MTHFR and MTRR gene polymorphisms in patients with chronic hepatitis B virus infections in Zigong, Sichuan Province.

BACKGROUND: Chronic hepatitis B virus (HBV) infection is a severe disease affecting the physical and economic well-being of patients. The relationship between polymorphisms in the MTHFR gene and disease progression following HBV infection remains a controversial topic. AIM: To study MTHFR and MTRR gene polymorphisms in patients with chronic HBV infections in Zigong, Sichuan Province. SUBJECTS AND METHODS: One hundred and ninety-one patients with chronic HBV infections were divided into three groups: the chronic hepatitis B (CHB) group (n = 71), the hepatitis B-induced liver cirrhosis (LC) group (n = 56), and the hepatitis B-related primary liver cancer (PLC) group (n = 64). The gene polymorphisms were detected using the PCR-melt curve method and analysed. RESULTS: The distributions of MTHFR C677T (CC: 41.2% vs. 41.8%; CT: 50% vs. 45.5%; TT: 8.8% vs. 12.7%; p = 0.714), MTHFR A1298C (AA: 70.6% vs. 72.7%; AC: 26.5% vs. 25.5%; CC: 2.9% vs. 1.8%; p = 1.000), and MTRR A66G (AA: 58.1% vs. 65.5%; AG: 39.0% vs. 29.1%; 2.9% vs. 5.5%; p = 0.353) genetic polymorphisms did not vary between male and female patients from Zigong. In addition, there were no differences in the distributions of MTHFR C677T (CC: 43.4% vs. 38.8%; CT: 49.1% vs. 48.2%; TT: 7.5% vs. 12.9%; p = 0.444), MTHFR A1298C (AA: 76.4% vs. 64.7%; AC: 20.8% vs. 32.9%; CC: 2.8% vs. 2.4%; p = 0.155), and MTRR A66G (AA: 62.3% vs. 57.6%; AG: 34.0% vs. 38.8%; 3.8% vs. 3.5%; p = 0.353) genetic polymorphisms between the patients <60 and >60 years of age. The distributions of MTHFR C677T (CHB vs. LC, p = 0.888; CHB vs. PLC, p = 0.661; PLC vs. LC, p = 0.926), MTHFR A1298C (CHB vs. LC, p = 0.12; CHB vs. PLC, p = 0.263; PLC vs. LC, p = 0.550), and MTRR A66G (CHB vs. LC, p = 0.955; CHB vs. PLC, p = 0.645; PLC vs. LC, p = 0.355) gene polymorphisms were comparable between the CHB, LC, and PLC groups. CONCLUSION: The distributions of MTHFR and MRRR genetic polymorphisms in the population with HBV infections in Zigong, Sichuan Province did not differ in age and sex. The MTHFR and MRRR genetic polymorphisms were comparable between the CHB, LC, and PLC groups.

Clinical application value of hepatitis B virus basal core promoter 1762/1764 and GGTII and GGT in patients with HBV-DNA-positive primary liver cancer.

BACKGROUND: Hepatitis B virus (HBV) is closely related to the occurrence and development of primary liver cancer (PLC). The early diagnosis of PLC is difficult. The study explored the clinical application value of the HBV gene basal core promoter (BCP) region 1762/1764 combined with gamma-glutamyl transpeptidase (GGT) and its isozyme II (GGTII) in PLC. METHODS: From June 2017 to June 2021, 145 hepatitis B surface antigen-positive and HBV DNA-positive patients were enrolled in the Third People Hospital of Zigong. Of them, 67 were chronic hepatitis B (CHB) patients, 30 were liver cirrhosis patients, and 48 were patients with hepatitis B-associated PLC. The HBV BCP 1762/1764 mutation was detected through the amplification refractory mutation system fluorescence PCR method, and GGTII was detected using the double-antibody sandwich method. RESULTS: The results showed that the serum GGT activity, GGTII level, aspartate aminotransferase (AST) activity, AST/alanine aminotransferase (ALT) ratio, GGT/ALT ratio, and GGT/AST ratio were significantly different between the PLC and CHB groups. Statistically significant differences in serum GGT activity, AST activity, and GGT/ALT ratio were observed between the PLC and LC groups. The BCP 1762/1764 mutation rate between the PLC and CHB groups was statistically significant. The GGTII level in the early PLC (stage I + II) group and the advanced PLC (stage III + IV) group was higher than that in the N-PLC group. Serum GGT activity in the early PLC and advanced PLC groups was higher than that in the N-PLC group. The area under the curve of the receiver operator characteristic curve of GGT and GGTII for diagnosing PLC was 0.775 (95% confidence interval [CI] [0.697, 0.854]) and 0.608 (95% CI [0.512, 0.704]), respectively. The area under curve of GGT and GGTII for diagnosing early PLC was 0.732 (95% CI [0.620, 0.845]) and 0.579 (95% CI [0.452, 0.706]), respectively. CONCLUSION: HBV gene BCP 1762/1764 mutation, GGT, and GGTII may be related to PLC occurrence. The HBV gene BCP region 1762/1764 combined with GGT has certain clinical diagnostic values for PLC and early PLC. However, GGTII is not a good indicator of early PLC and is more relevant to advanced PLC.