Theoretical overview of clinical and pharmacological aspects of the use of etelcalcetide in diabetic patients undergoing hemodialysis.

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Term Occurence Count Dictionary
Liraglutide 2 endocrinologydiseasesdrugs
diabetes mellitus 3 endocrinologydiseases
metformin 1 endocrinologydiseasesdrugs
vascular calcification 1 endocrinologydiseases
hypoglycemia 10 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
hyperphosphatemia 1 endocrinologydiseases
repaglinide 8 endocrinologydiseasesdrugs
secondary hyperparathyroidism 2 endocrinologydiseases
Insulin 2 endocrinologydiseasesdrugs
diabetic neuropathy 1 endocrinologydiseases
hyperinsulinemia 2 endocrinologydiseases
hyperparathyroidism 4 endocrinologydiseases
calcitriol 1 endocrinologydiseasesdrugs
glipizide 3 endocrinologydiseasesdrugs
hypokalemia 2 endocrinologydiseases
primary hyperparathyroidism 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 11525 aforementioned antidiabetic drugs as no interaction studies have been performed with etelcalcetide so far. Insulin and glucagon-like peptide 1 receptor agonistsAs the kidneys primarily excrete exogenous insulin, experts
Insulin 30671 (%)Possible clinical effectOral hypoglycemic agentsHypocalcemia/hypoglycemia Glipizide>99 Repaglinide>98 Insulin s Detemir>98 Degludec>99GLP-1 receptor agonists Liraglutide>98Abbreviation: GLP-1, glucagon-like
Liraglutide 12789 binding, free concentration of etelcalcetide may be affected by its co-administration with these insulins. Liraglutide has been suggested as one of the glucagon-like peptide 1 receptor agonists that do not require dose
Liraglutide 30732 agentsHypocalcemia/hypoglycemia Glipizide>99 Repaglinide>98Insulins Detemir>98 Degludec>99GLP-1 receptor agonists Liraglutide >98Abbreviation: GLP-1, glucagon-like peptide 1.Table 2Hypothetical influence of the treatment of secondary
calcitriol 2495 complication of chronic kidney disease (CKD).[1] Hypocalcemia, induced by phosphate retention and reduced calcitriol synthesis, typically occurs when the glomerular filtration rate (GFR) drops <40 mL/min/1.73 m2.[2] This
glipizide 10843 kidney dysfunction.[24] Oral antidiabetics recommended for use in patients undergoing hemodialysis are glipizide and repaglinide.[25] Both of these drugs may compete with etelcalcetide at the protein-binding level.
glipizide 25999 in >5%.[14],[15] Nausea and diarrhea are described as common adverse effects (≥1/100 to <1/10) of glipizide , while diarrhea commonly occurs with repaglinide.[26],[27] Clinicians should bear in mind that these
glipizide 28656 interactions with etelcalcetide may occur at the SA-binding level with the two recommended oral hypoglycemics, glipizide and repaglinide, as well as with insulins detemir and degludec, and the clinicians should avoid their
metformin 14044 poor dietary intake, increased magnesiuria, altered insulin metabolism, recurrent metabolic acidosis, metformin -and diabetic neuropathy-related diarrhea, etc.) and hypoalbuminemia (owing to nephrotic syndrome, hemodialysis
repaglinide 10857 dysfunction.[24] Oral antidiabetics recommended for use in patients undergoing hemodialysis are glipizide and repaglinide .[25] Both of these drugs may compete with etelcalcetide at the protein-binding level. Glipizide’s
repaglinide 11004 compete with etelcalcetide at the protein-binding level. Glipizide’s protein binding exceeds 99%, while repaglinide , the preferred glinide in hemodialysis patients, is bound to albumin over 98%.[26],[27] At the moment,
repaglinide 24925 purely speculative and theoretical.In studies designed to evaluate clinical efficacy and safety of repaglinide , arrhythmias were observed at ≤1% and no more frequently with this drug than with comparator drugs.[27]
repaglinide 25056 observed at ≤1% and no more frequently with this drug than with comparator drugs.[27] Nonetheless, repaglinide exerts its effect by closing ATP-dependent potassium channels, and in in vitro ion channel studies,
