The metabolism of isotopically labelled
vitamin D2 and D3 has been investigated in eight patients with
primary biliary cirrhosis and in five controls. The concentration of labelled
vitamin D2 was lower than that of
vitamin D3 in serum of patients with
primary biliary cirrhosis on days 1 and 2 after
intravenous injection (P less than 0.005 and P less than 0.05, respectively) but no difference was seen in controls. Similar amounts of labelled
25-hydroxyvitamin D2 and D3 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 D2 exceeded that of
24,25-dihydroxyvitamin D3 (significant for controls on day 2, P less than 0.02) but concentrations in the two groups were not different. Concentrations of labelled
25,26-dihydroxyvitamin D3 were significantly higher than those of 25,26-dihydroxyvitamin D2 in the
primary biliary cirrhosis group at all times and in the control group on days 2 and 3. Both 25,26-dihydroxyvitamin D2 and D3 were higher in the serum of patients with
primary biliary cirrhosis than in controls (significant on day 1; P less than 0.05). Urinary excretion over days 0-3 of radioactivity from both
vitamins D2 and D3 was significantly higher in the
primary biliary cirrhosis group than in controls: 12.03 vs 1.80% for
vitamin D2 and 8.98 vs 1.76% for
vitamin D3 (P less than 0.005).
Vitamin D2-derived urinary radioactivity in
primary biliary cirrhosis correlated strongly with serum
bilirubin (P = 0.005). The metabolism of labelled
vitamin D3 was studied in seven patients with
alcoholic liver disease, three of whom showed low serum concentrations of labelled
25-hydroxyvitamin D3 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 D3 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.