RESUMO
BACKGROUND/OBJECTIVE: Hepatitis B virus (HBV) infection is a major public health problem globally. Northeast India is home to indigenous tribes with different ethnicity and high rates of drug abuse and HIV infection. The study was designed to estimate the burden of HBV infection across various spectrums of liver diseases from this region. HBV genotypes and subgenotypes play a role in the chronicity of disease, response to treatment and its progression. As very limited data are available from this region, we tried to elucidate the role of HBV genotypes, HBV mutants and their phylogenetic analysis. METHOD: We designed a prospective multicentric study, and included 7464 liver disease cases, 7432 blood donors and 650 health care workers, who were screened for HBV infection. HBV DNA positive patients were genotyped and subjected to surface protein, precore and core mutation and phylogenetic analysis. RESULTS: The prevalence of HBV infection with respect to different types of liver diseases, blood donors and health care workers was 9.9% (1550/15,546). 49.5% (768/1550) cases were found to be HBV DNA positive. The most common genotype was found to be genotype D 74.2% (570/768), followed by genotype C 6.5% (50/768), A 4.4% (34/768) and I 0.9% (7/768). CONCLUSION: This study highlights the high hepatitis B burden in Northeast India, reflecting lacunae in health care needs of the region. Also, the different genotype distribution and presence of mutations may translate into different rates of liver disease progression, prognosis and ultimately, clinical significance. However, further prospective cohort study from Northeast India is warranted, to elucidate the clinical significance of multiple genotypes and mutation in this unique population.
RESUMO
BACKGROUND AND AIM: 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. METHODS: The study population comprised of 170 subjects; 120 cases (HBV inactive carrier, n = 30; HBV related chronic hepatitis, n = 30; HBV related cirrhosis, n = 30; cryptogenic cirrhosis, n = 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. RESULTS: The GSTM1 null genotype was seen more commonly in hepatitis B cirrhosis (n = 21; 70%), chronic hepatitis B (n = 19; 63.33%) and cryptogenic cirrhosis (n = 17; 56.67%) as compared with inactive carrier (n = 9; 30%) and controls (n = 13; 26%). The GSTT1 null genotype was seen less frequently in all the groups, the observed frequencies were controls (n = 7; 14%), inactive carrier (n = 5; 16.67%), chronic hepatitis B (n = 8; 26.67%) and hepatitis B cirrhosis (n = 7; 23.33%). The difference of GSTM1 null genotype frequencies was statistically significant for hepatitis B cirrhosis vs. controls (P = 0.0002), chronic hepatitis B vs. controls (P = 0.002) and cryptogenic cirrhosis vs. controls (P = 0.01). The GSTT1 null genotype was not found to vary significantly between the groups. CONCLUSION: 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.
RESUMO
BACKGROUND/OBJECTIVE: Quantification of serum hepatitis B antigen (HBsAg) is an important test that marks active infection with hepatitis B and helps in the prediction of the clinical outcome and management of hepatitis B virus (HBV) infection. Correlation with HBV DNA quantitative levels may help in developing strategies for antiviral treatment. This study is aimed to evaluate HBsAg titres in various phase of HBV infection in HBsAg positive patients, and its correlation with HBV DNA viral load levels. METHODS: 976 HBV related patients were analysed in this retrospective cross-sectional study. Patients were categorised on the basis of the phase of HBV infection: immune tolerant phase (IT, n = 123), immune clearance phase (IC, n = 192), low-replicative phase (LR, n = 476), and HBeAg-negative hepatitis (ENH, n = 185). HBsAg titres were quantified and correlated with HBV-DNA levels and clinical parameters. RESULTS: Median HBsAg titres were different between each phases of HBV infection (P < 0.001): (4.62 log10 IU/ml), IC (3.88 log10 IU/ml), LR (2.76 log10 IU/ml) and ENH (2.94 log10 IU/ml). HBsAg and HBV DNA levels showed significant correlation in the whole group (r = 0.694, P < 0.001), and this was also observed in different phases of HBV infection. Strong correlation in IT phase (r = 0.603, P < 0.001) and IC phase (r = 0.523, P < 0.001), moderate in LR phase (r = 0.362, P < 0.001) and weak in ENH (r = 0.110, P = 0.04). No correlation was observed between serum HBsAg levels and biochemical parameters. CONCLUSION: The study demonstrated significant difference in the median baseline values of serum HBsAg titres in different phases of HBV infection and provides additional information in understanding the natural history of HBV-infection.