Blog
About

1
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Comparison between 1α(OH)D 3 and 1,25(OH) 2D 3 on the Suppression of Plasma PTH Levels in Uremic Patients, Evaluated by the ‘Whole’ and ‘Intact’ PTH Assays

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background/Aims: The aim was to evaluate the acute effects of intravenous 1α(OH)D<sub>3</sub> and 1,25(OH)<sub>2</sub>D<sub>3</sub> on (1) plasma parathyroid hormone (PTH) and Ca<sup>2+</sup> 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 µg 1,25(OH)<sub>2</sub>D<sub>3</sub> (Calcijex, Abbott, USA), or 10 µg 1α(OH)D<sub>3</sub> (Etalpha, LEO, Denmark) or 10 ml of isotonic saline was injected as a bolus. Blood samples for analyses of plasma Ca<sup>2+</sup> 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 µg 1,25(OH)<sub>2</sub>D<sub>3</sub> intravenously. Results: No significant changes in plasma Ca<sup>2+</sup> and PTH were seen after administration of saline. Twenty-four hours after administration of 1,25(OH)<sub>2</sub>D<sub>3</sub>, plasma PTH decreased from a maximum level of PTH<sub>WHOLE</sub> 151 ± 27 to a minimum of 58 ± 13 pg/ml; from a maximum level of PTH<sub>TOTAL</sub> 247 ± 40 to a minimum of 99 ± 26 pg/ml and from a maximum level of PTH<sub>INTACT</sub> 205 ± 29 to a minimum of 83 ± 18 pg/ml (p < 0.001). Twenty-four hours after administration of 1α(OH)D<sub>3</sub>, plasma PTH levels decreased from a maximum level of PTH<sub>WHOLE</sub> 155 ± 21 to a minimum of 116 ± 15 pg/ml; from a maximum level of PTH<sub>TOTAL</sub> 265 ± 33 to a minimum of 221 ± 35 pg/ml and from a maximum level of PTH<sub>INTACT</sub> 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)<sub>2</sub>D<sub>3</sub> was approximately 60% and following administration of 1α(OH)D<sub>3</sub> 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 Ca<sup>2+</sup> remained stable after administration of saline. After 24 h, no increase in plasma Ca<sup>2+</sup> was observed after administration of 1α(OH)D<sub>3</sub> or after administration of 6 µg 1,25(OH)<sub>2</sub>D<sub>3</sub>, while plasma Ca<sup>2+</sup> after administration of 10 µg 1,25(OH)<sub>2</sub>D<sub>3</sub> increased to 1.31 ± 0.03 mmol/l (p < 0.008). After 72 h, 1α(OH)D<sub>3</sub> increased plasma Ca<sup>2+</sup> to 1.22 ± 0.02 mmol/l (p < 0.05) and 10 µg 1,25(OH)<sub>2</sub>D<sub>3</sub> 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)<sub>2</sub>D<sub>3</sub> (1.28 ± 0.12 mmol/l) and 1α(OH)D<sub>3</sub> (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)<sub>2</sub>D<sub>3</sub> and a maximum of 1.94 ± 0.31 mmol/l after administration of 1α(OH)D<sub>3</sub>. Plasma phosphate was significantly higher after 1,25(OH)<sub>2</sub>D<sub>3</sub> than after 1α(OH)D<sub>3</sub> at 48 (p = 0.016) and 72 h (p < 0.010). Conclusion: A single intravenous dose of both 10 µg 1,25(OH)<sub>2</sub>D<sub>3</sub> and 1α(OH)D<sub>3</sub> significantly suppressed plasma PTH. The acute suppressive effect of 1,25(OH)<sub>2</sub>D<sub>3</sub> was 3 times greater than that of 1α(OH)D<sub>3</sub>. The increase in plasma Ca<sup>2+</sup> after intravenous administration of 10 µg of 1,25(OH)<sub>2</sub>D<sub>3</sub> was, however, significantly greater than that of 10 µg of 1α(OH)D<sub>3</sub> (p < 0.005). The PTH response to acute administration of 10 µg 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 Ca<sup>2+</sup> or by the vitamin D analog given.

