TY - JOUR
T1 - Selective effects of thiazide therapy on serum 1α,25-dihydroxyvitamin D and intestinal calcium absorption in renal and absorptive hypercalciurias
AU - Zerwekh, J. E.
AU - Pak, C. Y C
N1 - Funding Information:
From the Section on Mineral Metabolism, Department of Internal Medicine, the University of Texas Healih Science Center at Dallas. Southwestern Medical School, Dallas. Tex. Receivedforp ublication September 27. 1978. Supported in part by grants from the USPHS P50-AM20543. ROI-AM16061. and MOl-RR00633. Address reprint requests to Dr. J. E. Zerwekh, Section on Mineral Metabolism. Department of Internal Medicine, University of Texas Health Science Center. Southwestern Medical School, 5323 Harry Hines Blvd. Dallas. Ter. 75235. cr)1 980 b.v Grune & Stratton, Inc. 0026&049S/80/290/LO003$l.00/0
PY - 1980/1
Y1 - 1980/1
N2 - The effect of long-term thiazide therapy (hydro-chlorothiazide, 50 mg twice/day) on intestinal calcium (Ca) absorption and serum 1α,25-dihydroxy-vitamin D [1α,25-(OH)2D] concentration was examined in 10 patients with renal hypercalciuria (RH), many of whom had hyperabsorption of Ca, and in 11 cases of absorptive hypercalciuria (AH), all of whom had intestinal hyperabsorption of Ca. In patients with RH, the intestinal Ca absorption decreased significantly during thiazide therapy (mean treatment period of 15 mo) from 0.68 ± 0.09 SD to 0.56 ± 0.10 (p < 0.01), commmensurate with the "correction" of the renal leak of Ca and secondary hyperparathyroidism. Furthermone, serum 1α,25-(OH)2D decreased significantly from 5.2 ± 2.2 SD ng/dl to 3.7 ± 0.8 ng/dl (p < 0.025) during thiazide therapy. In patiens with AH, the intestinal hyperabsorption of calcium persisted during thiazide treatment 0.69 ± 0.07 versus 0.69 ± 0.06), despite restoration of normal urinary Ca. Serum 1α,25-(OH)2D was virtually unchanged during treatment (4.5 ± 1.4 ng/dl versus 4.7 ± 0.9 ng/dl). The results support the hypothesis that the intestinal hyperabsorption of Ca in RH is a result of increased serum concentration of 1α,25-(OH)2D secondary to the hyperparathyroid state, while that in AH may not be totally dependent on increased concentrations of 1α,25-(OH)2D.
AB - The effect of long-term thiazide therapy (hydro-chlorothiazide, 50 mg twice/day) on intestinal calcium (Ca) absorption and serum 1α,25-dihydroxy-vitamin D [1α,25-(OH)2D] concentration was examined in 10 patients with renal hypercalciuria (RH), many of whom had hyperabsorption of Ca, and in 11 cases of absorptive hypercalciuria (AH), all of whom had intestinal hyperabsorption of Ca. In patients with RH, the intestinal Ca absorption decreased significantly during thiazide therapy (mean treatment period of 15 mo) from 0.68 ± 0.09 SD to 0.56 ± 0.10 (p < 0.01), commmensurate with the "correction" of the renal leak of Ca and secondary hyperparathyroidism. Furthermone, serum 1α,25-(OH)2D decreased significantly from 5.2 ± 2.2 SD ng/dl to 3.7 ± 0.8 ng/dl (p < 0.025) during thiazide therapy. In patiens with AH, the intestinal hyperabsorption of calcium persisted during thiazide treatment 0.69 ± 0.07 versus 0.69 ± 0.06), despite restoration of normal urinary Ca. Serum 1α,25-(OH)2D was virtually unchanged during treatment (4.5 ± 1.4 ng/dl versus 4.7 ± 0.9 ng/dl). The results support the hypothesis that the intestinal hyperabsorption of Ca in RH is a result of increased serum concentration of 1α,25-(OH)2D secondary to the hyperparathyroid state, while that in AH may not be totally dependent on increased concentrations of 1α,25-(OH)2D.
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U2 - 10.1016/0026-0495(80)90091-8
DO - 10.1016/0026-0495(80)90091-8
M3 - Article
C2 - 7351872
AN - SCOPUS:0018917132
SN - 0026-0495
VL - 29
SP - 13
EP - 17
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 1
ER -