肝源性糖尿病患者肝组织干扰素诱导蛋白-10表达变化

Hepatic expression of interferon inducible protein-10 in patients with hepatitis B liver cirrhosis and hepatogenic diabetes mellitus

目的观察肝源性糖尿病患者肝组织和血清干扰素诱导蛋白-10(IP-10)水平变化,并分析其在肝源性糖尿病发病过程中的可能作用。方法2016年3月~2018年5月我院诊治的乙型肝炎肝硬化并发肝源性糖尿病患者70例和不伴有糖尿病的乙型肝炎肝硬化患者70例,采用ELISA法检测血清IP-10水平,采用PCR法和免疫组化法分别检测肝组织IP-10 mRNA水平和蛋白表达。结果伴有糖尿病的肝硬化血清IP-10水平为(236.59±28.30)pg/mL,显著高于不伴有糖尿病的肝硬化患者【(205.31±26.92)pg/mL,P<0.001】;糖尿病患者肝组织IP-10 mRNA水平为(0.59±0.91)lg copies/ml,显著高于肝硬化患者【(0.21±0.66)lg copies/ml,P<0.05】,差异具有统计学意义;糖尿病患者肝组织IP-10表达阳性率为31.4%,显著高于肝硬化患者的12.9%,差异具有统计学意义(x2=7.002,P<0.05)。结论乙型肝炎肝硬化并发肝源性糖尿病患者血清和肝组织IP-10水平显著升高,其意义还有待于进一步探讨。

Objective To investigate hepatic expression of interferon inducible protein-10(IP-10)in patients with hepatitis B liver cirrhosis and hepatogenic diabetes mellitus.Methods The specimens of liver tissues from 70 patients with hepatitis B-induced liver cirrhosis and hepatogenic diabetes mellitus and another 70 patients with hepatitis B-induced liver cirrhosis were obtained by liver biopsies between March 2016 and May 2018,and serum IP-10 were assayed by ELISA,and hepatic IP-10 mRNA and its protein expression were detected by PCR and immunohistochemistry.Results Serum IP-10 level in patients with hepatitis B-induced liver cirrhosis and hepatogenic diabetes mellitus was(236.59±28.30)pg/mL,significantly higher than[(205.31±26.92)pg/mL,P<0.001]in patient with liver cirrhosis without hepatogenic diabetes mellitus;hepatic IP-10 mRNA was(0.59±0.91),significantly higher than[(0.21±0.66),P<0.05]in patients without diabetes mellitus;the immunohistochemical staining results showed that the hepatic IP-10 expression positive rate was 31.4%,significantly higher than(12.9%,x2=7.002,P<0.05)in patients without diabetes mellitus.Conclusion The expression of IP-10 in liver tissues and serum IP-10 levels in patients with hepatogenic diabetes mellitus with underlying hepatitis B liver cirrhosis is sig-nificantly increased,which might be involved in the pathogenesis of hepatogenic diabetes mellitus through inflammatory mechanism.