Effect of Antiviral Therapy on Serum Activity of Angiotensin Converting Enzyme in Patients with Chronic Hepatitis C

Introduction: Renin-angiotenzin system (RAS) is frequently activated in patients with chronic liver disease. Angiotenzin - II (AT-II), produced by angiotenzin converting enzyme (ACE), has many physiological effects, including an important role in liver fibrogenesis. Combined antiviral therapy with PEG-IFN and ribavirin besides its antiviral effect also leads to a reduction in liver parenchyma fibrosis. Aim of the study: Determining the value of ACE in serum of patients with chronic hepatitis C before and after combined antiviral therapy, as well as the value of ACE activities in sera of the control group. Materials and methods: We studied 50 patients treated at Gastroenterohepatology Department, in the time-period of four years. Value of ACE in serum was determined by Olympus AU 400 device, with application of kit “Infinity TN ACE Liquid Stable Reagent”. HCV RNA levels in sera were measured by real time PCR. HCV RNA test was performed with modular analysis of AMPLICOR and COBAS AMPLICOR HCV MONITOR test v2.0, which has proved infection and was used for quantification of the viruses and monitoring of the patients’ response to therapy. Liver histology was evaluated in accordance with the level of necroinflammation activity and stage of fibrosis. Results: Serum activities of ACE in chronic hepatitis C patients is statistically higher than the values in the control group (p=0.02). Antiviral therapy in chronic hepatitis C patients statistically decreases serum activities of ACE (p= 0.02) and indirectly affects fibrogenesis of the liver parenchyma. Correlation between ACE and ALT activity after the therapy was proved (0.3934). Conclusion: Our findings suggest that the activity of ACE in serum is a good indirect parameter of the liver damage, and could be used as an indirect prognostic factor of the level of liver parenchyma damage. Serum activity of ACE can be used as a parameter for non-invasive assessment of intensity of liver damage.

[1]  O. Guillaud,et al.  Angiotensin blockade does not affect fibrosis progression in recurrent hepatitis C after liver transplantation. , 2013, Transplantation proceedings.

[2]  H. Yoshiji,et al.  Blockade of renin–angiotensin system in antifibrotic therapy , 2007, Journal of gastroenterology and hepatology.

[3]  M. Shiffman,et al.  Approach to the management of patients with chronic hepatitis C who failed to achieve sustained virologic response. , 2005, Clinics in liver disease.

[4]  Stefano Colagrande,et al.  Fibrosis in chronic liver diseases: diagnosis and management. , 2005, Journal of hepatology.

[5]  X. Forns,et al.  Beneficial Effect of Angiotensin-Blocking Agents on Graft Fibrosis in Hepatitis C Recurrence after Liver Transplantation , 2004, Transplantation.

[6]  J. Dixon,et al.  Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss , 2004, Hepatology.

[7]  G. Ramadori,et al.  Portal tract fibrogenesis in the liver , 2004, Laboratory Investigation.

[8]  M. Yuen,et al.  Viral hepatitis C , 2003, The Lancet.

[9]  R. Schwabe,et al.  NADPH oxidase signal transduces angiotensin II in hepatic stellate cells and is critical in hepatic fibrosis. , 2003, The Journal of clinical investigation.

[10]  H. Yamauchi,et al.  Interferon alfa down‐regulates collagen gene transcription and suppresses experimental hepatic fibrosis in mice , 2003, Hepatology.

[11]  H. Yamauchi,et al.  Interferon alfa down-regulates collagen gene transcription and suppresses experimental hepatic fibrosis in mice. , 2003 .

[12]  K. Chayama,et al.  AT1A-deficient mice show less severe progression of liver fibrosis induced by CCl(4). , 2003, Biochemical and biophysical research communications.

[13]  Teruhiko Yoshida,et al.  Adenovirus-mediated gene transfer of interferon α improves dimethylnitrosamine-induced liver cirrhosis in rat model , 2003, Gene Therapy.

[14]  D. Schuppan,et al.  Hepatitis C and liver fibrosis , 2003, Cell Death and Differentiation.

[15]  S. Sakuta,et al.  Effect of angiotensin receptor antagonist on liver fibrosis in early stages of chronic hepatitis C , 2002, Hepatology.

[16]  H. Yoshiji,et al.  Inhibition of renin-angiotensin system attenuates liver enzyme-altered preneoplastic lesions and fibrosis development in rats. , 2002, Journal of hepatology.

[17]  M. Arthur,et al.  Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C. , 2002, Gastroenterology.

[18]  N. Leung.  Management of viral hepatitis C , 2002, Journal of gastroenterology and hepatology.

[19]  H. Yoshiji,et al.  Angiotensin‐II type 1 receptor interaction is a major regulator for liver fibrosis development in rats , 2001, Hepatology.

[20]  Bernt Schiele,et al.  Smart-Its Friends: A Technique for Users to Easily Establish Connections between Smart Artefacts , 2001, UbiComp.

[21]  J. Maher.  Interactions between Hepatic Stellate Cells and the Immune System , 2001, Seminars in liver disease.

[22]  S. Friedman,et al.  Hepatic fibrosis. Pathogenesis and principles of therapy , 2001 .

[23]  D. Valla,et al.  Regression of liver fibrosis after biliary drainage in patients with chronic pancreatitis and stenosis of the common bile duct. , 2001, The New England journal of medicine.

[24]  P. Bedossa,et al.  Natural history of HCV infection. , 2000, Bailliere's best practice & research. Clinical gastroenterology.

[25]  D. Purdie,et al.  Host genetic factors influence disease progression in chronic hepatitis C , 2000, Hepatology.

[26]  B. Lončar,et al.  Activity of serum angiotensin-converting enzyme as a tumour marker of hepatocellular carcinoma. , 1999, European journal of gastroenterology & hepatology.

[27]  D. Thabut,et al.  Natural history and predictors of disease severity in chronic hepatitis C. , 2006, Journal of hepatology.