Kapahtia Siddharth, Hazam Rajib K, Asim Mohammad, Karra Vijay K, Chowdhury Soumya J, Das Bhudev C, Kar Premashis
Department of Medicine, Maulana Azad Medical College, University of Delhi, India.
Dr B.R.Ambedkar Center for Biomedical Research, University of Delhi, India.
J Clin Exp Hepatol. 2018 Jun;8(2):169-172. doi: 10.1016/j.jceh.2017.05.208. Epub 2017 May 31.
Progression of hepatitis B virus infection (HBV) might be affected by host genetic factors. The present study was undertaken to study the role of glutathione S-transferases (GST)-M1 and T1 gene polymorphisms in different stages of HBV infection: HBV inactive carrier, chronic hepatitis B and cirrhosis, and cryptogenic cirrhosis.
The study population comprised of 170 subjects; 120 cases (HBV inactive carrier, = 30; HBV related chronic hepatitis, = 30; HBV related cirrhosis, = 30; cryptogenic cirrhosis, = 30) and 50 unrelated healthy adults without liver disease as controls. Analysis of GSTM1 and GSTT1 gene polymorphisms was done by multiplex polymerase chain reaction.
The GSTM1 null genotype was seen more commonly in hepatitis B cirrhosis ( = 21; 70%), chronic hepatitis B ( = 19; 63.33%) and cryptogenic cirrhosis ( = 17; 56.67%) as compared with inactive carrier ( = 9; 30%) and controls ( = 13; 26%). The GSTT1 null genotype was seen less frequently in all the groups, the observed frequencies were controls ( = 7; 14%), inactive carrier ( = 5; 16.67%), chronic hepatitis B ( = 8; 26.67%) and hepatitis B cirrhosis ( = 7; 23.33%). The difference of GSTM1 null genotype frequencies was statistically significant for hepatitis B cirrhosis vs. controls ( = 0.0002), chronic hepatitis B vs. controls ( = 0.002) and cryptogenic cirrhosis vs. controls ( = 0.01). The GSTT1 null genotype was not found to vary significantly between the groups.
The patients with GSTM1 null genotype are at risk of progression of liver disease as the frequency of GSTM1 null genotype was found to be significantly higher in chronic hepatitis B, hepatitis B cirrhosis and cryptogenic cirrhosis as compared with controls.
乙型肝炎病毒(HBV)感染的进展可能受宿主遗传因素影响。本研究旨在探讨谷胱甘肽S-转移酶(GST)-M1和T1基因多态性在HBV感染不同阶段(HBV非活动性携带者、慢性乙型肝炎、肝硬化以及隐源性肝硬化)中的作用。
研究人群包括170名受试者;120例患者(HBV非活动性携带者,n = 30;HBV相关慢性肝炎,n = 30;HBV相关肝硬化,n = 30;隐源性肝硬化,n = 30)以及50名无肝病的无关健康成年人作为对照。通过多重聚合酶链反应分析GSTM1和GSTT1基因多态性。
与非活动性携带者(n = 9;30%)和对照组(n = 13;26%)相比,GSTM1无效基因型在乙型肝炎肝硬化(n = 21;70%)、慢性乙型肝炎(n = 19;63.33%)和隐源性肝硬化(n = 17;56.67%)中更为常见。GSTT1无效基因型在所有组中出现频率较低,观察到的频率分别为对照组(n = 7;14%)、非活动性携带者(n = 5;16.67%)、慢性乙型肝炎(n = 8;26.67%)和乙型肝炎肝硬化(n = 7;23.33%)。GSTM1无效基因型频率在乙型肝炎肝硬化与对照组之间(P = 0.0002)、慢性乙型肝炎与对照组之间(P = 0.002)以及隐源性肝硬化与对照组之间(P = 0.01)差异具有统计学意义。未发现GSTT1无效基因型在各组之间有显著差异。
GSTM1无效基因型患者存在肝病进展风险,因为与对照组相比,慢性乙型肝炎、乙型肝炎肝硬化和隐源性肝硬化中GSTM1无效基因型的频率显著更高。