ngiotensin Converting Enzyme I/D Polymorphism and Chronic Hepatitis C Virus Infection
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- Category: Vol. 77, June 2009
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Angiotensin Converting Enzyme I/D Polymorphism and Chronic Hepatitis C Virus Infection, KHALDA S. AMR, WAFAA M. EZZAT, YASSER A. EL-HOSSARY, NOUR A. ABDULLA, HASSAN E. EL-BATAE and HALA M. RASLAN
Abstract
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 develop-ment.
Aim of the Work: This study aimed at investigating the role of angiotensin-converting enzyme (ACE) gene inser-tion/deletion (I/D) polymorphism in increasing the suscepti-bility 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: goup1 (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: D/D genotype was significantly more prevalent among HCV patients compared to controls (65.6% vs 48.2%, p=0.006). Degree of necroinflammation was significantly higher among patients with I/I genotype when compared to patients with D/D genotype (p=0.04). No significant difference in the distribution of the D/D and I/I genotypes between the fibrosis groups and between responders and non-responders to interferon therapy.
Conclusion: The D/D genotype may increase the suscep-tibility to infection with hepatitis C however, the ACE gene I/D polymorphism has no influence on hepatic fibrosis and patients' response to interferon treatment.