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      Treatment of Uremic Hyperparathyroidism with Percutaneous Ethanol Injection

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          Abstract

          The percutaneous ethanol injection (PEI) with ultrasound guidance has been suggested for the treatment of patients with hyperparathyroidism who are on dialysis, with the aim of selectively treating the parathyroid glands with nodular hyperplasia. We present our experience in 25 patients with chronic renal failure followed during 13.4 ± 10.6 months. A decrease in the levels of parathormone (PTH) (1,236.32 ± 129.8 vs. 721.66 ± 142.24 pg/ml), phosphatemia (6.16 ± 0.35 vs. 4.93 ± 0.36 mg/dl) and calcium-phosphorous product (60.82 ± 3.81 vs. 46.47 ± 3.46 mg<sup>2</sup>/dl<sup>2</sup>) was verified. In 56% of patients, PTH levels decreased (>50% of the baseline value) and 36% had final values <300 pg/ml. Patients in whom ultrasound showed a single gland responded better than those with more than one gland (83.3 vs. 30.8% of responders in each group). The procedures performed had a 4.9% complication rate: hematoma, symptomatic hypocalcemia, temporary paresis of the vocal cords. In summary, treatment with PEI is useful for the management of patients with hyperparathyroidism who are on dialysis, and the results achieved are better in patients who have a single gland identified by ultrasonography.

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          Most cited references 10

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          Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients.

          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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            Pathogenesis of secondary hyperparathyroidism

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              Clinical experience with percutaneous ethanol injection therapy in hemodialysis patients with renal hyperparathyroidism.

              Percutaneous ethanol injection therapy (PEIT) is a noteworthy method to treat patients with renal hyperparathyroidism (RHPT). This study was performed to enable the authors to propose appropriate indications for PEIT.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2005
                October 2005
                08 June 2005
                : 101
                : 2
                : c53-c57
                Affiliations
                Departments of aEndocrinology, Metabolism and Nuclear Medicine, bDiagnostic Imaging, and cNephrology, Hospital Italiano, Buenos Aires, Argentina
                Article
                86222 Nephron Clin Pract 2005;101:c53–c57
                10.1159/000086222
                15942251
                © 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
                Tables: 2, References: 21, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/86222
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