Enhanced purine degradation in muscles of patients with hypoparathyroidism

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Semiischemic forearm exercise tests were carried out in 14 patients with hypocalcemia (hypoparathyroidism) (n = 6), hypercalcemia (hyperparathyroidism) (n = 3), hypopotassemia (n = 3), hypothyroidism (n = 1), and drug - induced myopathy (n = 1) to investigate purine degradation in skeletal muscles. In control subjects, an increase in cubital venous ammonia was correlated with that in lactate (p<0.001). Two patients with hypoparathyroidism with elevated serum creatine kinase levels showed exaggerated ammonia and hypoxanthine responses although lactate responses were normal. The abnormal responses of ammonia and hypoxanthine were normalized 3 months after treatment with 1α-hydroxyvitamin D3. Ammonia and lactate responses in 12 other patients showed a similar correlation with that of controls. These findings suggest that excess purine degradation occurred in exercising muscles of patients with hypoparathyroidism (hypocalcemia) with elevated creatine kinase levels.
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