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Comparison between 1alpha(OH)D3 and 1,25(OH)2D3 on the suppression of plasma PTH levels in uremic patients, evaluated by the 'whole' and 'intact' PTH assays.
Nephron Clin Pract. 2005; 99(4):c128-37.NC

Abstract

BACKGROUND/AIMS

The aim was to evaluate the acute effects of intravenous 1alpha(OH)D3 and 1,25(OH)2D3 on (1) plasma parathyroid hormone (PTH) and Ca2+ levels in chronic uremic patients and (2) circulating large C-terminal PTH fragments as measured by the 'whole PTH' assay compared to two different 'intact PTH' assays.

METHODS

11 patients on chronic hemodialysis with plasma intact PTH >90 pg/ml were studied. At time zero 10 microg 1,25(OH)2D3 (Calcijex, Abbott, USA), or 10 microg 1alpha(OH)D3 (Etalpha, LEO, Denmark) or 10 ml of isotonic saline was injected as a bolus. Blood samples for analyses of plasma Ca2+ and plasma PTH were drawn at 0, 6, 12, 24, 48 and 72 h. The same patient was studied 3 times in a random fashion with an interval of 3 weeks. Further, 7 of the patients were studied after an injection of 6 microg 1,25(OH)2D3 intravenously.

RESULTS

No significant changes in plasma Ca2+ and PTH were seen after administration of saline. Twenty-four hours after administration of 1,25(OH)2D3, plasma PTH decreased from a maximum level of PTHWHOLE 151 +/- 27 to a minimum of 58 +/- 13 pg/ml; from a maximum level of PTHTOTAL 247 +/- 40 to a minimum of 99 +/- 26 pg/ml and from a maximum level of PTHINTACT 205 +/- 29 to a minimum of 83 +/- 18 pg/ml (p < 0.001). Twenty-four hours after administration of 1alpha(OH)D3, plasma PTH levels decreased from a maximum level of PTHWHOLE 155 +/- 21 to a minimum of 116 +/- 15 pg/ml; from a maximum level of PTHTOTAL 265 +/- 33 to a minimum of 221 +/- 35 pg/ml and from a maximum level of PTHINTACT 222 +/- 26 to a minimum of 182 +/- 23 pg/ml (p < 0.05). Regardless of which of the three assays that was applied, the percentage suppression of PTH following administration of 1,25(OH)2D3 was approximately 60% and following administration of 1alpha(OH)D3 approximately 20%. Significant correlations were demonstrated between the Whole and the intact PTH assays, and as expected between the 2 intact assays ('Whole'/'Intact', r = 0.92, p < 0.0001, 'Whole'/'Total', r = 0.94, p < 0.0001, 'Intact'/'Total', r = 0.97, p < 0.0001) with no influence of the two vitamin D analogs administered. Plasma Ca2+ remained stable after administration of saline. After 24 h, no increase in plasma Ca2+ was observed after administration of 1alpha(OH)D3 or after administration of 6 microg 1,25(OH)2D3, while plasma Ca2+ after administration of 10 microg 1,25(OH)2D3 increased to 1.31 +/- 0.03 mmol/l (p < 0.008). After 72 h, 1alpha(OH)D3 increased plasma Ca2+ to 1.22 +/- 0.02 mmol/l (p < 0.05) and 10 microg 1,25(OH)2D3 to 1.27 +/- 0.03 mmol/l. Plasma phosphate was within the normal range before administration of saline (1.24 +/- 0.13 mmol/l), 1,25(OH)2D3 (1.28 +/- 0.12 mmol/l) and 1alpha(OH)D3 (1.46 +/- 0.21 mmol/l). Plasma phosphate increased significantly after 24, 48 and 72 h to a maximum of 2.06 +/- 0.27 mmol/l after administration of 1,25(OH)2D3 and a maximum of 1.94 +/- 0.31 mmol/l after administration of 1alpha(OH)D3. Plasma phosphate was significantly higher after 1,25(OH)2D3 than after 1alpha(OH)D3 at 48 (p = 0.016) and 72 h (p < 0.010).

