C-terminal PTH (70-84) after biliary ligation in rats: implications for the diagnostic importance in hepatobiliary disease.
The pathogenesis of hepatic osteodystrophy is still poorly understood. To date, there is no convincing evidence for the involvement of one of the vitamin D metabolites. Recent observations provided evidence for an disturbed hepatic metabolism of intact PTH in patients with primary biliary cirrhosis and children with biliary atresia. To confirm these data experimentally, the extrahepatic bile-duct was ligated and dissected in rats. As expected GOT and AP activity increased in ligated group, calcium and mid-C-PTH remained constant for the first 44 days post-ligation. Similar to the data in the respective groups of patients, C-terminal PTH immunoreactivity increased after biliary ligation. The radioimmunological discrimination between intact PTH and the bone-seaking N-terminal PTH peptide is still impossible without further chromatographic procedures. Therefore, C-PTH may represent an important laboratory parameter for the evaluation of the hepatic metabolism of PTH which seems to be disturbed during severe longstanding cholestasis.
D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001647:Bile Acids and Salts / Q000032:analysis; D001660:Biliary Tract Diseases / Q000097:blood* / Q000150:complications; D002118:Calcium / Q000097:blood; D001651:Cholestasis, Extrahepatic / Q000378:metabolism; D004195:Disease Models, Animal; D008026:Ligation; D008107:Liver Diseases / Q000097:blood* / Q000150:complications; D010281:Parathyroid Hormone / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D051381:Rats
D001647:Bile Acids and Salts; D010281:Parathyroid Hormone; D010446:Peptide Fragments; D001219:Aspartate Aminotransferases; D000469:Alkaline Phosphatase; D002118:Calcium