Determination of plasma alpha-glutathione S-transferases in patients with HCV-related chronic infection: its significance and possible clinical relevance
ABSTRACT— Aims/Background: Alpha‐glutathione S‐transferases (α‐GST) are the cytoplasmatic class of enzymes responsible for cellular detoxifying processes. We evaluated the plasma α‐GST activity in relation to chronic infection caused by hepatitis C virus (HCV). Methods: Eighteen anti‐HCV‐negative he...
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Veröffentlicht in: | Liver (Copenhagen) 1998-06, Vol.18 (3), p.166-172 |
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Sprache: | eng |
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Zusammenfassung: | ABSTRACT— Aims/Background: Alpha‐glutathione S‐transferases (α‐GST) are the cytoplasmatic class of enzymes responsible for cellular detoxifying processes. We evaluated the plasma α‐GST activity in relation to chronic infection caused by hepatitis C virus (HCV). Methods: Eighteen anti‐HCV‐negative healthy subjects (controls), 32 anti‐HCV‐positive subjects with a constant normality of alanine aminotransferases (ALT) and gamma‐glutamyl transpeptidase (γ‐GT) levels (“apparently healthy carriers”), and 85 patients with HCV‐related chronic liver disease (40 chronic hepatitis, 27 cirrhosis, and 18 with hepatocellular carcinoma) were studied. We assayed plasma α‐GST in all subjects upon their entry into the study; and every 6 months for 3 years in the control group and in anti‐HCV apparently healthy carriers. Results: Alpha‐GST values were significantly higher than normal values in 57% of the 21 HCV‐RNA‐positive apparently healthy carriers and in none of 11 persistently HCV‐RNA‐negative subjects; the highest increment of α‐GST was documented in patients with chronic hepatitis. We did not observe correlation among HCV‐RNA, histological activity, γ‐GT and ALT or α‐GST values. Conclusions: Therefore, the increment of plasma α‐GST indicates a liver involvement even when ALT levels are normal. This may be clinically relevant to “apparently healthy carriers” whose plasma α‐GST values, when increased, might need further evaluation. |
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ISSN: | 0106-9543 1600-0676 |
DOI: | 10.1111/j.1600-0676.1998.tb00145.x |