Role of etelcalcetide in the management of secondary hyperparathyroidism in hemodialysis patients: a review on current data and place in therapy.

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Term Occurence Count Dictionary
hypercalcemia 1 endocrinologydiseases
hyperparathyroidism 4 endocrinologydiseases
hyperphosphatemia 1 endocrinologydiseases
paricalcitol 2 endocrinologydiseasesdrugs
secondary hyperparathyroidism 2 endocrinologydiseases
vascular calcification 1 endocrinologydiseases
calciphylaxis 2 endocrinologydiseases
calcitriol 11 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
calcitriol 1088 Outcomes chronic kidney disease – mineral and bone disorder clinical practice guidelines. Contrary to calcitriol or other vitamin D-receptor activators, calcimimetics reduce PTH without increasing serum-calcium, phosphorus,
calcitriol 4449 decreased serum-calcium levels, initial normophosphatemia followed by hyperphosphatemia, low 1,25(OH)2D3 ( calcitriol ) concentration, increasing levels of FGF23, a decrease in plasma-soluble Klotho and the development
calcitriol 5538 function.[14] PTH itself stimulates FGF23 secretion directly and indirectly through enhanced synthesis of calcitriol secondary to the PTH-induced stimulation of tubular 1α-hydroxylase.[15]–[17] On the other hand, FGF23
calcitriol 6223 parathyroid-cell hyperplasia.[20] Activation of the VDR lowers PTH transcription, whereas decreased calcitriol stimulates PTH synthesis.[21]Elevated phosphorus reduces the activity of tubular 1α-hydroxylase and
calcitriol 6359 synthesis.[21]Elevated phosphorus reduces the activity of tubular 1α-hydroxylase and lowers the synthesis of calcitriol .[22] Also, it stimulates PTH production independently of changes in calcium and calcitriol concentration[23]
calcitriol 6450 synthesis of calcitriol.[22] Also, it stimulates PTH production independently of changes in calcium and calcitriol concentration[23] and directly increases parathyroid-cell proliferation,[24] due to downregulation of
calcitriol 6696 serum concentrations of calcium and phosphorus and high PTH stimulate 1α-hydroxylase and increase calcitriol production, whereas FGF23 and calcitriol itself reduce enzyme activity.[26] With progressive sHPT, parathyroid-cell
calcitriol 6737 phosphorus and high PTH stimulate 1α-hydroxylase and increase calcitriol production, whereas FGF23 and calcitriol itself reduce enzyme activity.[26] With progressive sHPT, parathyroid-cell hyperplasia is characterized
calcitriol 7367 the use of phosphate binders; the inhibition of PTH synthesis and secretion by the supplementation of calcitriol or other VDR activators (VDRAs) or the use of calcimimetics; finally, surgical parathyroidectomy is
calcitriol 8676 achieving recommended target levels compared to patients treated with a standard regimen containing calcitriol or another VDRA.[33],[34] Even in patients with persistent or recurrent HPT after parathyroidectomy,
calcitriol 8845 or recurrent HPT after parathyroidectomy, cinacalcet is effective.[35] Experimental data has found calcitriol and paricalcitol induce soft-tissue and aortic calcification in uremic rats, while cinacalcet monotherapy
paricalcitol 8860 HPT after parathyroidectomy, cinacalcet is effective.[35] Experimental data has found calcitriol and paricalcitol induce soft-tissue and aortic calcification in uremic rats, while cinacalcet monotherapy did not cause
paricalcitol 19922 aortic calcium content and prevented medial aortic calcification in uremic rats with sHPT, whereas paricalcitol did not show these beneficial effects.[58] A direct effect on vascular endothelial[59] or smooth-muscle
Select Disease Character Offset Disease Term Instance
calciphylaxis 3385 implicated as risk factors for the very rare but devastating calcific and thrombotic arteriolopathy calciphylaxis [7] and lead to reduced health-related quality of life (HRQoL). The indication for sHPT treatment results
calciphylaxis 11282 of EVOLVE demonstrated a significant risk reduction for parathyroidectomy[40] or the development of calciphylaxis [42] with the use of cinacalcet.With regard to bone turnover and histology, cinacalcet has been shown
hypercalcemia 29218 concentration within the normal reference range in dialysis patients; rather, it suggests avoiding hypercalcemia and tolerates mild and asymptomatic calcimimetic-associated hypocalcemia to avoid inappropriate calcium
hyperparathyroidism 96 Title: Drug Design, Development and TherapyRole of etelcalcetide in the management of secondary hyperparathyroidism in hemodialysis patients: a review on current data and place in therapyClaudia FriedlEmanuel Zitt1Department
hyperparathyroidism 516 Feldkirch, AustriaPublication date (collection): /2018Publication date (epub): 6/2018AbstractSecondary hyperparathyroidism (sHPT) is a frequently occurring severe complication of advanced kidney disease. Its clinical consequences
hyperparathyroidism 2293 cardiovascular and survival benefits and better health-related quality of life.IntroductionSecondary hyperparathyroidism (sHPT) is common in hemodialysis patients. This complication of chronic kidney disease (CKD) is caused
hyperparathyroidism 4094 data of the new intravenous second-generation calcimimetic etelcalcetide.Pathogenesis of secondary hyperparathyroidism in chronic kidney diseasesHPT generally develops in stage 3 CKD with an estimated glomerular filtration
hyperphosphatemia 4413 characterized by normal or slightly decreased serum-calcium levels, initial normophosphatemia followed by hyperphosphatemia , low 1,25(OH)2D3 (calcitriol) concentration, increasing levels of FGF23, a decrease in plasma-soluble
secondary hyperparathyroidism 86 Title: Drug Design, Development and TherapyRole of etelcalcetide in the management of secondary hyperparathyroidism in hemodialysis patients: a review on current data and place in therapyClaudia FriedlEmanuel Zitt1Department
secondary hyperparathyroidism 4084 and clinical data of the new intravenous second-generation calcimimetic etelcalcetide.Pathogenesis of secondary hyperparathyroidism in chronic kidney diseasesHPT generally develops in stage 3 CKD with an estimated glomerular filtration
vascular calcification 10293 analysis of protocol-adherent patients in the same study, significantly attenuated progression of cardio vascular calcification was found, even using the Agatston score.[39] In the large randomized placebo-controlled, double-blind

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