Effect of Parathyroid Hormone on 1,25-Dihydroxyvitamin D Formation in Type I Pseudohypoparathyroidism*
Lage Aksnes, Dagfinn Aarskog, E. Bravo
Abstract
Lage Aksnes, Dagfinn Aarskog, E. Bravo
Abstract
The role of parathyroid hormone (PTH) and cAMP in the hydroxylation of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D [1,25-(OH)2D] was explored in two young male volunteers and a patient with pseudohypoparathyroidism type I. Parathyroid extract infusion resulted in a prompt and distinct increase in the plasma levels of cAMP and the urinary excretion of the nucleotide in the normal controls, whereas there was only a negligible increase in the patient. In both the patient and the control subjects, the serum concentration of 1,25-(OH)2D showed a distinct increase after the parathyroid extract infusion. The responses were similar in magnitude and were apparent after 2 h, with a further rise 4 h in the patient and one of the controls, whereas the other control subject only responded after 4 h. The findings are consistent with the assumption that a normal renal cAMP response to PTH is not essential for the PTH stimulation of the renal 25-hydroxyvitamin D-1 alpha-hydroxylase. The two other dihydroxymetabolites of vitamin D, 24,25-(OH)2D and 25,26-(OH)2D, showed no consistent response to the PTH infusion in either the controls or the patient.
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The role of parathyroid hormone (PTH) and cAMP in the hydroxylation of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D [1,25-(OH)2D] was explored in two young male volunteers and a patient with pseudohypoparathyroidism type I. Parathyroid extract infusion resulted in a prompt and distinct increase in the plasma levels of cAMP and the urinary excretion of the nucleotide in the normal controls, whereas there was only a negligible increase in the patient. In both the patient and the control subjects, the serum concentration of 1,25-(OH)2D showed a distinct increase after the parathyroid extract infusion. The responses were similar in magnitude and were apparent after 2 h, with a further rise 4 h in the patient and one of the controls, whereas the other control subject only responded after 4 h. The findings are consistent with the assumption that a normal renal cAMP response to PTH is not essential for the PTH stimulation of the renal 25-hydroxyvitamin D-1 alpha-hydroxylase. The two other dihydroxymetabolites of vitamin D, 24,25-(OH)2D and 25,26-(OH)2D, showed no consistent response to the PTH infusion in either the controls or the patient.
Key concepts: Pseudohypoparathyroidism, Endocrinology, Internal medicine, Parathyroid hormone, Vitamin D and neurology, Hormone, Stimulation, Medicine