Abnormal bone and calcium metabolism in patients after stroke

To review how mineral stores and endocrine factors affect bone mass in poststroke patients immobilized by hemiparesis.

Computer databases and published indexes.

Case-control studies of hemiparetic poststroke patients examined regarding bone metabolism.

References were obtained from MEDLINE; all data concerning the objective were used.

Bone loss occurs in affected extremities after stroke. Immobilization from hemiplegia causes hypercalcemia. Insufficiency or deficiency of 25-hydroxyvitamin D (25-OHD) is very common in stroke patients and may be caused by poor dietary intake, decreased sunlight exposure, or both. Compensatory hyperparathyroidism may not occur because hypercalcemia inhibits the parathyroid glands even when 25-OHD is in the insufficient range. However, hyperparathyroidism does occur when 25-OHD is in the deficient range, in which case the parathyroid response to hypovitaminosis D overrides effects of hypercalcemia. Increased bone resorption was observed during the first year after stroke, declining to normal during the second year. During the first year, determinants of bone mineral density (BMD) in hands affected by hemiplegia were age, severity of hemiplegia, duration of paralysis, serum calcium concentration, and 25-OHD concentration. In the second year, BMD determinants on the hemiplegic side were severity of hemiplegia and 25-OHD concentration, whereas 25-OHD concentration was the only BMD determinant on the intact side. Administering 1alpha-hydroxyvitamin D3, vitamin K2, or ipriflavone ameliorated osteopenia on both sides and decreased the frequency of hip fracture on the hemiplegic side.

Bone remodeling and determinants of bone mass for the affected and unaffected sides after stroke differ between the first and subsequent years.