BERNARD M. PATTEN, M.D.; JOHN P. BILEZIKIAN, M.D.; L. E. MALLETTE, M.D., Ph.D.; ALAN PRINCE, M.D.; W. KING ENGEL, M.D.; G. D. AURBACH, M.D.
PATTEN BM, BILEZIKIAN JP, MALLETTE LE, PRINCE A, ENGEL WK, AURBACH GD. Neuromuscular Disease in Primary Hyperparathyroidism. Ann Intern Med. 1974;80:182-193. doi: 10.7326/0003-4819-80-2-182
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Published: Ann Intern Med. 1974;80(2):182-193.
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.
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Endocrine and Metabolism, Neurology, Parathyroid Disorders.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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