+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Combination Therapy of Intravenous Maxacalcitol and Percutaneous Ethanol Injection Therapy Lowers Serum Parathyroid Hormone Level and Calcium × Phosphorus Product in Secondary Hyperparathyroidism

      Read this article at

          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.


          Background: Percutaneous ethanol injection therapy (PEIT) is an alternative treatment for secondary hyperparathyroidism (SHPT). Although maxacalcitol has been recently developed as a new vitamin D<sub>3</sub> and its efficacy is anticipated in SHPT, there are only few reports on the usefulness of combination therapy of intravenous maxacalcitol and selective PEIT. Methods: The study population comprised 10 hemodialysis patients (6 males and 4 females, mean age; 51.5 ± 13.5 years, mean HD period 13.7± 3.5 years), with high intact-PTH level (>400 pg/ml) and 1 or 2 enlarged parathyroid glands detected by power Doppler ultrasonography. Intravenous maxacalcitol therapy commenced one week after PEIT at 15 µg/week. The effect of combination therapy was monitored by measuring intact-PTH, serum Ca and P, bone metabolic markers, parathyroid gland volume and bone mineral density, prior to and at 6 and 12 months after PEIT. Results: Successful control of intact-PTH, bone metabolic markers and parathyroid gland volume was achieved using the combination therapy. Serum P and Ca×P productweresignificantly decreased 12 months after PEIT. The mean values of serum intact-PTH, P and Ca×P product fulfilled all of the K/DOQI guidelines at 12 months after PEIT. None of the patients developed complications related to PEIT-maxacalcitol therapy during 12 months following PEIT. Conclusion: Combination therapy of intravenous maxacalcitol therapy and selective PEIT is safe and effective for the treatment of refractory SHPT. This combination therapy results in suppression of PTH secretion, regression of parathyroid hyperplasia and the control of Ca×P product, which may prevent calcific uremic arteriolopathy in dialysis patients.

          Related collections

          Most cited references 25

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

          Decreased 1,25-dihydroxyvitamin D3 receptor density is associated with a more severe form of parathyroid hyperplasia in chronic uremic patients.

          The resistance of parathyroid cells to 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in uremic hyperparathyroidism is thought to be caused, in part, by a 1,25(OH)2D3 receptor (VDR) deficiency in the parathyroids. However, results of biochemical studies addressing VDR numbers in the parathyroids are controversial. Several studies have found VDR content to be decreased in the parathyroids of uremic patients and animals, while others have found no such decrease in the parathyroids of uremic animals. To clarify the role of VDR, we investigated VDR distribution in surgically-excised parathyroids obtained from chronic dialysis patients by immunohistochemistry. We classified the parathyroids as exhibiting nodular or diffuse hyperplasia. Our studies demonstrated a lower density of VDR in the parathyroids showing nodular hyperplasia than in those showing diffuse hyperplasia. Even in the parathyroids showing diffuse hyperplasia, nodule-forming areas were present; these areas were virtually negative for VDR staining. A significant negative correlation was found between VDR density and the weight of the parathyroids. These findings indicate that the conflicting results of biochemical studies may be caused by the heterogeneous distribution of VDR; the decreased VDR density in parathyroids may contribute to the progression of secondary hyperparathyroidism and to the proliferation of parathyroid cells that is seen in uremia.
            • Record: found
            • Abstract: found
            • Article: not found

            Parathyroid hormone, vitamin D, and cardiovascular disease in chronic renal failure.

            Parathyroid hormone and vitamin D have been shown to influence cardiac and vascular growth and function experimentally in human subjects with normal renal function. Because of the increased prevalence of hyperparathyroidism and altered vitamin D status in chronic renal failure, these alterations have been considered to contribute to the increased prevalence of cardiovascular disease and hypertension seen in this patient population. Methods and Results. In this article, we review experimental and clinical literature on the cardiovascular effects of parathyroid hormone and vitamin D and relate them to the development of cardiac and vascular dysfunction in uremia, such as: cardiomyopathy, myocardial hypertrophy, and fibrosis, as well as to myocardial ischemia; uremic glucose intolerance, dyslipidemia, and atherosclerosis; hypertension; and vascular and cardiac calcifications. The hyperparathyroid state and altered vitamin D status found in uremia contribute to the cardiovascular pathology seen clinically in uremia and also to the excess mortality from cardiovascular causes found in this patient group. The therapeutic implications of these observations are also discussed.
              • Record: found
              • Abstract: found
              • Article: not found

              Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia.

              The pathogeneses of parathyroid disease in patients with uremia and nonfamilial primary parathyroid hyperplasia are poorly understood. Because of multigland involvement, it has been assumed that these common diseases predominantly involve polyclonal (non-neoplastic) cellular proliferations, but an overall assessment of their clonality has not been done. We examined the clonality of these hyperplastic parathyroid tumors using X-chromosome inactivation analysis with the M27 beta (DXS255) DNA polymorphism and by searching for monoclonal allelic losses at M27 beta and at loci on chromosome band 11q13. Fully 7 of 11 informative hemodialysis patients (64%) with uremic refractory hyperparathyroidism harbored at least one monoclonal parathyroid tumor (with a minimum of 12 of their 19 available glands being monoclonal). Tumor monoclonality was demonstrable in 6 of 16 informative patients (38%) with primary parathyroid hyperplasia. Histopathologic categories of nodular versus generalized hyperplasia were not useful predictors of clonal status. These observations indicate that monoclonal parathyroid neoplasms are common in patients with uremic refractory hyperparathyroidism and also develop in a substantial group of patients with sporadic primary parathyroid hyperplasia, thereby changing our concept of the pathogenesis of these diseases. Neoplastic transformation of preexisting polyclonal hyperplasia, apparently due in large part to genes not yet implicated in parathyroid tumorigenesis and possibly including a novel X-chromosome tumor suppressor gene, is likely to play a central role in these disorders.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                January 2006
                14 September 2005
                : 102
                : 1
                : c1-c7
                aDepartment of Nephrology, Akebono Clinic, Shirafuji, Kumamoto, and bDivision of Nephrology and Dialysis Center, Kobe University Graduate School of Medicine, Kusunoki-cho, Chuo-ku, Kobe, Japan
                88163 Nephron Clin Pract 2006;102:c1–c7
                © 2006 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: 8, Tables: 1, References: 37, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/88163
                Original Paper


                Comment on this article