OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of clinical gastroenterology|
|State||Published - Jan 1 2006|
- Crohn's disease
- Tumor necrosis factor-α
ASJC Scopus subject areas