BACKGROUND: Patients with Crohn's disease (CD) have a high risk of developing osteoporosis, but the mechanisms underlying bone mass loss are unclear. Elevated proinflammatory cytokines, such as tumour necrosis factor-alpha (TNFalpha), have been implicated in the pathogenesis of bone resorption. AIM: To assess whether suppression of TNFalpha with infliximab treatment has a beneficial effect on lumbar bone mass. METHODS: Adult CD patients who had received infliximab treatment, and who underwent lumbar densitometric evaluation before and during treatment, were selected. Adult CD patients who had never received infliximab treatment were selected as controls. Information regarding age, sex, weight, duration of CD, use of glucocorticoids and bisphosphonates, and signs of disease activity between both densitometric measurements were collected. RESULTS: Data from 45 patients were analyzed. The control group (n=30, mean [+/- SD] 26.7+/-9 years of age) had a significantly higher increase in body weight between both evaluations (6.26%+/-8%) than the infliximab group (n=15, 30.6+/-13 years), which had an increase of 0.3%+/-7.4%. There was a strong correlation between the final weight and lumbar bone mineral content (BMC) in both groups. The infliximab group had a significant increase in lumbar bone area (4.15%+/-6.6%), BMC (12.8%+/-13.6%) and bone mineral density (8.13%+/-7.7%) between both evaluations (interval 22.6+/-11 months) compared with the control group. The increase in BMC in patients who had received infliximab treatment was significant when compared with control patients who had received glucocorticoids (n=8) or had evidence of disease activity (n=13). CONCLUSION: Infliximab therapy improved lumbar bone mass independent of nutritional status. This finding suggests that TNFalpha plays a role in bone loss in CD.
BACKGROUND:Patients with Crohn's disease (CD) have a high risk of developing osteoporosis, but the mechanisms underlying bone mass loss are unclear. Elevated proinflammatory cytokines, such as tumour necrosis factor-alpha (TNFalpha), have been implicated in the pathogenesis of bone resorption. AIM: To assess whether suppression of TNFalpha with infliximab treatment has a beneficial effect on lumbar bone mass. METHODS: Adult CDpatients who had received infliximab treatment, and who underwent lumbar densitometric evaluation before and during treatment, were selected. Adult CDpatients who had never received infliximab treatment were selected as controls. Information regarding age, sex, weight, duration of CD, use of glucocorticoids and bisphosphonates, and signs of disease activity between both densitometric measurements were collected. RESULTS: Data from 45 patients were analyzed. The control group (n=30, mean [+/- SD] 26.7+/-9 years of age) had a significantly higher increase in body weight between both evaluations (6.26%+/-8%) than the infliximab group (n=15, 30.6+/-13 years), which had an increase of 0.3%+/-7.4%. There was a strong correlation between the final weight and lumbar bone mineral content (BMC) in both groups. The infliximab group had a significant increase in lumbar bone area (4.15%+/-6.6%), BMC (12.8%+/-13.6%) and bone mineral density (8.13%+/-7.7%) between both evaluations (interval 22.6+/-11 months) compared with the control group. The increase in BMC in patients who had received infliximab treatment was significant when compared with control patients who had received glucocorticoids (n=8) or had evidence of disease activity (n=13). CONCLUSION:Infliximab therapy improved lumbar bone mass independent of nutritional status. This finding suggests that TNFalpha plays a role in bone loss in CD.
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