Combination therapy of intravenous maxacalcitol and percutaneous ethanol injection therapy lowers serum parathyroid hormone level and calcium x phosphorus product in secondary hyperparathyroidism.

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

Percutaneous ethanol injection therapy (PEIT) is an alternative treatment for secondary hyperparathyroidism (SHPT). Although maxacalcitol has been recently developed as a new vitamin D3 and its efficacy is anticipated in SHPT, there are only few reports on the usefulness of combination therapy of intravenous maxacalcitol and selective PEIT.

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.

N. Fukuda, H Tanaka, Y Tominaga … (1993)

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.

0 comments Cited 67 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

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

K S Rostand, T Drüeke (1999)

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.