Publication: Hepatitis G infection and therapeutic response to interferon in HCV-related chronic liver disease
Issued Date
1998-09-01
Resource Type
ISSN
01251562
Other identifier(s)
2-s2.0-0032149482
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Southeast Asian Journal of Tropical Medicine and Public Health. Vol.29, No.3 (1998), 480-490
Suggested Citation
Chutima Pramoolsinsap, Yong Poovorawan, Thanyachai Sura, Apiradee Theamboonlers, Nunta Busagorn, Sucha Kurathong Hepatitis G infection and therapeutic response to interferon in HCV-related chronic liver disease. Southeast Asian Journal of Tropical Medicine and Public Health. Vol.29, No.3 (1998), 480-490. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/18494
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Hepatitis G infection and therapeutic response to interferon in HCV-related chronic liver disease
Other Contributor(s)
Abstract
Circulating HGV-RNA was determined in 117 patients with HCV-related chronic liver disease and in 200 healthy blood donors. The patients, aged 50.8±13.8 years, were classified as chronic hepatitis (CH; n = 82), liver cirrhosis (n = 25) and hepatocellular carcinoma (HCC; n = 10). HGV-RNA was detected in 5 (4.3%) patients, all with CH and in 10 (5%) of blood donors The majority of all groups (52% to70%) were infected with HCV genotype II/1b, including 4/5 patients with HGV co-infection. Of 5 patients with HGV co-infection, 4 were positive for anti-HBs and anti-HBc and none exhibited jaundice. A 24-week course of interferon treatment with 12-month follow-up was achieved in 27 patients with chronic active hepatitis, including 3 with HGV co-infection. Of these, 55.6% responded to the therapy, but only 6/27 (22.2%) patients were sustained responders. The majority of sustained responders were HCV genotype III/ 2a (4/6) while genotype II/1b was found in the majority of patients with relapse (7/9) and non-responders (9/12). At the 48- month follow up, 2/6 sustained responders (one with HGV co-infection) became HCV RNA positive. These results show that the prevalence of HGV infection in HCV-related chronic liver disease is low, as in the general population, and is found in younger patients with chronic hepatitis. HGV coinfection does not interfere with clinical severity, disease progression or response to interferon in patients with HCV-related chronic liver disease. The favorable factors of interferon treatment for HCV infection are young age, low HCV-RNA levels and HCV genotype III/2a.