Neuromuscular Disease in Primary Hyperparathyroidism

Abstract

Fourteen of 16 patients with primary hyperparathyroidism studied prospectively had weakness, easy fatiguability, and atrophy of muscles—particularly of the lower extremities. Electromyograms of these patients showed short-duration, low-amplitude motor unit potentials in some patients and abnormally high amplitude, long-duration polyphasic potentials in others. Motor nerve conduction velocities and distal sensory latencies were normal. The major finding on muscle biopsy was atrophy of both type I and type II muscle fibers, with type II fibers more extensively involved. Typical myopathic features were absent. A low concentration of phosphate in about half the patients was the only cerebrospinal-fluid abnormality noted. No patient had elevated serum glutamicoxalacetic transaminase, creatinine Phosphokinase, or aldolase values. All patients from whom a parathyroid adenoma was removed were significantly better within days to a few weeks of surgery. We conclude that many patients with hyperparathyroidism have treatable neuromuscular disease that is neuropathic in origin.