抄録
1, 25-dihydroxyvitamin D production in response to two successive infusions of synthetic active 1-34 fragment of human PTH [hPTH-(1-34)] was evaluated in order to develop an understanding of the vitamin D metabolism and the rationale of vitamin D therapy in calcium disorders. Five normal controls, six hypoparathyroid patients, two patients with hypophosphatemic vitamin-Dresistant rickets, one patient with Lowe's synd. and one patient with primary Fanconi's synd. were investigated, and the following results were obtained.
All normal controls showed a significant increase in serum 1, 25 (OH) 2D [43± 3.8 (m± SEM, n=5, basal), 53±4.3 (three hours after the first PTH infusion), 65±7.7 (six hours) and 66±4.4 (nine hours) pg/ml]. All patients with PTHdeficient 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 of dibutyryl cyclic AMP. On the other hand, 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 two patients with hypophosphatemic vitamin-D-resistant rickets, one with Lowe's syndrome and the other with primary Franconi's syndrome.
We conclude that these results are important in obtaining an understanding of calcium and vitamin D metabolism in these disorders and that this PTH stimulation test is a useful method to use in evaluating renal responsiveness in 1, 25 (OH) 2D production to PTH in various calcium disorders.
