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Liver and Bone
Author(s) -
NAKANO ATSUSHI,
KANDA TSUTOMU,
ABE HIROKO
Publication year - 1996
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1996.tb01843.x
Subject(s) - medicine , pathogenesis , thioacetamide , endocrinology , osteomalacia , bone resorption , carbon tetrachloride , cirrhosis , osteopenia , creatinine , vitamin d and neurology , osteoporosis , pathology , bone mineral , chemistry , organic chemistry
To investigate the pathogenesis of hepatic osteodystrophy (HOD) in parenchymal liver disease, we developed a laboratory model in animals using carbon tetrachloride (CCl 4 ) and thioacetamide. Biochemical and histological parameters in the model were measured. In rats with both chronic non‐cirrhotic liver injury and CCl 4 ‐induced cirrhosis, tibial bone volume was significantly lower than in controls. In CCl 4 ‐treated cirrhotic rats, the osteoid volume decreased while the urinary calcium/creatinine ratio increased. In all CCl 4 ‐treated rats, bone volume was significantly correlated with both the serum albumin concentration and the number of goblet cells reflecting intestinal villous atrophy. The serum concentration of vitamin D metabolites was not correlated with bone volume. Whole body retention of 47 Ca was significantly lower in CCl 4 ‐treated cirrhotic rats than in controls. Furthermore, the bone volume in thioacetamide‐treated cirrhotic rats was significantly lower than in controls. 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.