repaglinide 25168 exerts its effect by closing ATP-dependent potassium channels, and in in vitro ion channel studies, repaglinide was shown to inhibit all of the tested ionic currents in a concentration-dependent manner, significantly
repaglinide 25398 the action potential duration in isolated rabbit Purkinje fibers.[86] Although it has been shown that repaglinide ’s pharmacokinetics and safety are not influenced by severe renal impairment, there are no data regarding
repaglinide 26046 described as common adverse effects (≥1/100 to <1/10) of glipizide, while diarrhea commonly occurs with repaglinide .[26],[27] Clinicians should bear in mind that these effects may be potentiated when these hypoglycemics
repaglinide 28670 etelcalcetide may occur at the SA-binding level with the two recommended oral hypoglycemics, glipizide and repaglinide , as well as with insulins detemir and degludec, and the clinicians should avoid their use. While an
Select Disease Character Offset Disease Term Instance
diabetes mellitus 3687 40% of patients with the end-stage renal disease.[7],[8] An Indian study showed that >60% of type 2 diabetes mellitus (T2DM) patients with Stage 3 and 4 CKD suffer from sHPT, while 28.9% of T2DM patients undergoing outpatient
diabetes mellitus 8655 common transporter proteins.[16] Pharmacokinetic alterations of etelcalcetide potentially induced by diabetes mellitus , such as an impaired drug absorption (owing to changes in subcutaneous adipose blood flow, muscle blood
diabetes mellitus 30962 hyperparathyroidism with etelcalcetide versus cinacalcet as a function of clinical alterations associated with diabetes mellitus Clinical alterations in diabetesPossible influence of etelcalcetidePossible influence of cinacalcetLower
diabetic neuropathy 14058 intake, increased magnesiuria, altered insulin metabolism, recurrent metabolic acidosis, metformin-and diabetic neuropathy -related diarrhea, etc.) and hypoalbuminemia (owing to nephrotic syndrome, hemodialysis itself, poor
hyperinsulinemia 23423 overnight death in diabetic patients on insulin treatment.[73]–[75] Even nondiabetic persons with hyperinsulinemia were found to have QTc interval prolongation, and this effect was observed in both acute and chronic
hyperinsulinemia 23551 to have QTc interval prolongation, and this effect was observed in both acute and chronic states of hyperinsulinemia .[76],[77] Two principal mechanisms by which insulin affects the QTc interval have been proposed: direct
hyperparathyroidism 644 4/2018AbstractEtelcalcetide is the first intravenous calcimimetic agent authorized for the treatment of secondary hyperparathyroidism (sHPT) in patients undergoing hemodialysis in Europe, the US, and Japan. The relationship between sHPT
hyperparathyroidism 2202 clinicians should be cautious when using this calcimimetic in patients with diabetes.IntroductionSecondary hyperparathyroidism (sHPT), characterized by elevated levels of parathyroid hormone (PTH) in response to derangements in
hyperparathyroidism 27101 mechanism may be partially responsible for the higher prevalence of diabetes among patients with primary hyperparathyroidism .[93]In in vitro models, it has been shown that the activation of CaR using receptor-specific calcimimetics
hyperparathyroidism 30851 agonists Liraglutide>98Abbreviation: GLP-1, glucagon-like peptide 1.Table 2Hypothetical influence of the treatment of secondary hyperparathyroidism with etelcalcetide versus cinacalcet as a function of clinical alterations associated with diabetes
hyperphosphatemia 13867 hemodialysis suffer from sHPT.[10] The principal reason for this high prevalence is kidney-related hyperphosphatemia and vitamin D deficiency, while hypomagnesemia (owing to poor dietary intake, increased magnesiuria,
hypoglycemia 1343 patients undergoing hemodialysis and insulins detemir and degludec, causing unexpected hypocalcemia or hypoglycemia . More importantly, hypocalcemia, a common side effect of etelcalcetide, may cause decompensation of
