PEDIATRICS Vol. 53 No. 1 January 1974, pp. 100-105
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High-Dosage Intravenous Calcium Therapy for Osteoporosis and Osteomalacia in Anticonvulsant Therapy With Hypomobilization

Humberto Latorre M.D.1 and Frederic M. Kenny M.D.1

1 Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania

Approximately 25% of those receiving the anticonvulsants diphenylhydantoin and phenobarbital have low serum calcium and elevated alkaline phosphatase levels which may be secondary to hepatic hydroxylase induction and inactivation of principal vitamin D metabolites. We found hypocalcemia, hypophosphatemia, and x-ray evidence of rickets in three children undergoing such therapy. Healing occurred in two patients who were maintained on anticonvulsants during two and four months of therapy with vitamin D, calcium and phosphorus supplement. Thereafter, vitamin D alone maintained the healing. A third patient with spastic quadriplegia, immobilized from infancy, had seizures treated with diphenylhydantoin and phenobarbital. At 9 years of age she had osteoporosis, osteomalacia, and spontaneous fracture. Rickets and secondary hyperparathyroidism were characterized by hypocalcemia, hypophosphatemia, elevated alkaline phosphatase, elevated phosphate clearance and low percent tubular reabsorption of phosphorus. Intravenous calcium gluconate (270 mg of elemental calcium/24 hours; total, 15 gm) over several two- to three-week periods resulted in healing of rickets and osteoporosis without deleterious side effects. Intravenous calcium therapy probably suppresses endogenous parathormone and may stimulate thyrocalcitonin. It deserves trial use in juvenile osteoporosis when rapid correction is necessary.

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