Enhanced release of ammonia and hypoxanthine from exercising muscles in patients with idiopathic hypoparathyroidism
- 1 September 1987
- journal article
- research article
- Published by Wiley in Muscle & Nerve
- Vol. 10 (7) , 599-602
- https://doi.org/10.1002/mus.880100703
Abstract
Semiischemic forearm exercise tests were carried out in two patients with idiopathic hypoparathyroidism who had muscle cramps and high serum levels of creatine kinase. Although cubital venous lactate levels increased normally after forearm exercise, venous ammonia and hypoxanthine were greatly increased. The abnormal responses of ammonia and hypoxanthine were normalized 3 months after treatment with 1 α‐hydroxyvitamin D3. These findings suggest that excess purine degradation occurred in exercising muscles of patients with idiopathic hypoparathyroidism.This publication has 11 references indexed in Scilit:
- ATP degradation products after ischemic exerciseNeurology, 1985
- Excess purine degradation in exercising muscles of patients with glycogen storage disease types V and VII.Journal of Clinical Investigation, 1985
- Metabolic basis of improved exercise toleranceNeurology, 1984
- A comparative study on glucagon effect between mcardle disease and tarui diseaseMuscle & Nerve, 1984
- Hypoxanthine and McArdle disease: A clue to metabolic stress in the working forearmMuscle & Nerve, 1983
- Increased ammonia production during forearm ischemic work test in McArdle's diseaseJournal of Molecular Medicine, 1981
- Pseudohypoparathyroidism and hypocalcemic “myopathy”Klinische Wochenschrift, 1981
- Metabolic adaptation in phosphorylase kinase deficiency. Changes in metabolite concentrations during tetanic stimulation of mouse leg musclesBiochemical Journal, 1980
- Myoadenylate Deaminase Deficiency: A New Disease of MuscleScience, 1978
- Phosphorylase a deficiency in pseudohypoparathyroidismNeurology, 1969