Objective: To assess the influence of immobilization upon vitamin D status and bone mass in chronically hospitalized, disabled, elderly patients following stroke.
Design: cross-sectional study.
Setting: Department of geriatric neurology in a Japanese hospital.
Subjects: 129 chronically hospitalized, disabled, elderly stroke patients and 28 age-matched controls.
Results: We observed a deficiency of both 1,25-dihydroxyvitamin D (1,25-[OH]2D; 24.3 pg/ml) and 25-hydroxyvitamin D concentrations (25-OHD; 11.7 ng/ml) in stroke patients compared with controls. A high serum ionized calcium (mean; 2.648 mEq/l) was an independent determinant of the Barthel index (66) and 1,25-[OH]2D. When the patients were categorized into three groups by 25-OHD level (deficient, insufficient and sufficient), there was no difference in the mean 1,25-[OH]2D levels. Parathyroid hormone levels were normal or low and did not correlate with 25-OHD. Serum bone turnover variables and bone mineral density (BMD) of the second metacarpal in patients were significantly decreased compared to control subjects. Independent determinants of BMD included Barthel index, 25-OHD and 1,25-[OH]2D.
Conclusions: 1,25-[OH]2D deficiency in immobilized stroke patients is not caused by substrate (25-OHD) deficiency but by hypercalcaemia. Immobilization-induced hypercalcaemia may inhibit parathyroid hormone secretion and thus 1,25-[OH]2D production, resulting in decreased BMD. Immobilization itself also may be responsible for decreased BMD. Exogenous 1,25-[OH]2D (calcitriol) rather than dietary vitamin D supplementation may be required in disabled elderly stroke patients who have a deficiency of 1,25-[OH]2D in order to prevent hip fractures, which frequently occur in this population.