Bone changes and mineral metabolism disorders in rats with experimental liver cirrhosis.

@article{Nakano1996BoneCA,
  title={Bone changes and mineral metabolism disorders in rats with experimental liver cirrhosis.},
  author={Aoi Nakano and Tsutomu Kanda and Hiroko Abe},
  journal={Journal of gastroenterology and hepatology},
  year={1996},
  volume={11 12},
  pages={1143-54}
}
To investigate the pathogenesis of hepatic osteodystrophy (HOD) in parenchymal liver disease, we developed a laboratory model in animals using carbon tetrachloride (CCl4) and thioacetamide. Biochemical and histological parameters in the model were measured. In rats with both chronic non-cirrhotic liver injury and CCl4-induced cirrhosis, tibial bone volume was significantly lower than in controls. In CCl4-treated cirrhotic rats, the osteoid volume decreased while the urinary calcium/creatinine… CONTINUE READING

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These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis ( i.e. HOD ) due to a combination of low bone formation rates and high resorption rates , that HOD begins at the stage of chronic non - cirrhotic liver injury , that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy , while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD .
These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis ( i.e. HOD ) due to a combination of low bone formation rates and high resorption rates , that HOD begins at the stage of chronic non - cirrhotic liver injury , that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy , while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD .
These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis ( i.e. HOD ) due to a combination of low bone formation rates and high resorption rates , that HOD begins at the stage of chronic non - cirrhotic liver injury , that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy , while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD .
These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis ( i.e. HOD ) due to a combination of low bone formation rates and high resorption rates , that HOD begins at the stage of chronic non - cirrhotic liver injury , that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy , while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD .
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