with active CD.Sera from 38 prospectively enrolled CD patients were examined for levels of bone alkaline phosphatase (BAP), N-telopeptide of type I collagen (NTX), immunoreactive parathyroid hormone (iPTH), calcium, and pro-inflammatory cytokines at baseline and 4 weeks following infliximab infusion. Crohn's Disease Activity Index (CDAI), Inflammatory Bowel Disease Questionnaire (IBDQ), and glucocorticoid dose also were collected.In this cohort, CDAI and IBDQ scores were significantly improved at week 4 (P < 0.001). Infliximab therapy was associated with an increase in BAP, a marker of bone formation (P = 0.010), whereas NTX, a marker of bone resorption, was not increased (P = 0.801). Among 22 patients who were taking glucocorticoids, mean glucocorticoid dose decreased 36% (P < 0.001; −7.9 mg).Treatment with infliximab was associated with increased markers of bone formation (BAP) without increasing bone resorption (NTX). This effect may be due to a beneficial effect of TNF-α blockade on bone turnover, a beneficial effect on CD activity resulting in decreased glucocorticoid dose, or both. Studies of longer duration are needed to assess the effect of infliximab on bone mineral density.