A low aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio and low HCV load were independently associated with SVR, but core mutations were not.
A past or present GBV-C/HGV contact was statistically correlated with the duration of HD and hepatitis C virus (HCV) infection, but was independent of age, hepatitis B virus (HBV) infection, and alanine aminotransferase (ALT) level.
A positive correlation between H2O2 production by PMA-stimulated cells and serum levels of alanine aminotransferase and aspartate aminotransferase was found in the HCV-infected patients (r = 0.877, P <0.01 and r = 0.9351, P <0.001, respectively).
A prospective follow-up study on HCV infection was conducted in 3 HD units from April 1990 to June 2001 to study clinical outcomes after acute hepatitis C. A total of 781 patients were tested monthly for alanine aminotransferase and anti-HCV in serum.
A significant association between the combined presence of HCV and MTHFR C677T polymorphism and grades 2-4 hepatotoxicity as alanine aminotransferase (ALT), AST, and alkaline phosphatase (ALP) elevation was observed (P values <0.001, 0.02, and 0.001, respectively).
A significantly high HHV-8 seroprevalence is already present in patients with chronic hepatitis before the development of cirrhosis, particularly in patients with HCV infection and/or higher plasma ALT levels.
A sustained response was defined as either negative hepatitis C virus (HCV) RNA by polymerase chain reaction and/or normal alanine aminotransferase (ALT) level (only in those treated before availability of HCV RNA testing) 6 months following completion of therapy.
A threshold HCV RNA level of 400,000 IU/mL is optimal for differentiating high and low probability of SVR in genotype 1-infected individuals with elevated ALT.
A total of 103 liver biopsy-proven chronic HCV patients with genotype 3, having alanine aminotransferase levels >1.2 x ULN and positive HCV-RNA were randomized into two groups: group I (n = 76; age, 43.1 +/- 11.4 years; male/female, 67/9) received peg-IFN 1.0 mug/kg/week + ribavirin 10.6 mg/kg/day, while group II (n = 27; age, 37.3 +/- 11.6 years; male/female, 21/6) received peg-IFN 1.5 microg/kg/week + ribavirin 10.6 mg/kg/day.
A total of 23 subjects with chronically raised alanine transaminase and a liver biopsy in whom all known causes of liver disease had been excluded, and 40 subjects with hepatitis C virus-related chronic liver disease.
A trend for the SEN V--positive group to have a greater mean ALT level (82 v 41 U/L; P =.067) was attributable to the subgroup with HCV recurrence because there was no difference in mean ALT levels (34.9 v 34.5 U/L; P =.968) in non--HCV-infected transplant recipients.
Additional, but statistically non-significant, univariate predictors of response were lower serum HCV-RNA (P = 0.07) and higher alanine aminotransferase levels (P = 0.055) at baseline.
Administration of the mitochondria-targeted anti-oxidant mitoquinone significantly decreased plasma ALT and aspartate aminotransferase in patients with chronic HCV infection, and this suggests that mitoquinone may decrease necroinflammation in the liver in these patients.
Advanced hepatic fibrosis and steatosis are associated with persistent alanine aminotransferase elevation in chronic hepatitis C patients negative forhepatitis C virus RNA during pegylated interferon plus ribavirin therapy.
AHCV was diagnosed by acute serum alanine aminotransferase elevation with anti-hepatitis C virus (HCV) seroconversion, HCV-RNA fluctuations above 1 log, and/or recent high-risk exposure without prior HCV infection, excluding those with human immunodeficiency virus infection.
All participants were typed for HLA class II antigens (DR and DQ) using National Institutes of Health recommended microlymphocytotoxicity test and were followed up by means of alanine aminotransferase and HCV testing for at least 1 year.