09 September 2002
Influence of the hepatocellular damage on the clinical usefulness of biochemical markers of bone metabolism and parathormon in haemodialysed patients
Andrzej J. Jaroszyński, Andrzej Książek, Wojciech ZałuskaMed Sci Monit 2002; 8(9): CR652-656 :: ID: 13490
Abstract
Background: The present study was undertaken to determine if hepatitis C virus (HCV) and cytomegalovirus (CMV) infections, as well as biochemical indices of liver damage, can significantly influence the relationships occurring between markers of bone formation, resorption
and PTH in hemodialysis patients.
Material/Methods: 76 HD patients were tested for anti-HCV and anti-CMV antibodies. Serum intact PTH osteocalcin, total and bone isoenzyme of alkaline phosphatase, and plasma tartrate-resistant acid
phosphatase were determined as bone metabolism indices. Serum alanine aminotransferase (ALT) and gamma-glutamyl transferase (γ-GT) were measured as markers of hepatocyte function.
The patients were divided into subgroups according to serological and enzymatic status.
Results: 37 patients were anti-HCV positive, 61 were anti-CMV positive, and 35 were both anti-HCV and anti-CMV positive. 13 patients were free of viruses. Elevated ALT and γ-GT activity was
found in 26 and 15 patients respectively. Indices of bone formation, resorption and PTH values showed no significance differences in the respective subgroups. Markers of bone formation significantly correlated with one another, as well as markers of bone resorption and intact PTH in all patients. In the subgroup of patients with increased γ-GT activity, significant differences were found in the slopes of the regression lines occurring in most of the estimated correlations
in comparison with all other subgroups.
Conclusions: In renal osteodystrophy, hepatocellular damage indicated by an increase of γ-GT influences the relationship between the biochemical markers of bone metabolism and parathormon levels,
but the presence of anti-HCV and anti-CMV antibodies does not.
Keywords: Hepatitis C - metabolism
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