ABSTRACT
THE PURPOSE: To evaluate the effect of diet on the development of hepatic osteodystrophy in patients with primary biliary cirrhosis. MATERIALS AND METHODS: In 24 women with PBC, including signs of autoimmune hepatitis (PBC/AIH)--9 persons and 19 women in the control group were analyzed the daily diet, body composition, as well as bone mineral density in the lumbar spine and femur by dual-energy X-ray adsorbtsiometrii (DEXA). THE RESULTS: In PBC incidence of osteoporosis and severe osteoporosis was 22.7% and 9.1%, respectively, and osteopenia--59.1%, with a lesion predominantly lumbar spine. Inadequate intake of calcium in patients with PBC is associated with lower density of the femur. The high protein content in the diet has a protective effect on bone mineral density, associating with the development of osteopenia.
Subject(s)
Liver Cirrhosis, Biliary/diet therapy , Osteoporosis/diet therapy , Aged , Aged, 80 and over , Bone Density , Female , Humans , Liver Cirrhosis, Biliary/complications , Liver Cirrhosis, Biliary/metabolism , Middle Aged , Osteoporosis/etiology , Osteoporosis/metabolism , Spine/metabolismABSTRACT
The common bile duct-ligated (CBDL) rat, which is widely used as a model of human cirrhosis, rapidly develops secondary biliary cirrhosis (SBC) within 4 weeks. The CBDL rat shows poor viability, however, a detailed examination of the causes of its death has not been made. In this study, we investigated the outcome of bile duct ligation in detail and attempted to extend the life span of this model by feeding the animals a diet supplemented with nutrients. Survival rate, blood chemistry, blood cell counts, plasma levels of K vitamins and liver histology were compared among CBDL rats fed a standard diet and an enriched diet. Sham-operated rats were used as a control. Six out of 18 CBDL rats fed the standard diet died within 32 days of operation. The cause of death was massive internal hemorrhage in various organs or body cavities. All CBDL rats fed the enriched diet survived more than 31 days, but the viability of CBDL rats was not significant between those fed the standard diet and the enriched diet. The degree of anemia correlated significantly with the prolongation of prothrombin time. Plasma vitamin K1 levels in CBDL rats were significantly lower than those in sham-operated rats, but vitamin K2 levels were similar. We suggest that massive hemorrhage, which was the direct cause of death, is caused by the impairment of hemostasis resulting from vitamin K deficiency. The enriched diet with vitamin K nutritional supplements seemed to contribute to the prolongation of the life span of CBDL rats.
Subject(s)
Liver Cirrhosis, Biliary/blood , Liver Cirrhosis, Biliary/etiology , Vitamin K 1/blood , Animals , Disease Models, Animal , Hemorrhage/diet therapy , Hemorrhage/etiology , Hemostasis , Ligation/adverse effects , Liver Cirrhosis, Biliary/diet therapy , Liver Cirrhosis, Biliary/mortality , Male , Rats , Rats, Sprague-Dawley , Survival Rate , Vitamin K/administration & dosage , Vitamin K 2/blood , Vitamin K Deficiency/complications , Vitamin K Deficiency/physiopathologyABSTRACT
To study the mechanism of the reduced serum selenium concentration in patients with liver damage we administered 200 micrograms (2.53 mumol) selenium daily as selenium-rich yeast to 8 patients with primary biliary cirrhosis and 8 healthy controls over 16 weeks. Initially selenium concentrations in serum were 24% lower (P less than 0.001) in patients than controls. During supplementation serum selenium levels increased in both groups but the difference between them persisted. Throughout the study whole blood selenium levels and glutathione peroxidase activities were also somewhat lower (P = NS) in patients than controls. Selenium supplementation had no effect on whole blood glutathione peroxidase activities in either group. The basal 24 h urinary excretion of selenium was similar in both groups but was increased more by supplementation in patients than controls. Selenium administration did not influence the liver function of the patients. We conclude that impaired hepatic production of selenium-containing serum compounds is the most likely explanation for the reduced serum selenium concentration in patients with primary biliary cirrhosis.
