Skeletal morbidity in inflammatory bowel disease

Skeletal morbidity in inflammatory bowel disease
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炎症性肠病的骨骼发病率

DOI:
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发表时间:
2006
期刊:
Scandinavian Journal of Gastroenterology, Supplement
影响因子:
--
通讯作者:
N. Hamdy
N. Hamdy
中科院分区:
--
文献类型:
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作者:
R. V. van Hogezand;N. Hamdy

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克罗恩病患者发生骨和矿物质代谢紊乱的风险增加,这是由于几个因素,包括炎性肠病的精氨酸介导的性质、疾病活动或广泛肠切除导致的肠吸收不良以及使用葡萄糖皮质激素控制疾病活动。在儿童期发病时无法达到峰值骨量,营养不良,固定,低BMI,吸烟和性腺功能减退也可能在骨丢失的发病机制中发挥作用。长期使用糖皮质激素治疗任何疾病适应症与骨质疏松症和骨折风险增加之间的关系已得到充分证实。然而,克罗恩病和溃疡性结肠炎与骨丢失之间的关系仍然存在争议。根据研究的人群,骨质疏松症的患病率在炎症性肠病(IBD)患者中的范围为12%至42%。在IBD中,大多数研究表明骨矿物质密度(BMD)和糖皮质激素使用之间呈负相关,但并非所有作者都同意长期糖皮质激素使用和持续骨丢失之间的关系。尽管前瞻性研究确实表明长期使用糖皮质激素的炎症性肠病患者的骨小梁和皮质部位存在持续的骨丢失,但在不使用糖皮质激素的活动性克罗恩病患者中也观察到骨量减少,并且在使用口服或直肠给药糖皮质激素的克罗恩病患者中并不普遍观察到骨丢失。关于脊椎骨折的数据很少,关于克罗恩病患者的非脊椎骨折风险没有一致意见,尽管有人认为IBD患者的非脊椎骨折风险可能增加高达60%。最近的一篇出版物报告了克罗恩病中髋部骨折的风险增加,与当前和累积使用皮质类固醇和使用阿片类药物有关,尽管这些骨折与骨质疏松症的严重程度无关。骨质疏松症问题的严重性问题在克罗恩病中变得特别相关,因为在骨质疏松症患者中已经清楚地确定了治疗干预对骨骼发病率的有利影响的能力,无论是绝经后妇女、男性还是糖皮质激素使用者。出现的主要问题是,是否所有克罗恩病患者都应该接受骨保护剂治疗,假设他们都有可能发展为骨质疏松症,或者是否应该将这些药物的使用限制在明确存在骨质疏松症和骨折风险的患者中,前提是这些患者可以被识别。我们建议,根据现有的文献和我们自己的经验,所有克罗恩病患者除了完全纠正任何潜在的钙和维生素D缺乏症外,还应通过骨矿物质密度测量筛查骨质疏松症,以便对有风险的患者进行及时的治疗干预,同时避免绝大多数不必要的药物治疗。
Patients with Crohn's disease are at increased risk of developing disturbances in bone and mineral metabolism because of several factors, including the cytokine-mediated nature of the inflammatory bowel disease, the intestinal malabsorption resulting from disease activity or from extensive intestinal resection and the use of glucucorticoids to control disease activity. Inability to achieve peak bone mass when the disease starts in childhood, malnutrition, immobilization, low BMI, smoking and hypogonadism may also play a contributing role in the pathogenesis of bone loss. The relationship between long-term use of glucocorticoids for any disease indication and increased risk for osteoporosis and fractures is well established. However, the relationship between Crohn's disease and ulcerative colitis and bone loss remains controversial. Depending on the population studied the prevalence of osteoporosis has thus been variably reported to range from 12 to 42% in patients with inflammatory bowel disease (IBD). In IBD most studies demonstrate a negative correlation between bone mineral density (BMD) and glucocorticoid use, but not all authors agree on the relationship between long-term glucocorticoid use and continuing bone loss. Whereas prospective studies do suggest sustained bone loss at both trabecular and cortical sites in long-term glucocorticoid users with inflammatory bowel disease, a decrease in bone mass is also observed in patients with active Crohn's disease not using glucocorticoids, and bone loss is not universally observed in patients with Crohn's disease using orally or rectally administered glucocorticoids. Data on vertebral fractures are scarce and there is no agreement about the risk of non-vertebral fractures in patients with Crohn's disease, although it has been suggested that non-vertebral fracture risk may be increased by up to 60% in patients with IBD. A recent publication reports an increased risk of hip fractures in Crohn's disease related to current and cumulative corticosteroid use and use of opiates, although these fractures could not be related to the severity of osteoporosis. The issue of the magnitude of the problem of osteoporosis has become particularly relevant in Crohn's disease, since the ability of therapeutic interventions to beneficially influence skeletal morbidity has been clearly established in patients with osteoporosis, whether post-menopausal women, men or glucocorticoid users. The main question that arises is whether all patients with Crohn's disease should be treated with bone protective agents on the assumption that they all have the potential to develop osteoporosis or whether the use of these agents should be restricted to patients clearly at risk of osteoporosis and fractures, providing these can be identified. We recommend, based on the available literature and our own experience, that all patients with Crohn's disease should be screened for osteoporosis by means of a bone mineral density measurement in addition to full correction of any potential calcium and vitamin D deficiency, to allow timely therapeutic intervention of the patient at risk while sparing the vast majority unnecessary medical treatment.
DOI: 10.1210/endo.140.9.7131
发表时间: 1999-09
期刊: Endocrinology
影响因子: 4.8
作者:
L. Hofbauer;S. Khosla;C. Dunstan;D. Lacey;T. Spelsberg;B. Riggs
通讯作者: L. Hofbauer;S. Khosla;C. Dunstan;D. Lacey;T. Spelsberg;B. Riggs
骨质疏松症:儿童克罗恩病的一种不寻常表现。
DOI: 10.1210/jcem.85.6.6640
发表时间: 2000
期刊: The Journal of clinical endocrinology and metabolism
影响因子: --
作者:
Thearle,M;Horlick,M;Bilezikian,JP;Levy,J;Gertner,JM;Levine,LS;Harbison,M;Berdon,W;Oberfield,SE
通讯作者: Oberfield,SE
DOI: 10.1016/8756-3282(95)00180-l
发表时间: 1995-08-01
期刊: BONE
影响因子: 4.1
作者:
MANOLAGAS, SC
通讯作者: MANOLAGAS, SC
DOI: 10.1172/jci2799
发表时间: 1998-07-15
影响因子: 15.9
作者:
Weinstein, RS;Jilka, RL;Manolagas, SC
通讯作者: Manolagas, SC