Saturday, 18 November 2017

Smileband Health issues


We tested HGV RNA in serum in addition to HBV DNA and HCV RNA to study the causative agents involved in chronic non-B, non-C hepatitis. Twenty five patients diagnosed as having chronic non-B, non-C hepatitis(negative for HBsAg and HCV-Ab), were investigated in this study. HGV RNA was detected by nested RT-PCR using primers in 5′-untranslated, NS3 and NS5 regions. Of the 25 patients, 4(16%) were positive for HGV RNA, only 1(4%) was positive for HBV DNA and none were positive for HCV RNA. Of the 4 patients with HGV RNA, 2 histologically has mild fibrosis and the remaining 2 had cirrhosis. One patient with cirrhosis also had hepatocellular carcinoma; HBV DNA was positive in this patient. All 3 patients with only the HGV infection had a mild histological grade. In conclusion, HGV infection was involved in 16% of Japanese patients with chronic non-B, non-C hepatitis. Chronic Hepatitis G seemed to exhibit mild hepatitis activity.  

Abstract

Background—The hepatitis G virus (HGV), a recently identified member of the Flaviviridae family, can cause chronic infection in man but the role of this agent in chronic liver disease is poorly understood.
Aims—To evaluate the prevalence and meaning of HGV infection in a large series of patients with chronic liver disease.
Subjects—Two hundred volunteer blood donors, 179 patients with chronic hepatitis C, 111 with chronic hepatitis B, 104 with alcoholic liver disease, 136 with hepatocellular carcinoma, and 24 with cryptogenic chronic liver disease were studied.
Methods—HGV RNA was investigated in serum samples by reverse transcription and polymerase chain reaction amplification of the 5′ non-coding region of HCV and hybridisation to a specific probe. The main features of HGV RNA seropositive and seronegative patients were compared.
Results—The prevalence of HGV infection was 3% in blood donors, 7% in chronic hepatitis C, 8% in chronic hepatitis B, 2% in alcoholic liver disease, 4% in hepatocellular carcinoma, and 8% in cryptogenic chronic liver disease. HGV infected patients tended to be younger than non-infected patients but no differences concerning sex, possible source of infection, clinical manifestations, biochemical and virological parameters, or severity of liver lesions were found.
Conclusions—The prevalence of HGV infection in chronic liver disease seems to be relatively low in our area. Infection with HGV does not seem to play a significant pathogenic role in patients with chronic liver disease related to chronic HBV or HCV infection or to increased alcohol consumption, or in those with cryptogenic chronic liver disease.

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