L ow bone density has long been associated with inflamma- tory bowel disease (IBD) through a complex interplay of factors, including glucocorticoid use, suppression of gonadal function, low body weight, vitamin D deficiency, and systemic effects of chronic inflammation through cytokines. 1 Glucocorticoid use, both short-and long-term, adds significant risk by increasing bone resorption, inhibiting bone formation, and altering the intestinal absorption and renal excretion of calcium. 2 The true causal effect of steroids on bone mass in IBD has been difficult to separate from disease activity, as patients with more severe disease are also more likely to require steroids.
Bisphosphonates have become an important tool in the treatment and prevention of osteoporosis. The goal of this study was to examine the effects of the oral bisphosphonate risedronate on bone mass in patients with both Crohn's disease (CD) and ulcerative colitis (UC). This randomized, double-blind, placebo-controlled trial involved a total of 61 patients (48 of whom completed the trial) with a bone mineral density (BMD) T-score of less than or equal to ฯช1, who were randomized to receive either 5 mg daily of oral risedronate or identical placebo for 12 months. Patients were divided into separate groups based on gender, menopausal status, and cumulative steroid dose. All patients received 600 mg of calcium daily. Patients were excluded if they had abnormal calcium or abnormal bone chemistries, liver disease, pregnancy/ breastfeeding, and previous hormone replacement or bisphosphonate therapy. Disease activity was measured by the Truelove and Witts index for UC and the Harvey Bradshaw index for CD as well as laboratory data (Creactive protein [CRP], erythrocyte sedimentation rate [ESR], and full blood count), and patient self-reported disease activity.
BMD was measured using dual x-ray absorptiometry at baseline and 12 months for the spine, total hip, femoral neck, trochanter, and intertrochanteric region. The primary end-