Plasma 25-hydroxyvitamin D concentrations and bone histomorphometry were investigated in 24 grossly obese subjects. The mean plasma 25OHD concentration was significantly lower in the obese group than in age-matched, healthy controls. Subnormal values were found in four obese subjects and in a further two subjects, who were investigated at the end of the summer, plasma 25-hydroxyvitamin D levels were at the lower end of the normal winter range. Bone histology was abnormal in two patients. In one, mild osteomalacia and secondary hyperparathyroidism were present while in the other patient the appearance suggested increased bone turnover, possibly as a result of healing osteomalacia. We conclude that gross obesity is associated with an increased risk of vitamin D deficiency, probably because of reduced exposure to uv radiation. Histological evidence of metabolic bone disease may also occur. Preoperative vitamin D deficiency may contribute in some patients to the development of metabolic bone disease after intestinal bypass.

SUMMARY Biliary radioactivity excretion was studied in 10 patients with postcholecystectomy T-tube drainage after intravenous administration of 3H-1,25-dihydroxyvitamin D3. The mean±SD radioactivity excreted in T-tube bile expressed as a percentage of the administered dose was 18.9±10*7% per 24 hours. After correction for incomplete bile collection the value obtained was 28-8±12-8%. The mean chloroform solubility of the biliary radioactivity increased from 17-0±8-4% to 69.4±15*1% after incubation with jI-glucuronidase. High performance liquid chromatography of chloroform extracts of bile revealed that most of the eluted radioactivity was more polar than 1,25(OH)2D3. The percentage radioactivity eluting as 3H-1,25(OH)2D3increased from approximately 2X4±+19 to 16-2±8*0 after incubation with P-glucuronidase. We conclude that significant amounts of intravenously administered 3H-1,25(OH)2D3 are excreted in bile, mostly as more polar metabolites. The increase in free 3H-1,25(OH)2D3 after incubation with ,3-glucuronidase indicates that glucuronides of 1,25(OH)2D3 are present in bile.It is well established that vitamin D and its metabolites are excreted in bile, both in animals and in man.1-9 The biliary excretion of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is of particular interest because this metabolite is believed to be the major active form of vitamin D. It is known to undergo side chain oxidation to calcitroic acid in the liver and intestine,10 11 conversion to a 26,23-lactone in the intestine12 and 24-hydroxylation in the kidney and intestine.13 In addition, excretion of metabolites of 1,25(OH)2D3 has been demonstrated in urine, bile, and faeces.5 Weisner et a19 reported a mean biliary excretion of 15-6% of an intravenous dose of 3H-1,25-dihydroxyvitamin D3 after six hours in five normal subjects, whereas in rats, dose dependent values of between 25 and 72%/24 hours were found.6 8 These values are higher than those mostly reported for vitamin D and 250HD1 3 14-16 and suggest that biliary excretion may play a quantitatively important role in the metabolism of 11,25(OH)2D3.In this study we have measured biliary radioactivity excretion after intravenous administration of 3H-1,25(OH)2D3 in 10 patients with T-tube drainage after cholecystectomy and have examined the nature of the radioactivity by high performance

SUMMARY Faecal tritium excretion after intravenous 3H-25-hydroxyvitamin D3 administration was measured in three control subjects and in six patients with small intestinal resection or bypass. The mean daily faecal tritium excretion over four to six days ranged from 0.8-1.6% of the injected dose in the controls (mean 1.2) and 0.9-6.8% in the patients (mean 3.7). There was a significant positive correlation between stool volume and the mean daily faecal tritium excretion. No correlation was found between the faecal tritium excretion and the plasma 25-hydroxyvitamin D concentration. Between 2.5 and 19.0% of faecal radioactivity eluted as 'H-25-hydroxyvitamin D3 on silicic acid chromatography. We conclude that faecal loss of endogenous 25-hydroxyvitamin D may be increased after small intestinal resection or bypass. Although the amount lost by this route is relatively small, it may contribute to the development of vitamin D deficiency in patients with malabsorption when endogenous vitamin D, synthesis is also reduced.Low plasma 25-hydroxyvitamin D (250HD) concentrations, indicating vitamin D deficiency, are common in patients with small intestinal disease, resection or bypass'-5 and histological evidence ofosteomalacia may also occur.`4 The pathogenesis of vitamin D deficiency and osteomalacia in these patients is not fully understood. As endogenous vitamin D3 synthesis is normally the major source of vitamin D in man,67 a poor dietary intake or malabsorption of dietary vitamin D cannot explain vitamin D deficiency provided that exposure to ultraviolet irradiation is adequate.Evidence that 250HD may undergo enterohepatic circulation in man8 has led to the suggestion that malabsorption of the metabolite from an enterohepaticcirculation could account for loss of both endogenously and exogenously derived vitamin D in patients with small intestinal disease. Arnaud et al.9 reported that the plasma half-life of intravenously administered 3H-250HD, was reduced in four patients with coeliac dis-

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