          Related collections

          Most cited references 30

          • Record: found
          • Abstract: not found
          • Article: not found

          Clinical epidemiology of cardiovascular disease in chronic renal disease.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Electron beam computed tomography in the evaluation of cardiac calcification in chronic dialysis patients.

            The purpose of this study was to assess the value of electron beam computed tomography in the detection of cardiac calcifications in coronaries and valves of dialysis patients and to determine the rate at which calcification progresses. Forty-nine chronic hemodialysis patients aged 28 to 74 years were compared with 102 non-dialysis patients aged 32 to 73 years with documented or suspected coronary artery disease, all of whom underwent coronary angiography. We used high-resolution electron beam computed tomography scanning to make 30 axial slices with a distance of 3 mm between each slice. The number of calcifications, the surface area, and the average and highest density values were measured. We calculated a quantitative coronary artery calcium score and assessed calcification of mitral and aortic valves. In dialysis patients, the measurements were repeated after 12 months. The coronary artery calcium score was from 2.5-fold to fivefold higher in the dialysis patients than in the non-dialysis patients. Hypertensive dialysis patients had higher calcium scores than non-hypertensive dialysis patients (P < 0.05). A stepwise, multiple regression analysis confirmed the importance of age and hypertension. No correlation between calcium, phosphate, or parathyroid hormone values and the coronary calcium score was identified; however, the calcium score was inversely correlated with bone mass in the dialysis patients (r = 0.47, P < 0.05). The mitral valve was calcified in 59% of dialysis patients, while the aortic valve was calcified in 55%. The coronary artery calcium score was correlated with aortic valvular, but not mitral valvular calcification. A repeat examination of the dialysis patients at an interval of 1 year showed a disturbing tendency for progression. Our data under-score the frequency and severity of coronary and valvular calcifications in dialysis patients, and illustrate the rapid progression of this calcification. Finally, they draw attention to hypertension as an important risk factor in this process.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Randomized, double-blind, placebo-controlled, dose-titration, phase III study assessing the efficacy and tolerability of lanthanum carbonate: a new phosphate binder for the treatment of hyperphosphatemia.

               Paul W. Finn,  Parijat Joy,   (2003)
              Lanthanum carbonate is a novel, non-calcium, non-aluminum phosphate binder under evaluation for the treatment of hyperphosphatemia in end-stage renal disease (ESRD) patients receiving either hemodialysis or continuous ambulatory peritoneal dialysis. This 16-week study assessed the control of serum phosphorus with lanthanum carbonate, and its effects on serum calcium, calcium x phosphorus product, and parathyroid hormone (PTH). Hemodialysis patients > or =18 years old entered into a 1- to 3-week washout period during which serum phosphorus levels rose to >5.9 mg/dL (1.90 mmol/L). In total, 126 patients were titrated with lanthanum carbonate at doses containing 375, 750, 1,500, 2,250, or 3,000 mg/d elemental lanthanum, given in divided doses with meals over a 6-week period, to achieve serum levels < or =5.9 mg/dL. By the end of dose titration, 11/126 (9%) patients received < or =750 mg/d of lanthanum, 25 (20%) received 1,500 mg/d, 37 (29%) received 2,250 mg/d, and 53 (42%) received 3,000 mg/d. Following titration, patients were randomized to receive either lanthanum carbonate or placebo during a 4-week, double-blind maintenance phase. At the study endpoint, the mean difference in serum phosphorus between the lanthanum carbonate and placebo treatment arms was 1.91 mg/dL (0.62 mmol/L) (P < 0.0001). Calcium x phosphorus product (P < 0.0001) and serum PTH levels (P < 0.01) were also significantly lower with lanthanum carbonate versus placebo. The incidence of drug-related adverse events was similar between placebo- and lanthanum carbonate-treated patients. Lanthanum carbonate is an effective and well-tolerated agent for the treatment of hyperphosphatemia in patients with ESRD.
                Bookmark

                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2005
                April 2005
                22 February 2005
                : 99
                : 4
                : c128-c137
                Affiliations
                Nephrological Department P, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
                Article
                83979 Nephron Clin Pract 2005;99:c128–c137
                10.1159/000083979
                15722644
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 2, References: 42, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/83979
                Categories
                Original Paper

                Comments

                Comment on this article