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Hypercalcemia clinical trials

View clinical trials related to Hypercalcemia.

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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: 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: NCT01226810 Not yet recruiting - Hyperparathyroidism Clinical Trials

The Novel Approach of Minimally Invasive Parathyroid Surgery Requires Precise Identification and Localization of the Lesion Prior to Exploration

Start date: January 2011
Phase: N/A
Study type: Observational

Purpose of this study is to compare the image quality and diagnostic accuracy obtained with ultrafast solid state short SPECT in comparison with the routine SPECT protocol.

NCT ID: NCT01021280 Not yet recruiting - Hypocalcemia Clinical Trials

Parathyroid Hormone (PTH) Homeostasis in Bartter Syndrome

Start date: January 2013
Phase: N/A
Study type: Observational

Parathyroid hormone (PTH) gland calcium sensing receptor (CASR) regulates PTH secretion. CASR is also expressed in nephron thick ascending limb (TAL). Bartter syndrome (BS), a normotensive hypokalemic tubulopathy, may be due to mutations in different TAL channels, including the potassium channel ROMK. Mutations in CASR may also cause BS through its effects on ROMK function. However, it is unknown whether ROMK mutations exert any effects on CASR function and PTH physiology. Preliminary data from our center shows that PTH levels were specifically elevated in type II (where ROMK is mutated) and not in type IV (where another gene, Barttin is defective) BS, without a common explanation. We assume that the mutation in ROMK may cause a dysregulation of PTH secretion via possible interaction with CASR. The purpose of this study is: to investigate the PT-gland function and regulation in BS. Methods: Patients with BS type II and IV and normal controls will undergo a standard protocol of controlled ionic hypo- and hypercalcemia, during which PTH secretion, phosphate balance and calcium excretion will be followed. Calcium Vs PTH response curves will be generated and compared. Expected impact and benefit: the results of this study will help understand the mechanisms of PTH regulation beyond CASR.