肝炎后肝硬化患者血清TNF-α、BGP及尿Crosslaps变化与骨代谢的关系

Relationship between serum TNF-α,BGP and urine crosslaps and bone metabolism in patients with posthepatitic cirrhosis

目的探讨肝炎后肝硬化患者骨代谢异常的发病机制。方法分别测定36例乙型肝炎后肝硬化患者血清TNF-α、骨钙素(BGP)、尿骨胶原交联(Crosslaps)水平及骨密度,并与15例健康者对照。结果肝硬化组血清肿瘤坏死因子α(TNF-α)、尿Crosslaps水平较对照组显著升高(P<0.01,<0.05),其中骨质疏松(OP)组较非骨质疏松(NOP)组升高明显(P<0.01,<0.01),而肝硬化组血清BGP水平较对照组明显降低(P<0.01),其中OP组较NOP组降低更明显(P<0.05)。OP组血清TNF-α、尿Crosslaps均与尺桡骨密度呈负相关(r=-0.483,P<0.05;r=-0.624,P<0.01),而血清BGP与尺桡密度呈正相关(r=0.51,P<0.05)。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TNF-α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TNF-α水平,对HBD防治可能有一定意义。

Objective To discuss the pathogenesis of abnormal bone metabolism in patients with posthepatitic cirrhosis.Methods Levels of serum TNF-α,osteocalcin (BGP) and urine crosslaps were detected in 36 male cirrhosis and 15 age-matched healthy controls.Results Serum TNF-α and urine crosslaps in cirrhosis increased more than those of controls (P<0.01,<0.05),and above items in osteoporosis (OP) group were much higher than those in non-osteoporosis (NOP) group(P<0.01,<0.01).Serum BGP levels of cirrhosis were lower than the controls (P<0.01),and much lower in OP group than in NOP group (P<0.05).TNF-α and crosslaps had negative correlation with mean ulnoradial density (r=-0.483,P<0.01; r=-0.624,P<0.01 ) respectively in OP group.Positive correlation was found between serum BGP and mean ulnoradial density (r=0.51,P<0.05).Conclusions Bone formation is weakened and bone resorption is strengthened in patients with posthepatitic cirrhosis,which lead to hepatic bone disease (HBD).Elevation of serum TNF-α can accelerate bone resorption and cause HBD.Reducing the level of serum TNF-α may be very important for prevention and treatment of HBD.