The Effect of Cinacalcet on Gastric Acid Output in Healthy Subjects

This study has been completed.
Sponsor:
Information provided by:
Tufts University
ClinicalTrials.gov Identifier:
NCT00336739
First received: June 12, 2006
Last updated: July 20, 2007
Last verified: June 2007

June 12, 2006
July 20, 2007
April 2006
Not Provided
Compare change in gastric acid output in response to an 11-day course of daily cinacalcet or placebo in subjects on a fixed protein metabolic diet. [ Time Frame: 11 days ]
Compare change in gastric acid output in response to an 11-day course of daily cinacalcet or placebo in subjects on a fixed protein metabolic diet.
Complete list of historical versions of study NCT00336739 on ClinicalTrials.gov Archive Site
  • Compare serum gastrin levels in subjects before and after an 11-day course of cinacalcet or placebo and on a fixed protein metabolic diet. [ Time Frame: 11 days ]
  • Compare 24-hour urinary calcium excretion before and after an 11-day course of cinacalcet or placebo and on a fixed protein metabolic diet. [ Time Frame: 11 days ]
  • Compare serum IGF-1 levels before and after an 11-day course of cinacalcet or placebo and on a fixed protein metabolic diet. [ Time Frame: 11 days ]
  • Compare change in urinary magnesium excretion in response to an 11-day course of daily cinacalcet or placebo in subjects on a fixed protein metabolic diet. [ Time Frame: 11 days ]
  • Compare serum gastrin levels in subjects before and after an 11-day course of cinacalcet or placebo and on a fixed protein metabolic diet.
  • Compare 24-hour urinary calcium excretion before and after an 11-day course of cinacalcet or placebo and on a fixed protein metabolic diet.
  • Compare serum IGF-1 levels before and after an 11-day course of cinacalcet or placebo and on a fixed protein metabolic diet.
Not Provided
Not Provided
 
The Effect of Cinacalcet on Gastric Acid Output in Healthy Subjects
Not Provided

The purpose of this study is to determine whether cinacalcet will increase gastric acid secretion in healthy volunteers.

The calcium sensing receptor (CaSR) was originally found on parathyroid and renal cells and more recently it has been identified on cells that regulate gastric acid secretion (G cells and parietal cells). However, its role in regulating acid secretion in humans is completely unknown and is of potential importance because an acid environment in the stomach enhances intestinal calcium absorption. In this pilot project, we will stimulate the CaSR with a CaSR-agonist called cinacalcet. Our hypothesis is that activation of the CaSR will in turn increase gastric acid production in healthy volunteers.

Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Pharmacodynamics Study
Intervention Model: Parallel Assignment
Masking: Double-Blind
Primary Purpose: Diagnostic
Healthy
Drug: cinacalcet
Not Provided
Ceglia L, Harris SS, Rasmussen HM, Dawson-Hughes B. Activation of the calcium sensing receptor stimulates gastrin and gastric acid secretion in healthy participants. Osteoporos Int. 2009 Jan;20(1):71-8. Epub 2008 Jun 7.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
17
March 2007
Not Provided

Inclusion Criteria:

  • Healthy ambulatory men and postmenopausal women
  • Age 45 to 70
  • Avoid alcohol, antacids, H2 blockers, proton pump inhibitors, or antihistamines during the study.

Exclusion Criteria:

  • Ionized Ca++ level <4.39 mg/dl or >5.02 mg/dl (normal reference range 4.18- 5.02).
  • 24-hour UCa++ excretion >350 mg.
  • Cr >1.3.
  • AST/ALT values >10% beyond reference range.
  • Hgb level <11.7 g/dl in women and <13.2 g/dl in men.
  • MCV level >102 UM3.
  • Basal acid output >5 mEq/h in men and >3.8 mEq/h in women.
  • Basal acid output <1 mEq/h in men and <0.2 mEq/h in women.
  • Age <45 or >70.
  • Premenopausal or <1 year post-menopause.
  • Individuals following vegan diets.
  • Current EtOH abuse.
  • Lidocaine allergy. Medications
  • Antacids
  • H2 blockers
  • Proton pump inhibitors
  • Carafate
  • Anticholinergic agents (i.e. TCA)
  • Cholinergic agents
  • Antihistamines in the last 3 weeks
  • Cogentin
  • Adrenergic blockers
  • Thiazide diuretics
  • Antiplatelet drugs
  • Oral and Inhaled Glucocorticoids
  • Bisphosphonates
  • Raloxifene, Tamoxifen
  • Tobacco
  • EtOH during study
  • rPTH
  • Calcitonin
  • Ketoconazole/Itraconazole
  • Calcitriol
  • Paricalcitol
  • Drisdol, Ergocalciferol
  • Phosphate binders
  • Anticoagulant
  • Erythromycin
  • Hormone replacement therapy except vaginal estrogen creams

Exclusion Diseases

  • Achlorhydria
  • Pernicious anemia
  • Zollinger Ellison syndrome
  • Congestive heart failure
  • Esophageal strictures or motility problems
  • History of a GI bleed
  • Prior upper GI surgery
  • Malabsorption
  • History of GI malignancy
  • GERD, gastritis, duodenitis
  • Active peptic ulcer disease
  • Gallbladder disease
  • Liver disease
  • Pancreatitis
  • Current kidney stone
  • Renal disease
  • Current hypoparathyroidism or hyperparathyroidism
  • Moderate to Severe coronary artery disease
  • Aortic aneurysm
  • Seizure disorder
  • Current Arrhythmia
Both
45 Years to 70 Years
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00336739
2455
No
Not Provided
Tufts University
Not Provided
Principal Investigator: Bess Dawson-Hughes, MD Human Nutrition Research Center on Aging at Tufts University
Tufts University
June 2007

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP