Department of Gastroenterology, University Hospital Virgen Macarena, Seville, Spain.
Department of Gastroenterology, University Hospital Virgen Macarena, Seville, Spain.
J Clin Densitom. 2019 Apr-Jun;22(2):195-202. doi: 10.1016/j.jocd.2018.07.010. Epub 2018 Aug 13.
BACKGROUND/OBJECTIVE: Osteoporosis and osteoporotic fracture risk are extraintestinal manifestations of the inflammatory bowel disease, whose etiopathogenic mechanisms have not been determined yet. Anti-tumor necrosis factor (TNF)-α are used in treatment of inflammatory bowel disease (IBD), but it is unknown if they play a role in osteoporotic fracture prevention. The objective of this study was to know if anti-TNF decreases fracture risk or modifies bone mineral density. To determine the possible risk factors associated with fractures, and assess the incidence of vertebral fractures in IBD patients.
Longitudinal prospective cohort study (7 yr of follow-up); which included 71 IBD patients, 23 received anti-TNF-α; the remaining 48 received conventional treatment, constituted the control group. Patients participated in a questionnaire which gathered risk factors associated with the development of osteoporosis and fractures. Radiographs of the dorsolumbar-spine were performed and also a bone density measurement. Their biochemical and bone remodeling parameters were determined.
Although patients who did not receive anti-TNF-α, suffered more fractures but biologic therapy did not reduce the risk of new vertebral fractures. The increase of bone mass was significantly higher the group treated with anti-TNF-α. The increase in the lumbar spine was of 8% and in the femoral neck was of 6.7%. The only determinant factor for the incidence of vertebral fractures was a history of previous fractures (odds ratio of 12.8; confidence interval 95% 2.37-69.9; p = 0.003). The incidence of vertebral fractures in IBD patients was considerably high: 26.7/700 patient-yr.
Anti-TNF-α, although increased bone mass in these patients, did not reduce the risk of new vertebral fractures. In this study, patients with IBD have a considerably high incidence of fractures. Only the existence of previous vertebral fractures was a predictive factor for consistent fractures.
背景/目的：骨质疏松症和骨质疏松性骨折风险是炎症性肠病的肠外表现，其发病机制尚未确定。抗肿瘤坏死因子（TNF）-α 用于治疗炎症性肠病（IBD），但尚不清楚其是否在预防骨质疏松性骨折中发挥作用。本研究旨在了解抗 TNF 是否会降低骨折风险或改变骨密度。确定与骨折相关的可能危险因素，并评估 IBD 患者的椎体骨折发生率。
这是一项 7 年随访的纵向前瞻性队列研究；其中包括 71 例 IBD 患者，23 例接受了抗 TNF-α 治疗；其余 48 例接受了常规治疗，作为对照组。患者参与了一项问卷调查，其中包括与骨质疏松症和骨折发生相关的危险因素。对患者的胸腰椎进行 X 线检查，并进行骨密度测量。还测定了他们的生化和骨重塑参数。
尽管未接受抗 TNF-α 治疗的患者骨折发生率更高，但生物治疗并不能降低新发椎体骨折的风险。接受抗 TNF-α 治疗的患者骨量增加更为显著。腰椎增加了 8%，股骨颈增加了 6.7%。椎体骨折发生率的唯一决定因素是既往骨折史（比值比 12.8；95%置信区间 2.37-69.9；p=0.003）。IBD 患者的椎体骨折发生率相当高：26.7/700 患者-年。
尽管抗 TNF-α增加了这些患者的骨量，但并未降低新发椎体骨折的风险。在这项研究中，IBD 患者的骨折发生率相当高。只有既往椎体骨折的存在是持续骨折的预测因素。