hypoglycemia 1733 diabetic patients, hypocalcemia may lead to dangerous ventricular arrhythmias, as both insulin-related hypoglycemia and hemodialysis prolong QT interval. Patients with diabetes, therefore, should be strictly monitored
hypoglycemia 10627 metabolism, inactive or weakly active metabolites that are excreted in the urine, and a low risk of hypoglycemia , as the pharmacokinetic properties of many of the available oral hypoglycemic agents are altered by
hypoglycemia 11214 moment, it is not known whether this protein-binding displacement could lead to clinically significant hypoglycemia s and/or increased free concentrations of etelcalcetide and consequent hypocalcemias. However, the clinicians
hypoglycemia 23836 into the cytoplasm by increasing the activity of the Na+/K+-ATPase pump and sympathetic stimulation by hypoglycemia and hypokalemia.[78],[79] As reported in a recent study that investigated the effects of hypoglycemia
hypoglycemia 23938 hypoglycemia and hypokalemia.[78],[79] As reported in a recent study that investigated the effects of hypoglycemia induced by the administration of human insulin to diabetic patients, insulin-induced hypoglycemia causes
hypoglycemia 24036 of hypoglycemia induced by the administration of human insulin to diabetic patients, insulin-induced hypoglycemia causes a significant QT prolongation in comparison with baseline values and is associated with hypokalemia
hypoglycemia 24422 controls independently from glucose disturbances and insulin administration.[81]–[85] Knowing that hypoglycemia is frequent in insulin-treated diabetic patients undergoing hemodialysis and that this procedure itself
hypoglycemia 30002 ventricular arrhythmias in diabetic patients treated with etelcalcetide, as insulin treatment/insulin-induced hypoglycemia has been linked with QTc prolongation and hypocalcemia is a known risk factor for this ECG alteration.In
hypoglycemia 30627 protein-binding levelDrugsAlbumin binding (%)Possible clinical effectOral hypoglycemic agentsHypocalcemia/ hypoglycemia Glipizide>99 Repaglinide>98Insulins Detemir>98 Degludec>99GLP-1 receptor agonists Liraglutide>98Abbreviation:
hypokalemia 23853 by increasing the activity of the Na+/K+-ATPase pump and sympathetic stimulation by hypoglycemia and hypokalemia .[78],[79] As reported in a recent study that investigated the effects of hypoglycemia induced by the
hypokalemia 24144 hypoglycemia causes a significant QT prolongation in comparison with baseline values and is associated with hypokalemia and sympathoadrenal activation.[80] In addition to these findings, many studies have confirmed a significant
primary hyperparathyroidism 27093 This mechanism may be partially responsible for the higher prevalence of diabetes among patients with primary hyperparathyroidism .[93]In in vitro models, it has been shown that the activation of CaR using receptor-specific calcimimetics
secondary hyperparathyroidism 634 4/2018AbstractEtelcalcetide is the first intravenous calcimimetic agent authorized for the treatment of secondary hyperparathyroidism (sHPT) in patients undergoing hemodialysis in Europe, the US, and Japan. The relationship between sHPT
secondary hyperparathyroidism 30841 agonists Liraglutide>98Abbreviation: GLP-1, glucagon-like peptide 1.Table 2Hypothetical influence of the treatment of secondary hyperparathyroidism with etelcalcetide versus cinacalcet as a function of clinical alterations associated with diabetes
type 2 diabetes mellitus 3680 approximately 40% of patients with the end-stage renal disease.[7],[8] An Indian study showed that >60% of type 2 diabetes mellitus (T2DM) patients with Stage 3 and 4 CKD suffer from sHPT, while 28.9% of T2DM patients undergoing outpatient
vascular calcification 3100 CKD patients.[5] Untreated sHPT eventually leads to renal osteodystrophy, as well as to accelerated vascular calcification and consequent myocardial infarctions, atrioventricular conduction disorders, and abnormalities in valvular

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