Angiotensin Converting Enzyme I/D Polymorphism and Chronic Hepatitis C Virus Infection

Background: Patients with hepatitis C usually develop hepatic fibrosis. Experimental and clinical studies suggest that the renin-angiotensin system and its inhibitors may play a role in regulating the mechanisms of liver fibrosis development. Aim of the Work: This study aimed at investigating the role of angiotensin-converting enzyme (ACE) gene insertion/ deletion (I/D) polymorphism in increasing the susceptibility to virus C infection, progression of hepatic fibrosis and prediction of treatment response among Egyptian patients with chronic hepatitis C. Patients and Methods: This study included 90 patients with chronic hepatitis C, 68 males and 22 females. Their ages ranged from 21 to 59 (mean age = 42.6 years). All patients received antiviral therapy in the form of interferon. Patients were grouped according to the stage of liver fibrosis by biopsy into: goupl (fibrosis: 0 or 1); group2 (fibrosis: 2 or 3) and group 3 (fibrosis from 4 to 6). The study included also 170 healthy subjects, age and sex matched as a control group. Polymerase chain reaction was carried out to detect the different ACE genotypes in all subjects. Results: DID genotype was significantly more prevalent among HCV patients compared to controls (65.6% vs 48.2%, p=0.006). Degree of necrointlammation was significantly higher among patients with III genotype when compared to patients with DID genotype (p=0.04). No significant difference in the distribution of the DID and 1/1 genotypes between the fibrosis groups and between responders and non-responders to interferon therapy. Conclusion: The DID genotype may increase the susceptibility to infection with hepatitis C however, the ACE gene I/D polymorphism has no influence on hepatic fibrosis and patients response to interferon treatment.