1,25-Dihydroxyvitamin D production after stimulation with synthetic human parathyroid hormone (1-34) in hypoparathyroid and renal tubular disorders.

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Abstract
1,25-Dihydroxyvitamin D 1,25(OH)2D production in response to 2 successive infusions of synthetic active 1-34 fragment of human PTH [hPTH-(1-34)] was evaluated to develop an understanding of the vitamin D metabolism and the rationale of vitamin D therapy in Ca disorders. Five normal controls, 6 hypoparathyroid patients, 2 patients with hypophosphatemic vitamin-D-resistant rickets, 1 patient with Lowe''s synd. [syndrome] and 1 patient with primary Fanconi''s synd. were investigated. All normal controls showed a significant increase in serum 1,25(OH)2D[43 .+-. 3.8 (m .+-. standard error of the mean, n = 5, basal), 53 .+-. 4.3 (3 h after the 1st PTH infusion), 65.+-. 7.7 (6 h) and 66 .+-. 4.4 (9 h) pg/ml]. All patients with PTH-deficient hypoparathyroidism showed a significant increase in serum 1,25(OH)2D, and serum 1,25(OH)2D values were within the normal range after hPTH-(1-34) stimulation. Serum 1,25(OH)2D remained low after hPTH-(1-34) infusions in a patient with pseudohypoparathyroidism type I who showed a significant increase in this value after infusion or dibutyryl cAMP. A patient with normocalcemic pseudohypoparathyroidism type I had a high basal 1.25(OH)2D value, which increased further after hPTH-(1-34) infusions. An almost normal increase in serum 1,25(OH)2D was observed in 2 patients with hypophosphatemic vitamin-D-resistant rickets, 1 with Lowe''s synd. and the other with primary Franconi''s synd. These results are important in obtaining an understanding of C and vitamin D metabolism in these disorders and this PTH stimulation test is a useful method to use in evaluating renal responsiveness in 1,25(OH)2D production to PTH in various C disorders.