title: Possible role of angiotensin-converting enzyme polymorphism on progression of hepatic fibrosis in chronic hepatitis C virus infection.
abstract: Many functional polymorphisms in the rennin-angiotensin system (RAS) have been described; these polymorphisms have been postulated to contribute to fibrosis in several diseases. Our aim was to study the frequency of ACE I/D polymorphism in chronic hepatitis C virus (HCV) infection and its association with liver fibrosis and response to treatment. This study included 90 patients with chronic hepatitis C. All patients received antiviral therapy in the form of pegylated interferon and ribavirin. Patients were grouped according to the stage of liver fibrosis by biopsy into: group 1 (fibrosis: 0 or 1); group 2 (fibrosis: 2 or 3) and group 3 (fibrosis: 4 or 5). The study included also 170 healthy subjects, as a control group. Polymerase chain reaction was carried out to detect the different ACE genotypes. The 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 ACE I/D genotypes between the fibrosis groups and between responders and non responders to interferon therapy. The D/D genotype may increase the susceptibility to infection with hepatitis C.
authors.affiliation: Internal Medicine Department, National Research Centre, Elbohoos Street, Dokki, Giza, Egypt.
authors.forename: Hala M
authors.initials: HM
authors.lastname: Raslan
authors.forename: Khalda S
authors.initials: KS
authors.lastname: Amr
authors.forename: Yasser A
authors.initials: YA
authors.lastname: Elhosary
authors.forename: Wafaa M
authors.initials: WM
authors.lastname: Ezzat
authors.forename: Nour A
authors.initials: NA
authors.lastname: Abdullah
authors.forename: Hassan E
authors.initials: HE
authors.lastname: El-Batae
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000201:enzymology*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D008103:Liver Cirrhosis / Q000201:enzymology* / Q000473:pathology; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011092:Polyethylene Glycols / Q000627:therapeutic use; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; D007703:Peptidyl-Dipeptidase A; C100416:peginterferon alfa-2a