Studies With Vitamin D - Full Text View

Sponsor:	National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Information provided by:	National Institutes of Health Clinical Center (CC)
ClinicalTrials.gov Identifier:	NCT00001151

Purpose

Vitamin D in the diet undergoes changes in the liver and kidneys to several forms. Patients suffering from disorders with Vitamin D resistance are unable to absorb calcium from food. Patients diagnosed with these disorders will be evaluated and treated with high doses of another form of Vitamin D (1,25-dihydroxyvitamin D3). Patients will be monitored and observed throughout the study to avoid experiencing side effects from the medication.

Condition	Intervention	Phase
Hypocalcemia Rickets	Drug: 1,25-Dihydroxycholecalciferol	Phase II

Study Type:	Interventional
Study Design:	Primary Purpose: Treatment
Official Title:	Studies With 1,25-Dihydroxycholecalciferol

Resource links provided by NLM:

Genetics Home Reference related topics: carbamoyl phosphate synthetase I deficiency hereditary hypophosphatemic rickets

MedlinePlus related topics: Calcium Rickets Vitamin D

U.S. FDA Resources

Further study details as provided by National Institutes of Health Clinical Center (CC):

Primary Outcome Measures:

Normal serum calcium concentration. [ Time Frame: Throughout drug administration. ] [ Designated as safety issue: No ]

Estimated Enrollment:	200
Study Start Date:	March 1976
Study Completion Date:	October 2009
Primary Completion Date:	October 2009 (Final data collection date for primary outcome measure)

Intervention Details:

N/A

Detailed Description:

Patients with extreme resistance to 1,25-dihydroxyvitamin D will be evaluated and treated with high doses of 1,25-dihydroxyvitamin D3.

Plan: In previously untreated patients the study will be divided into a control and one or more treatment periods. During the control period, parathyroid status will be assessed by parameters nos. 1& 2 (below). In previously treated patients maintenance vitamin D will be gradually replaced with 1,25(OH)2D3. This will be accomplished by withdrawal of vitamin D and institution of 1,25(OH)2D3 when the serum calcium shows a downward trend.

1,25(OH)2D3 as 0.25 or 0.5 ug capsules (though IND 20,889) or as a solution of I microgram per ml will be administered orally. In most cases, because of consideration of time and expense, the cooperation of the patient's local physician will be enlisted. The following will be monitored:

Serum calcium, phosphorus,alkaline phosphatase,creatinine at twice weekly intervals. After a maintenance dose has been established, this will be decreased to a monthly, and subsequently 3-6 monthly interval.
Urine calcium, phosphorus,creatinine and cAMP before therapy and, when appropriate, during therapy.

The dose of 1,25(OH)2D3 will be 0.125 to 50.0 ug/day. Serum calcium will not be allowed to rise above the normal range (2.0 -2.4 mM at NIH). Should hypercalcemia occur, appropriate treatment will be initiated and the drug dosage will be decreased.

Eligibility

Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No

Criteria

INCLUSION CRITERIA:

Patients with hereditary resistance to calcitrol.

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00001151

Locations

United States, Maryland
National Institutes of Health Clinical Center, 9000 Rockville Pike
Bethesda, Maryland, United States, 20892

Sponsors and Collaborators

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

More Information

Publications:

Marx SJ, Swart EG Jr, Hamstra AJ, DeLuca HF. Normal intrauterine development of the fetus of a woman receiving extraordinarily high doses of 1,25-dihydroxyvitamin D3. J Clin Endocrinol Metab. 1980 Nov;51(5):1138-42.

Fraser D, Kooh SW, Kind HP, Holick MF, Tanaka Y, DeLuca HF. Pathogenesis of hereditary vitamin-D-dependent rickets. An inborn error of vitamin D metabolism involving defective conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D. N Engl J Med. 1973 Oct 18;289(16):817-22. No abstract available.

Marx SJ, Spiegel AM, Brown EM, Gardner DG, Downs RW Jr, Attie M, Hamstra AJ, DeLuca HF. A familial syndrome of decrease in sensitivity to 1,25-dihydroxyvitamin D. J Clin Endocrinol Metab. 1978 Dec;47(6):1303-10.

Responsible Party:	Stephen J. Marx, M.D./National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health
ClinicalTrials.gov Identifier:	NCT00001151 History of Changes
Other Study ID Numbers:	760081, 76-DK-0081
Study First Received:	November 3, 1999
Last Updated:	July 29, 2010
Health Authority:	United States: Federal Government

Keywords provided by National Institutes of Health Clinical Center (CC):

Calciferol
Hypocalcemia
Rickets

Additional relevant MeSH terms:

Hypocalcemia
Rickets
Calcium Metabolism Disorders
Metabolic Diseases
Water-Electrolyte Imbalance
Bone Diseases, Metabolic
Bone Diseases
Musculoskeletal Diseases
Vitamin D Deficiency
Avitaminosis
Deficiency Diseases
Malnutrition
Nutrition Disorders
Calcitriol

Dihydroxycholecalciferols
Vitamins
Micronutrients
Growth Substances
Physiological Effects of Drugs
Pharmacologic Actions
Bone Density Conservation Agents
Calcium Channel Agonists
Membrane Transport Modulators
Molecular Mechanisms of Pharmacological Action
Vasoconstrictor Agents
Cardiovascular Agents
Therapeutic Uses

ClinicalTrials.gov processed this record on February 09, 2012