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October 1979

HypocalcemiaDifferential Diagnosis and Mechanisms

Author Affiliations

From the Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical College of Ohio, St Vincent Hospital and Medical Center, Toledo, Ohio.

Arch Intern Med. 1979;139(10):1166-1171. doi:10.1001/archinte.1979.03630470074022

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidity of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminished to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.

(Arch Intern Med 139:1166-1171, 1979)