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Hypercalcemia clinical trials

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NCT ID: NCT04198480 Not yet recruiting - Clinical trials for Hypercalcemia of Malignancy

A Clinical Trial to Assess the Efficacy and Safety of JMT103 in Patients With Refractory HCM

Start date: January 24, 2020
Phase: Phase 1/Phase 2
Study type: Interventional

The purpose of this study is to determine the potential of JMT103 to treat hypercalcemia of malignancy in patients with elevated serum calcium who do not respond to recent treatment with intravenous bisphosphonates.

NCT ID: NCT03935984 Recruiting - Clinical trials for Primary Hyperparathyroidism

Calcitonin Pre-treatment to Improve SPECT-CT Sensitivity

Start date: May 29, 2019
Phase: Phase 4
Study type: Interventional

Patients with biochemically confirmed primary hyperparathyroidism and non-localizing SPECT-CT exam within the past year will be included. Subjects will be treated with calcitonin to lower calcium levels immediately prior to reimaging. The goal of this study is to determine whether lowering calcium will improve uptake/retention of sestamibi and improve sensitivity of SPECT-CT to localize parathyroid adenoma.

NCT ID: NCT03516747 Withdrawn - Hypercalcemia Clinical Trials

Preoperational Fine Needle Aspiration of Pathological Parathyroid Gland

Start date: June 9, 2018
Phase: N/A
Study type: Interventional

Identification and localization of pathological parathyroid gland before parathyroidectomy is traditionally done by a combination of two methods: ultrasound and sestamibi scan. The investigators would like to show that one exam that includes ultrasound and fine needle aspiration of the parathyroid gland for parathyroid hormone level is as accurate as the traditional method.

NCT ID: NCT03384121 Recruiting - Clinical trials for Idiopathic Infantile Hypercalcemia - Mild Form

The Antibiotic Rifampin to Reduce High Levels of Blood and Urine Calcium in IIH

Start date: February 22, 2018
Phase: Phase 1
Study type: Interventional

Idiopathic infantile hypercalcemia(IIH) is a rare,genetic disorder of mineral metabolism. Biallelic loss of functions mutations of CYP24A1, the gene encoding the 24-hydroxylase enzyme that represents the principal pathway for inactivation of vitamin D metabolites, cause the most common and severe form of IIH.Investigators have preliminary data supporting a novel therapeutic approach to suggest rifampin as an investigational drug to induce over-expression of CYP3A4, an important enzyme that provides an alternate catabolic pathway for inactivation of vitamin D metabolites. In this study, investigators will recruit 5 patients with biallelic inactivating mutations of CYP24A1. Participants will be followed prospectively for a total 6-11 months. This will include 2 months of observation, 2 months of receiving the starting dose of rifampin, followed by 2 month washout phase. Efficacy of the starting dose of rifampin will be determined prior to proceeding only in non responders to the escalation dose of rifampin 10mg/kg/day.

NCT ID: NCT03301038 Recruiting - Genetic Disease Clinical Trials

Rifampin in CYP24A1-related Hypercalcemia and Hypercalciuria

RICHH
Start date: July 25, 2018
Phase: Phase 2
Study type: Interventional

This study evaluates the efficacy of rifampin in the treatment of hypercalcemia and/or hypercalciuria in participants with at least one inactivating mutation of the CYP24A1 gene. Eligible subjects will receive rifampin for a total of 16 weeks during this study.

NCT ID: NCT03280264 Completed - Clinical trials for Primary Hyperparathyroidism

Phase 3 Study of KHK7580 for the Treatment of Hypercalcemia in Patients With Parathyroid Carcinoma or Primary Hyperparathyroidism

Start date: August 30, 2017
Phase: Phase 3
Study type: Interventional

To evaluate the efficacy of KHK7580 orally administered up to 24 weeks for hypercalcemia in patient with parathyroid carcinoma or primary hyperparathyroidism who are unable to undergo parathyroidectomy or relapse after parathyroidectomy.

NCT ID: NCT02908542 Completed - Hypercalcemia Clinical Trials

Search for New Genetic Causes of Hypercalcemia by Massively Parallel Sequencing of a Genes Panel

