In a study of 56 alcoholics with liver cirrhosis, 18 (32%) had decreased bone density and low levels of serum 25-hydroxyvitamin D (25-OH-D) (<20 ng per ml). To compare the efficacy of vitamin Da and 25-OH-D treatment in correcting the metabolic bone disease in alcoholic cirrhosis, the 18 patients were randomized in the following manner, in groups of six patients each: Group 1, control (received no supplemental vitamin D treatment); Group 2, given vitamin Df! (50,000 IU p.0.) two to three times weekly, and Group 3, treated with 25-OH-D (20 to 50 mg p.0.) daily as required to attain normal serum 25-OH-D levels. The study period lasted 6 to 12 months (mean, 10.7 months). Initial histomorphometric study of transiliac bone biopsy with double tetracycline labeling in nine patients in whom biopsy was feasible showed only osteoporosis without evidence of osteomalacia. By the end of the study, serum 25-OH-D levels in the control group (Group 1) raised slightly while showing marked improvement in Groups 2 and 3. Bone density results remained unchanged in control patients but demonstrated a significant increase in both treatment groups. Vitamin D2 and 25-OH-D were equally effective in increasing bone density measurements. Posttreatment biopsies were performed in three patients of Group 2 and two patients of Group 3. While the histomorphometric results in Group 3 were not conclusive, in Group 2 improvement in static measures of bone remodeling was noted. Osteoporosis is the usual form of bone disease in alcoholic cirrhosis and a response to either vitamin Da or 25-OH-D treatment is suggested.
It has been shown that there is a higher prevalence of metabolic bone disease among alcoholic patients (1-3), especially in those with liver disease as compared to age matched controls (4-8). Similar findings have been reported in other forms of chronic liver disease such as primary biliary cirrhosis (9-16). In patients with alcoholic cirrhosis, osteoporosis is the predominant form of bone disease and it is usually associated with decreased levels of serum 25-hydroxyvitamin D (25-OH-D) (8,(17)(18)(19). Until a few years ago, defective hydroxylation of vitamin D in the liver was considered to be a possible cause of bone abnormalities in patients with cirrhosis