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      New clinical guidelines for selective direct injection therapy of the parathyroid glands in chronic dialysis patients

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          Abstract

          In 2000, the Japanese Society for Parathyroid Intervention issued the ‘Guidelines for percutaneous ethanol injection therapy of the parathyroid glands in chronic dialysis patients’. Since then, the concept of ‘selective PEIT’ has been well accepted and the number of patients treated by this method in Japan has increased. Recently, it has been reported that the effect of PEIT differs depending on the degree of nodular hyperplasia. Several new drugs have become available since 2000, and active vitamin D and its analogue have also been used for direct injection into the parathyroids. We present the new ‘Guidelines for selective direct injection therapy of the parathyroid glands in chronic dialysis patients’, a revised version of the 2000 Guidelines. We believe that these new guidelines are useful for selecting direct injection therapy in patients with advanced secondary hyperparathyroidism.

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          Most cited references23

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          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.
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            Depressed expression of calcium receptor in parathyroid gland tissue of patients with hyperparathyroidism.

            The factors involved in abnormal parathyroid cell secretory function and growth in patients with primary (I degree) and secondary (II degree) hyperparathyroidism are still incompletely understood. We compared the expression of the calcium-sensing receptor (CaR) at the gene message and the protein level in parathyroid tissue obtained from patients with I degree non-uremic or II degree uremic hyperparathyroidism with that in normal parathyroid tissue, using in situ hybridization and immunohistochemistry techniques. The expression of the CaR mRNA and protein was reduced in most cases of I degree adenoma and II degree hyperplasia, compared with strong expression normal parathyroid tissue. In II degree hyperparathyroidism, expression of both receptor mRNA message and protein was often particularly depressed in nodular areas, compared with adjacent non-nodular hyperplasia. Decreased Ca-R expression in adenomatous and hyperplastic parathyroid glands would be compatible with a less efficient control of PTH synthesis and secretion by plasma calcium than in normal parathyroid tissue.
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              Histopathology, pathophysiology, and indications for surgical treatment of renal hyperparathyroidism.

              Morphological changes in the parathyroid glands evidently occur early during renal failure. Histopathological investigations have suggested that parathyroid cells initially increase diffusely with a normal lobular structure (diffuse hyperplasia). The parathyroid glands then become hyperplastic with some nodules (nodular hyperplasia). Cells in nodules grow monoclonally and proliferate aggressively, possibly induced by some kind of genetic abnormality. Pathophysiologically, in cells consisting of hyperplastic nodules, suppression of parathyroid hormone (PTH) secretion under the influence of excess extracellular calcium is more deranged, possibly due to a reduction of calcium-sensing receptors. Vitamin D receptor density decreases more severely in these cells, possibly causing abnormal PTH synthesis, PTH secretion, and even parathyroid cell proliferation. According to histopathological and pathophysiological findings, patients with nodular hyperplasia during renal hyperparathyroidism may be refractory to medical treatments, including calcitriol pulse therapy, and parathyroidectomy will become necessary. There is a relationship between the pattern of parathyroid hyperplasia and glandular weight in which glands weighing more than 500 mg may be pathognomonic of nodular hyperplasia. Glandular volume, estimated by ultrasonography, is one of several important criteria indicating parathyroidectomy. In order to prevent a recurrence of hyperparathyroidism, all nodular hyperplastic tissue should be extirpated.
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                Author and article information

                Journal
                NDT Plus
                NDT Plus
                ckj
                ndtplus
                NDT Plus
                Oxford University Press
                1753-0784
                1753-0792
                August 2008
                August 2008
                : 1
                : Suppl 3 , Parathyroid Intervention - Current themes and future perspectives
                : iii26-iii28
                Author notes
                Noritaka Onoda, Division of Endocrinology and Metabolism, Sekishin-kai Sayama Hospital, 1-33 Unoki, Sayana-shi, Saitaka-ken 350-1323, Japan. E-mail: noritaka-onoda@ 123456sayamahp.org
                Article
                sfn083
                10.1093/ndtplus/sfn083
                4421126
                25983969
                c098743a-ec65-4dde-985f-d73e00178ea6
                © The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 2 March 2008
                : 17 March 2008
                Categories
                Original Article

                Nephrology
                percutaneous ethanol injection therapy (peit),percutaneous vitamin d injection therapy (pdit),secondary hyperparathyroidism,ultrasonography,nodular hyperplasia

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