Association of ANGPT2 and NOS3 Gene Variants With Esophageal Variceal Progression in HCV-Induced Cirrhosis.

Esophageal varices (EV) are observed in 60%-85% of patients with decompensated cirrhosis at the time of diagnosis and in 30%-40% of patients with compensated cirrhosis. Hemorrhaging from these varices is a critical medical event and is associated with a mortality rate of approximately 40%. Therefore, it is essential to assess varices that show a risk for bleeding and then implement preventive measures. This urgency has sparked interest in several factors, including genetic polymorphisms, that influence the development of EV. To assess the prognostic value of specific single-nucleotide polymorphisms (SNPs) in ANGPT2 (rs2442598) and NOS3 (rs2070744) genes involved in EVdevelopment. Four-hundred fifty patients were enrolled: (1) 150 patients with hepatitis C (HCV)-related cirrhosis and endocscopically detected varices (Group I), (2) 150 patients with HCV-related cirrhosis and no varices (Group II), and 150 apparently healthy people as controls (Group III). Liver function tests, hepatitis viral markers, complete blood count {CBC}, abdominal ultrasonography, and detection of ANGPT2 (rs2442598) and NOS3 (rs2070744) based on real-time polymerase chain reaction were obtained for all participants. No significant differences in the genotype distribution or allele frequencies of ANGPT2 (rs2442598) and NOS3 (rs2070744) between patients with or without EV (p > 0.05) were found. However, significant differences were noted for ANGPT2 rs2442598 in relation to the presence of varices, ascites, Child-Pugh scores, hypertension (HTN), and levels of alanine and aspartate aminotransferase (ALT and AST, respectively; p < 0.05), while other parameters did not show significant differences (p > 0.05). Similarly, for NOS3 rs2070744, significant differences were found in Child-Pugh scores, HTN, and levels of ALT and AST (p < 0.05). The ANGPT2 (rs2442598) variant is a promising noninvasive indicator to confirm the absence of varices with portal hypertension to predict the absence of EV as a complication of cirrhosis.