Severity of liver disease predicts the development of glucose abnormalities in patients with chronic hepatitis B or C following achievement of sustained virological response to antiviral therapy.
A higher prevalence of glucose abnormalities has been reported in patients with hepatitis C virus (HCV) infection compared to patients with hepatitis B virus (HBV) infection. However, previous studies considered some confounding factors and ignored others, which might influence the comparative risk assessment between HBV and HCV infections. Fasting plasma glucose concentration, severity of liver disease and viral load were determined in 220 patients with HCV genotype 4 infection, and 200 patients with HBV infection. Patients completing antiviral therapy were followed-up, and the fasting plasma glucose levels were determined in patients with and without sustained virological response. The prevalence of glucose abnormalities in HCV infection (41%) was significantly higher than that in HBV infection (16%). However, when controlling the severity of liver disease and other risk factors, the prevalence of glucose abnormalities in patients with HCV infection was comparable to that in patients with HBV infection. After attaining of sustained virological response, a decrease of the median fasting plasma glucose value was observed only in chronic hepatitis C. In the group of patients with normal fasting plasma glucose levels, an association of nonsustained virological response with the development of impaired fasting glucose was only observed in chronic hepatitis C. The severity of liver disease was a common predictor of impaired fasting glucose in hepatitis B and C infections. These results indicate that high prevalence of glucose abnormalities can be associated with HBV- and HCV-related liver disease, and that clearance of HCV, but not HBV, may improve glucose metabolism.
Chehadeh
Wassim
W
Faculty of Medicine, Department of Microbiology, Kuwait University, Safat, Kuwait. wchehadeh@hsc.edu.kw
Al-Nakib
Widad
W
D000998:Antiviral Agents / Q000494:pharmacology / Q000627:therapeutic use; D001786:Blood Glucose / Q000032:analysis; D005215:Fasting; D005234:Fatty Liver / Q000188:drug therapy / Q000503:physiopathology / Q000821:virology; D005260:Female; D044882:Glucose Metabolism Disorders / Q000453:epidemiology*; D016174:Hepacivirus / Q000187:drug effects / Q000472:pathogenicity*; D006515:Hepatitis B virus / Q000187:drug effects / Q000472:pathogenicity*; D019694:Hepatitis B, Chronic / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology / Q000821:virology; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology / Q000821:virology; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012307:Risk Factors; D012720:Severity of Illness Index; D019562:Viral Load
D000998:Antiviral Agents; D001786:Blood Glucose