Silvennoinen J, Risteli L, Karttunen T, Risteli J
Department of Internal Medicine, University of Oulu, Finland.
Gut. 1996 Feb;38(2):223-8. doi: 10.1136/gut.38.2.223.
To assess the mechanisms of osteopenia in inflammatory bowel disease (IBD), the serum markers of bone formation (osteocalcin and carboxyterminal propeptide of type I procollagen (PICP)) and bone degradation (carboxyterminal telopeptide of type I collagen (ICTP)), the bone mineral density (BMD) of the lumbar spine and the proximal femur and calcium intake of 150 unselected IBD patients and 73 healthy controls were investigated. The patients had higher ICTP values (3.69 (SD 1.40) microgram/l) than the healthy controls (3.25 (1.00) microgram/l, p = 0.035), but no differences in serum PICP and osteocalcin between these groups were detected. In the patients, the ICTP, PICP, and osteocalcin values did not have any significant correlation with BMD, but the patients with ICTP values above 3.6 microgram/l had significantly lower Z scores than those with lower ICTP. In the controls, however, a positive correlation between serum ICTP and BMD was found. The ulcerative colitis patients with total colitis had higher values of ICTP (3.96 (1.58) microgram/l) than those with a left sided disease (3.04 (0.86) micrograms/l, p = 0.009). The patients with a history of clinically active disease (n = 20) had higher ICTP (4.58 (1.55) microgram/l) and osteocalcin (12.56 (5.64) microgram/l) values than the patients (n = 130) with quiescent disease (ICTP 3.56 (1.33), p = 0.002, and osteocalcin 9.76 (3.62), p = 0.017). Increased serum osteocalcin, PICP, and ICTP concentrations and reduced BMD Z scores were found in a subgroup of Crohn's disease patients with a history of an active disease (n = 11). Raised serum ICTP and normal values of osteocalcin and PICP in IBD patients show increased breakdown of type I collagen without a compensatory increase in its synthesis suggesting an increased rate of bone degradation as a probable mechanism for osteopenia in IBD. Raised ICTP values are related to reduced bone mineral densities.
为评估炎症性肠病(IBD)中骨质减少的机制,对150例未经挑选的IBD患者和73名健康对照者的骨形成血清标志物(骨钙素和I型前胶原羧基末端前肽(PICP))、骨降解血清标志物(I型胶原羧基末端肽(ICTP))、腰椎和股骨近端的骨矿物质密度(BMD)以及钙摄入量进行了研究。患者的ICTP值(3.69(标准差1.40)微克/升)高于健康对照者(3.25(1.00)微克/升,p = 0.035),但两组间血清PICP和骨钙素无差异。在患者中,ICTP、PICP和骨钙素值与BMD均无显著相关性,但ICTP值高于3.6微克/升的患者Z评分显著低于ICTP值较低者。然而,在对照者中,发现血清ICTP与BMD呈正相关。全结肠炎的溃疡性结肠炎患者的ICTP值(3.96(1.58)微克/升)高于左侧病变患者(3.04(0.86)微克/升,p = 0.009)。有临床活动病史的患者(n = 20)的ICTP(4.58(1.55)微克/升)和骨钙素(12.56(5.64)微克/升)值高于病情静止的患者(n = 130)(ICTP 3.56(1.33),p = 0.002,骨钙素9.76(3.62),p = 0.017)。在有活动病史的克罗恩病患者亚组(n = 11)中发现血清骨钙素、PICP和ICTP浓度升高以及BMD Z评分降低。IBD患者血清ICTP升高而骨钙素和PICP值正常,表明I型胶原分解增加而其合成无代偿性增加,提示骨降解速率增加可能是IBD中骨质减少的机制。ICTP值升高与骨矿物质密度降低有关。