CONCLUSION

A single intravenous dose of both 10 microg 1,25(OH)2D3 and 1alpha(OH)D3 significantly suppressed plasma PTH. The acute suppressive effect of 1,25(OH)2D3 was 3 times greater than that of 1alpha(OH)D3. The increase in plasma Ca2+ after intravenous administration of 10 microg of 1,25(OH)2D3 was, however, significantly greater than that of 10 microg of 1alpha(OH)D3 (p < 0.005). The PTH response to acute administration of 10 microg of the two vitamin D analogs was in principle the same, when measured by the three different assays and resulted in a parallel shift of the PTH response curves. Thus, circulating levels of large C-terminal PTH fragments were not influenced by differences in plasma Ca2+ or by the vitamin D analog given.

Authors+Show Affiliations

Nephrological Department P, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. Lisbet.Brandi@dadlnet.dkNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15722644

Citation

Brandi, Lisbet, et al. "Comparison Between 1alpha(OH)D3 and 1,25(OH)2D3 On the Suppression of Plasma PTH Levels in Uremic Patients, Evaluated By the 'whole' and 'intact' PTH Assays." Nephron. Clinical Practice, vol. 99, no. 4, 2005, pp. c128-37.
Brandi L, Egfjord M, Olgaard K. Comparison between 1alpha(OH)D3 and 1,25(OH)2D3 on the suppression of plasma PTH levels in uremic patients, evaluated by the 'whole' and 'intact' PTH assays. Nephron Clin Pract. 2005;99(4):c128-37.
Brandi, L., Egfjord, M., & Olgaard, K. (2005). Comparison between 1alpha(OH)D3 and 1,25(OH)2D3 on the suppression of plasma PTH levels in uremic patients, evaluated by the 'whole' and 'intact' PTH assays. Nephron. Clinical Practice, 99(4), c128-37.
Brandi L, Egfjord M, Olgaard K. Comparison Between 1alpha(OH)D3 and 1,25(OH)2D3 On the Suppression of Plasma PTH Levels in Uremic Patients, Evaluated By the 'whole' and 'intact' PTH Assays. Nephron Clin Pract. 2005;99(4):c128-37. PubMed PMID: 15722644.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Comparison between 1alpha(OH)D3 and 1,25(OH)2D3 on the suppression of plasma PTH levels in uremic patients, evaluated by the 'whole' and 'intact' PTH assays. AU - Brandi,Lisbet, AU - Egfjord,Martin, AU - Olgaard,Klaus, Y1 - 2005/02/17/ PY - 2004/04/06/received PY - 2004/12/08/accepted PY - 2005/2/22/pubmed PY - 2006/6/15/medline PY - 2005/2/22/entrez SP - c128 EP - 37 JF - Nephron. Clinical practice JO - Nephron Clin Pract VL - 99 IS - 4 N2 - BACKGROUND/AIMS: The aim was to evaluate the acute effects of intravenous 1alpha(OH)D3 and 1,25(OH)2D3 on (1) plasma parathyroid hormone (PTH) and Ca2+ levels in chronic uremic patients and (2) circulating large C-terminal PTH fragments as measured by the 'whole PTH' assay compared to two different 'intact PTH' assays. METHODS: 11 patients on chronic hemodialysis with plasma intact PTH >90 pg/ml were studied. At time zero 10 microg 1,25(OH)2D3 (Calcijex, Abbott, USA), or 10 microg 1alpha(OH)D3 (Etalpha, LEO, Denmark) or 10 ml of isotonic saline was injected as a bolus. Blood samples for analyses of plasma Ca2+ and plasma PTH were drawn at 0, 6, 12, 24, 48 and 72 h. The same patient was studied 3 times in a random fashion with an interval of 3 weeks. Further, 7 of the patients were studied after an injection of 6 microg 1,25(OH)2D3 intravenously. RESULTS: