36例乙型肝炎病人病毒核糖核酸、肌钙蛋白Ⅰ与心电图改变关系的探讨

目的:研究乙型肝炎(HB)病人血清乙型肝炎病毒脱氧核糖核酸(HBV-DNA)、肌钙蛋白Ⅰ(cTnⅠ)与心电图(ECG)改变三者的关系,探讨HBV对心肌损伤的机理。方法:收集36例HB的临床资料及ECG的变化,并检测血清HBV-DNA、cTn Ⅰ含量。结果:急性肝炎患者血清HBV-DNA含量明显高于慢性肝炎;各型肝炎cTn Ⅰ的阳性率不等,总阳性率为22.2%(8 36)。急性、慢性重度、慢性中度、肝硬化、慢性轻度的阳性率分别为50%(2/4)、25%(1/4)、23.4%(3、1 3)、14.2%、(1 7)、12.1%(1/8),急性肝炎明显高于其它各组(P<0.01)。慢性中度、莺度与慢性轻度、肝硬化之间也有显著差异(P<0.01)。慢性轻度与肝硬化之间、慢性中度与慢性重度之间无显著差异。HB病人ECG异常发生率为36.1%(13/36),4例急性肝炎患者均有过ECG改变,显著高于其它各组(P<0.01)。结论:1)cTn Ⅰ阳性与ECG异常表现并不一致,cTn Ⅰ可以作为判断HB心肌损伤的敏感和特异性指标;2)在HB急性期的心肌损伤可能是HBV直接作用,慢性HB心肌损伤是自身免疫作用的结果。

Relationship of Hepatitis B DNA, Cardiac Troponin I and Abnormal of Electrocardiogram in 36 Patients with Hepatitis B Infection

Objective:To study the associations of hepatitis B virus DNA ( HBV-DNA),cardiac troponin I(cTn I)and abnormal of electrocardiogram ( ECG) in hepatitis B ( HB) patients and to investigate the mechanism of myocardium hurt caused by HBV. Methods: Clinical data including Serum HBV-DNA,cTn I and abnormal of ECG in 36 cases of HB patients were collected and analyzed. . Results: Level of HBV-DNA in acute hepatitis was higher than that of chronic hepatitis. The cTn I positive rate of different clinical types were different, total positive rate is 22. 2%( 8/36 ). Acute hepatitis is 50%(2 4). Inchronic hepatitis,sever is 25% (1/4) middle is 23. 4%(3/13) liver cirrhosis is 14. 2% (1/7) and mild is 12. 1 %(1/8). Positive rate in acute group was obviously higher than that of other groupst P<(>. 01). There were significant differences among chronic middle.sever and chronic mild, liver cirrhosis groups ( P<0. 01 ). but no difference between chronic mild and liver cirrhosis. chronic middle and sever, exist 36. 1 %(13/36) of HB had abnormal ECG. All four acute hepatitis patients had abnormal ECG. which was obviously higher than other groups(P<0. 01). Conclusion: 1 ) The positive rate of cTn 1 and abnormal of ECG is different. cTn I might be a sensitive and specific marker for estimating myocardium hurt caused by HBV:2 ) Myocardium hurt might he due to direct action of HBV in acute hepatitis,and auto-immune action caused by HBV in chronic hepatitis B.