Metabolism of vitamin D in patients with primary biliary cirrhosis and alcoholic liver disease

The metabolism of isotopically labelled vitamin D 2 and D 3 has been investigated in eight patients with primary biliary cirrhosis and in five controls. The concentration of labelled vitamin D 2 was lower than that of vitamin D 3 in serum of patients with primary biliary cirrhosis on days 1 and 2 after intravenous injection (P <0.005 and P <0.05, respectively) but no difference was seen in controls. Similar amounts of labelled 25-hydroxyvitamin D 2 and D 3 were seen in serum of the control group; the same pattern was observed in the primary biliary cirrhosis group, and no significant differences were observed between the two groups. In both control and primary biliary cirrhosis groups, the serum concentration of labelled 24,25-dihydroxyvitamin D 2 exceeded that of 24,25-dihydroxyvitamin D 3 (significant for controls on day 2, P <0.02) but concentrations in the two groups were not different. Concentrations of labelled 25,26-dihydroxyvitamin D 3 were significantly higher than those of 25,26-dihydroxyvitamin D 2 in the primary biliary cirrhosis group at all times and in the control group on days 2 and 3. Both 25,26-dihydroxyvitamin D 2 and D 3 were higher in the serum of patients with primary biliary cirrhosis than in controls (significant on day 1; P <0.05). Urinary excretion over days 0-3 of radioactivity from both vitamins D 2 and D 3 was significantly higher in the primary biliary cirrhosis group than in controls: 12.03 vs 1.80% for vitamin D 2 and 8.98 vs 1.76% for vitamin D 3 (P <0.005). Vitamin D 2-derived urinary radioactivity in primary biliary cirrhosis correlated strongly with serum bilirubin (P = 0.005). The metabolism of labelled vitamin D 3 was studied in seven patients with alcoholic liver disease, three of whom showed low serum concentrations of labelled 25-hydroxyvitamin D 3 suggesting impaired hepatic synthesis. The 25-hydroxylation response was quantified as the relative index of 25-hydroxylation and was significantly related to two other indices of liver function. It is concluded that impaired 25-hydroxylation of vitamin D may occur in alcoholic liver disease and results from hepatocellular dysfunction. Less than the predicted amounts of 1,25-dihydroxyvitamin D 3 were produced in four of the seven patients with alcoholic liver disease; this defect may be attributable in part to decreased precursor 25-hydroxyvitamin D and to poor renal function.