HyCaGene
Start date: December 2015
Phase:
Study type: Observational

Hypercalcemia, whether chronic or acute, exposes the patient to potentially serious complications (arrhythmias, nephrolithiasis, nephrocalcinosis, ...). Prevention relies primarily on effective etiological necessary for taking matched load. Under the French reference center for rare disorders of calcium and phosphorus, the investigators looked for mutations in the coding sequence of the CYP24A1 gene (encoding the enzyme responsible for the breakdown of vitamin D), among patients with hypercalcemia without hyperparathyroidism with hypersensitivity to vitamin D. However, only 25% of these patients have a genetic anomaly suggesting the involvement of other genes (Molin et al. 2015). Recently our team, combined with Kaufmann et al. (2014 JCEM) validated the interest of the determination of metabolites of vitamin D by liquid chromatography-tandem mass spectrometry (LC-MS / MS), as biological pre-screening stage for patients with hypercalcemia. The objective of this project is to complement the molecular and biochemical studies of patients without mutation of the coding sequence of CYP24A1, in a gene candidate approach using massively parallel sequencing (MPS) which allows to study a panel of gene potentially involved in disorder of metabolism of calcium and phosphorus. Highlighted variations will be tested in silico, and if possible in vitro. The investigators will also use LC-MS / MS to evaluate in vivo the effects of these variations on the metabolism of vitamin D, to develop a genotype / phenotype correlation. The work carried out within the Genetics Department Caen University Hospital in collaboration with physicians of the rare disease reference center of the metabolism of calcium and phosphorus should identify new genetic mechanisms underlying hypercalcemia. At the time of development of personalized medicine, it will adapt the therapy in patients at risk for metabolic complications and / or kidney following administration of vitamin D and finally to offer genetic counseling.

NCT ID: NCT02711059 Withdrawn - Diabetes Clinical Trials

Insulin Resistance in Primary Hyperparathyroidism

IRIPH
Start date: October 2015
Phase: N/A
Study type: Interventional

The aims of this study is to analyse if insulin resistance in primary hyperparathyroidism (pHPT) is normalised after parathyroid adenomectomy and if glucose tolerance test may be useful as a diagnostic tool by predicting potential improvement of insulin sensitivity after biochemical cure of pHPT.

NCT ID: NCT02155803 Not yet recruiting - Sarcoidosis Clinical Trials

ACTHAR GEL for Sarcoidosis-Associated Calcium Dysregulation: An Open-label Pilot Study

Start date: February 2015
Phase: Phase 2/Phase 3
Study type: Interventional

ACTHAR Gel has activity in sarcoidosis associated hypercalciuria and calcium dysregulation.

NCT ID: NCT02023489 Recruiting - Healthy Volunteers Clinical Trials

Lipid and Glycogen Metabolism in Patients With Impaired Glucose Tolerance and Calcium Sensing Receptor Mutations

RISC_7T
Start date: July 2013
Phase: N/A
Study type: Interventional

Background: Type 2 diabetes mellitus is a main risk factor for cardiovascular disease and heart failure, in part due to diabetic cardiomyopathy. However, the association between intracellular lipid accumulation and (myocardial) functional impairment is likely more complex than originally imagined. Recent studies suggest that not fat per se, but the content of saturated or unsaturated fatty acids might predict the development of cardiac steatosis and myocardial dysfunction. In addition skeletal muscle and hepatic glycogen metabolism is impaired in patients with diabetes mellitus. Data from animal experiments suggest a relevant role of myocardial glycogen stores in ischemic preconditioning. Due to methodological limitations so far data on myocardial glycogen stores and myocardial lipid composition in humans are missing. Hypothesis: In addition to total ectopic lipid deposition in the myocardium, myocardial lipid composition, i.e. the relative abundance of saturated and unsaturated fatty acids, and impaired myocardial glycogen metabolism may play an important role in the development cardiac lipotoxicity leading to diabetic cardiomyopathy. Pancreatic endocrine function and myocardial morphology and function is altered in patients with heterozygote inactivating mutations of the CaSR-gene / FHH. Aims: - Metabolic virtual biopsy of the myocardium for identification of specific patterns of intracellular lipid composition and myocardial glycogen metabolism as possible critical determinants of metabolic cardiomyopathy - Characterization of the metabolic interplay between the myocardium, skeletal muscle, liver and adipose tissues in different stages of development of type 2 diabetes compared to patients with calcium sensing receptor mutation Methods: - 1H/13C and 31P magnetic resonance spectroscopy and imaging for measurements of myocardial, skeletal and liver lipid and glycogen content, abdominal adipose tissue distribution and composition, ATP synthesis and myocardial functional parameters - Mixed meal tolerance tests to trace the postprandial partitioning of substrates between insulin sensitive tissues (myocardium, skeletal muscle, liver, adipose tissue). - Hyperinsulinemic-hyperglycemic glucose clamp (HHC) with enrichment of the infused glucose with the stable isotope [1-13C]glucose to trace the incorporation of circulating glucose into myocardial glycogen in healthy insulin sensitive volunteers, prediabetic insulin resistant volunteers with impaired glucose tolerance, healthy subjects, patients suffering from type 2 diabetes mellitus, patients suffering from type 1 diabetes and patients with heterozygote mutation in calcium sensing receptor.