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Regulation of 1,25 (OH)2D synthesis in hypoparathyroidism and pseudohypoparathyroidism

Regulation of 1,25 (OH)2D synthesis in hypoparathyroidism and pseudohypoparathyroidism 1,25(OH)2D that results in the characteristic hypocalcemia and hyperphosphatemia of hypoparathyroidism. Several reports have indicated that the circulating concentration of 1,25(OH)zD is reduced (11, 19). However, the mechanism for the deficiency of 1,25(OH)zD in the various. forms of hypoparathyroidism remains unclear and requires further elucidation. Thus one may hypothesize that in PTH-deficient hypoparathyroidism (postsurgical or idiopathic), decreased of 1,25(OH)zD may be explained by the absence of two recognized stimuli for the renal lahydroxylase, i.e., PTH (13, 27) and hypophosphatemia (16, 30). Provision of either one of these stimuli would then be expected to raise serum 1,25(OH)zD levels. This in turn should permit greater mobilization of calcium from bone with a rise in serum calcium, as well as an augmented intestinal calcium absorption. Pseudohypoparathyroidism (PHP) is characterized by the same biochemical derangements as hypoparathyroidism but is due to PTH resistance rather than PTH deficiency. In almost all patients with PHP, urinary adenosine 3’,5’-cyclic monophosphate (CAMP) excretion after PTH infusion is significantly reduced (7), implicating a defect in the hormone receptor adenylate cyclase complex (PHP type I). Receptors are coupled to adenylate cyclase by stimulatory guanine nucleotide-binding proteins (G, proteins), which are deficient in patients with PHP type Ia (29). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

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