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Neuromuscular Disease in Secondary Hyperparathyroidism

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Grant support: in part by a grant from The Muscular Dystrophy Associations of America.

▸Requests for reprints should be addressed to Dr. L. E. Mallette, Bldg. 10, Rm. 9D20, National Institutes of Health, Bethesda, MD 20014.

Bethesda, Maryland

Ann Intern Med. 1975;82(4):474-483. doi:10.7326/0003-4819-82-4-474
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Neuromuscular function was evaluated in six patients with osteomalacia or secondary hyperparathyroidism, or both, as demonstrated by bone biopsy showing osteomalacia or increased immunoreactive parathyroid hormone, or both. Each patient had weakness, atrophy, and fatigability of proximal muscles, especially of the lower extremities. Most also showed involuntary fine movements of the tongue, hyperactive tendon reflexes with abnormal spread, and decreased vibration sensation, abnormalities similar to those observed in primary hyperparathyroidism. Every patient studied had evidence of neuropathic muscle disease, either on electromyography or muscle biopsy studied histochemically or both. Muscle biopsies showed no definite myopathic features. Treatment of the osteomalacia improved muscle strength. Patients with osteomalacia therefore have a treatable neuromuscular disease that is neuropathic in nature and resembles closely that found in primary hyperparathyroidism.





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