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Current evidence suggests that administration of 1,25(OH)2D3 to patients with chronic renal insufficiency results in suppression of secondary hyperparathyroidism only if hypercalcemia occurs. However, since the parathyroid glands possess specific receptors for 1,25(OH)2D3 and a calcium binding protein, there is considerable interest in a possible direct effect of 1,25(OH)2D3 on parathyroid hormone (PTH) secretion independent of changes in serum calcium. Recent findings indicate substantial degradation of 1,25(OH)2D3 in the intestine, therefore, it is possible that while oral administration of the vitamin D metabolite increases intestinal calcium absorption, the delivery of 1,25(OH)2D3 to peripheral target organs may be limited. We therefore compared the effects of orally or intravenously administered 1,25(OH)2D3 on the plasma levels of 1,25(OH)2D3 and the effects of these two modes of treatment on PTH secretion. Whereas oral administration of 1,25(OH)2D3 in doses adequate to maintain serum calcium at the upper limits of normal did not alter PTH levels, a marked suppression (70.1 +/- 3.2%) of PTH levels was seen in all 20 patients given intravenous 1,25(OH)2D3. Temporal studies suggested a 20.1 +/- 5.2% decrease in PTH without a significant change in serum calcium with intravenous 1,25(OH)2D3. In five patients the serum calcium was increased by the oral administration of calcium carbonate, the decrement in serum i-PTH was only 25 +/- 6.65% when compared with 73.5 +/- 5.08% (P less than 0.001) obtained by the administration of intravenous 1,25(OH)2D3. Thus, a similar serum calcium achieved by intravenous 1,25(OH)2D3 rather than calcium carbonate has a greater suppressive effect in the release of PTH. These studies indicate that 1,25(OH)2D3 administered intravenously rather than orally may result in a greater delivery of the vitamin D metabolite to peripheral target tissues other than the intestine and allow a greater expression of biological effects of 1,25(OH)2D3 in peripheral tissues. The use of intravenous 1,25(OH)2D3 thus provides a simple and extremely effective way to suppress secondary hyperparathyroidism in dialysis patients.
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J Thielan, and
R Horst, and
H Harter, and
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January 1989,
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K J Martin
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E Slatopolsky, and
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May 1996,
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E Slatopolsky, and
C Weerts, and
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R Horst, and
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September 1993,
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E Slatopolsky, and
C Weerts, and
J Thielan, and
R Horst, and
H Harter, and
K J Martin
August 1986,
Scandinavian journal of immunology,
E Slatopolsky, and
C Weerts, and
J Thielan, and
R Horst, and
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K J Martin
June 2020,
Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia,
E Slatopolsky, and
C Weerts, and
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R Horst, and
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K J Martin
September 1981,
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E Slatopolsky, and
C Weerts, and
J Thielan, and
R Horst, and
H Harter, and
K J Martin
May 1984,
Acta paediatrica Scandinavica,
E Slatopolsky, and
C Weerts, and
J Thielan, and
R Horst, and
H Harter, and
K J Martin
January 2002,
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association,
E Slatopolsky, and
C Weerts, and
J Thielan, and
R Horst, and
H Harter, and
K J Martin
January 1989,
Anales de la Real Academia Nacional de Medicina,
