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目的 :探讨乙肝后肝硬化骨代谢异常的发病机制。方法 :分别测定 36例乙肝后肝硬化患者血清 IL - 1β、骨钙素 (BGP)、尿骨胶原交联 (Crosslaps)水平及骨密度测量 ,并与 15例健康者对照。结果 :肝硬化组血清 IL - 1β、尿 Crosslaps较对照组显著升高 (P<0 .0 0 1,P<0 .0 5 ) ,其中肝硬化骨质疏松 (OP)组较非骨质疏松 (NOP)组升高明显 (P<0 .0 0 1,P<0 .0 1)。肝硬化组血清 BGP水平较对照组明显降低 (P<0 .0 1) ,其中 OP组较 NOP组降低更明显 (P<0 .0 5 )。 OP组血清IL - 1β、尿 Crosslaps均与尺桡密度呈负相关 (r=- 0 .6 38,P<0 .0 1,r=- 0 .6 2 4,P<0 .0 1) ,而血清 BGP与尺桡密度呈正相关 (r=0 .5 1,P<0 .0 5 )。结论 :乙肝后肝硬化患者存在骨形成减弱 ,骨吸收加强 ,从而导致肝性骨病 (HBD)发生。血清IL - 1β水平升高可引起骨吸收加强 ,是 HBD发生的重要原因之一。降低体内血清 IL - 1β水平 ,对 HBD防治可能有一定意义。
Objective: To explore the pathogenesis of abnormal bone metabolism in patients with posthepatitic cirrhosis. Methods: The levels of serum IL - 1β, BGP, Crosslaps and bone mineral density (BMD) in 36 patients with posthepatitic cirrhosis were measured and compared with 15 normal controls. Results: The levels of serum IL - 1β and urine Crosslaps in cirrhosis group were significantly higher than those in control group (P <0.01, P <0.05), and the serum levels of IL - 1β and urine in cirrhosis group were significantly higher than those in non - osteoporosis (NOP) group increased significantly (P <0.01, P <0.01). The level of serum BGP in cirrhosis group was significantly lower than that in control group (P <0.01). The level of BGP in OP group was significantly lower than that in NOP group (P <0.05). The levels of IL - 1β and urine Crosslaps in OP group were negatively correlated with ulnar radial densities (r = - 0.388, P <0.01, r = - 0.644, P <0.01) Serum BGP and ulnar radial density was positively correlated (r = 0.51, P <0.05). Conclusions: Bone formation is weakened and bone resorption is increased in patients with posthepatitic cirrhosis, leading to hepatic osteodystrophy (HBD). Serum IL - 1β levels can lead to increased bone resorption, HBD is one of the important causes. Decreasing serum IL - 1β level may have some significance for the prevention and treatment of HBD.