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目的探讨乙型肝炎肝硬化患者骨代谢异常的发病机制。方法用NM-300单光子骨密度测量系统检测61例乙型肝炎肝硬化患者的骨密度;抽取空腹血检测血清钙调节激素:1,25二羟维生素D3[1,25(OH)2D3]、甲状旁腺素、降钙素、骨钙素、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、尿骨胶原交联水平。根据尺桡骨密度将肝硬化患者分为骨质疏松组和非骨质疏松组,分别与30例健康者的各项检测指标做对照。结果肝硬化组尺骨密度、桡骨密度、尺桡密度均较对照组明显降低;肝硬化组血清1,25(OH)2D3、骨钙素水平较对照组明显降低,其中骨质疏松组较非骨质疏松组降低更明显;尿骨胶原交联水平肝硬化组较对照组明显升高,其中骨质疏松组较非骨质疏松组升高更明显。对血清1,25(OH)2D3、骨钙素、尿骨胶原交联水平与尺桡密度进行了统计学处理,发现血清1,25(OH)2D3、骨钙素水平与尺桡密度呈正相关。骨质疏松组尿骨胶原交联水平与尺桡密度呈负相关,而与非骨质疏松组无相关性。肝硬化组血清IL-1β、IL-6、TNF-α水平较对照组明显升高,骨质疏松组较非骨质疏松组升高显著;肝硬化组IL-1β、IL-6、TNF-α水平与尺桡密度呈负相关;其中骨质疏松组较非骨质疏松组相关性更明显。结论乙型肝炎肝硬化患者存在骨形成减少和骨破坏过多两种因素,从而引起肝性骨病;在骨形成减弱的过程中1,25(OH)2D3起着主要作用,在骨吸收增强的过程中IL-1β、IL-6、TNF-α起着重要的作用。适当补充维生素D3、降低体内IL-1β、IL-6和TNF-α水平,对防治肝性骨病可能具有重要意义。
Objective To investigate the pathogenesis of abnormal bone metabolism in patients with hepatitis B cirrhosis. Methods The bone mineral density (BMD) of 61 cirrhotic patients with hepatitis B was detected by NM-300 single-photon bone density measurement system. Serum calcium-regulated hormones: 1,25-dihydroxyvitamin D3 [1,25 (OH) 2D3] Parathyroid hormone, calcitonin, osteocalcin, interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF- Link level. The patients with cirrhosis were divided into osteoporosis group and non-osteoporosis group according to the radius and radial bone density, respectively, with 30 healthy controls. Results In the cirrhosis group, the ulnar, radial and ulnar radial densities were significantly lower than those in the control group. The levels of serum 1,25 (OH) 2D3 and osteocalcin in the cirrhosis group were significantly lower than those in the control group Osteoporosis group decreased more obvious; urinary collagen cross-linked level of cirrhosis group was significantly higher than the control group, of which osteoporosis group increased more significantly than the non-osteoporosis group. The levels of serum 1,25 (OH) 2D3, osteocalcin, urinary collagen cross-linking and ulnar radial density were statistically analyzed. It was found that serum 1,25 (OH) 2D3 and osteocalcin levels were positively correlated with ulnar radial . The level of urinary collagen cross-linking in osteoporosis group was negatively correlated with ulnar radial density, but not with non-osteoporosis group. The levels of IL-1β, IL-6 and TNF-α in cirrhosis group were significantly higher than those in the control group, while those in the osteoporosis group were significantly higher than those in the non-osteoporosis group. The levels of IL-1β, IL-6 and TNF- α level and ulnar radial density was negatively correlated; which osteoporosis group than non-osteoporosis group more obvious. Conclusions Hepatocirrhosis is caused by the reduction of bone formation and excessive destruction of bone in patients with hepatitis B cirrhosis. 1,25 (OH) 2D3 plays a major role in the process of weakened bone formation and plays an important role in the enhancement of bone resorption IL-1β, IL-6, TNF-α play an important role in the process of. Proper supplementation of vitamin D3 and lower levels of IL-1β, IL-6 and TNF-α in vivo may be of great significance for prevention and treatment of hepatic osteodystrophy.