No significant changes in plasma Ca2+ and PTH were seen after administration of saline. Twenty-four hours after administration of 1,25(OH)2D3, plasma PTH decreased from a maximum level of PTHWHOLE 151 +/- 27 to a minimum of 58 +/- 13 pg/ml; from a maximum level of PTHTOTAL 247 +/- 40 to a minimum of 99 +/- 26 pg/ml and from a maximum level of PTHINTACT 205 +/- 29 to a minimum of 83 +/- 18 pg/ml (p < 0.001). Twenty-four hours after administration of 1alpha(OH)D3, plasma PTH levels decreased from a maximum level of PTHWHOLE 155 +/- 21 to a minimum of 116 +/- 15 pg/ml; from a maximum level of PTHTOTAL 265 +/- 33 to a minimum of 221 +/- 35 pg/ml and from a maximum level of PTHINTACT 222 +/- 26 to a minimum of 182 +/- 23 pg/ml (p < 0.05). Regardless of which of the three assays that was applied, the percentage suppression of PTH following administration of 1,25(OH)2D3 was approximately 60% and following administration of 1alpha(OH)D3 approximately 20%. Significant correlations were demonstrated between the Whole and the intact PTH assays, and as expected between the 2 intact assays ('Whole'/'Intact', r = 0.92, p < 0.0001, 'Whole'/'Total', r = 0.94, p < 0.0001, 'Intact'/'Total', r = 0.97, p < 0.0001) with no influence of the two vitamin D analogs administered. Plasma Ca2+ remained stable after administration of saline. After 24 h, no increase in plasma Ca2+ was observed after administration of 1alpha(OH)D3 or after administration of 6 microg 1,25(OH)2D3, while plasma Ca2+ after administration of 10 microg 1,25(OH)2D3 increased to 1.31 +/- 0.03 mmol/l (p < 0.008). After 72 h, 1alpha(OH)D3 increased plasma Ca2+ to 1.22 +/- 0.02 mmol/l (p < 0.05) and 10 microg 1,25(OH)2D3 to 1.27 +/- 0.03 mmol/l. Plasma phosphate was within the normal range before administration of saline (1.24 +/- 0.13 mmol/l), 1,25(OH)2D3 (1.28 +/- 0.12 mmol/l) and 1alpha(OH)D3 (1.46 +/- 0.21 mmol/l). Plasma phosphate increased significantly after 24, 48 and 72 h to a maximum of 2.06 +/- 0.27 mmol/l after administration of 1,25(OH)2D3 and a maximum of 1.94 +/- 0.31 mmol/l after administration of 1alpha(OH)D3. Plasma phosphate was significantly higher after 1,25(OH)2D3 than after 1alpha(OH)D3 at 48 (p = 0.016) and 72 h (p < 0.010). CONCLUSION: A single intravenous dose of both 10 microg 1,25(OH)2D3 and 1alpha(OH)D3 significantly suppressed plasma PTH. The acute suppressive effect of 1,25(OH)2D3 was 3 times greater than that of 1alpha(OH)D3. The increase in plasma Ca2+ after intravenous administration of 10 microg of 1,25(OH)2D3 was, however, significantly greater than that of 10 microg of 1alpha(OH)D3 (p < 0.005). The PTH response to acute administration of 10 microg of the two vitamin D analogs was in principle the same, when measured by the three different assays and resulted in a parallel shift of the PTH response curves. Thus, circulating levels of large C-terminal PTH fragments were not influenced by differences in plasma Ca2+ or by the vitamin D analog given. SN - 1660-2110 UR - https://www.unboundmedicine.com/medline/citation/15722644/Comparison_between_1alpha_OH_D3_and_125_OH_2D3_on_the_suppression_of_plasma_PTH_levels_in_uremic_patients_evaluated_by_the_'whole'_and_'intact'_PTH_assays_ L2 - https://www.karger.com?DOI=10.1159/000083979 DB - PRIME DP - Unbound Medicine ER -