Neuromuscular involvement in mild, asymptomatic primary hyperparathyroidism

Abstract

Purpose: The classic neuromuscular abnormalities of primary hyperparathyroidism are based on observations from an earlier time when the disease presented commonly with signs and symptoms. The purpose of the present study was to test for neuromuscular abnormalities among patients currently seen with primary hyperparathyroidism, in whom the vast majority are asymptomatic.

Patients, methods, and results: Forty-two patients (30 women, 12 men) were studied. Serum calcium level was 11.1 +/- 0.1 mg/dL (normal, 8.7 to 10.7 mg/dL); phosphorus level was 2.8 +/- 0.1 mg/dL (normal, 2.5 to 4.5 mg/dL). Parathyroid hormone levels by radioimmunoassay for N-terminal and for mid-molecule regions were 32.6 +/- 2.4 pg/mL (normal, 8 to 24 pg/mL) and 831 +/- 127 pg/mL (normal, 50 to 330 pg/mL), respectively. Although generalized weakness and easy fatigability were common complaints, they were not seen on neurologic examination. No patient showed typical neuromuscular findings such as muscle weakness or atrophy, hyperreflexia, abnormal gait, tongue fasciculations, or objective changes in mental status. On the other hand, paresthesias and muscle cramps were reported by 22 patients (52%). Neurologic examination in 12 patients (29%) demonstrated findings consisting of either stocking-glove loss of pain sensation or loss of vibratory sensation with diminished reflexes. Creatine phosphokinase levels were normal in all patients. Electromyography and nerve conduction studies were performed in nine patients. None showed myopathy or signs of motor unit denervation. Isolated nerve abnormalities (n = 6) and nonspecific sensory neuropathy (n = 2) were observed.

Conclusion: We conclude that the classic neuromuscular syndrome of primary hyperparathyroidism is rarely seen among a typical modern-day group of patients with primary hyperparathyroidism. The results suggest that the neurologic component of primary hyperparathyroidism should be included among those features of the disease that have changed along with other aspects of the clinical profile of primary hyperparathyroidism.