Neoplasms

Symptoms and General Pathology

All Conditions

Gland and Hormone Related Diseases

Nutritional and Metabolic Diseases

Neoplasm Metastasis

Hyperparathyroidism

Hyperparathyroidism, Secondary

Vitamin D Deficiency

Neoplastic Processes

Parathyroid Diseases

Endocrine System Diseases

Micronutrients

All Drugs and Chemicals

Bone Density Conservation Agents

Vitamins

Vitamin D

Cholecalciferol

Hydroxycholecalciferols

Teriparatide

Calcifediol

Parathyroid Hormone

Hormones

Calcium

Calcium, Dietary

Vitamin D3

Calciferol

Patient with secondary hyperparathyroidism

Teriparatide will be given by continuous intravenous infusion at a rate of 12 pmol/kg/hr for 8 hours to both "patients" and "controls"

Elizabeth A Streeten, MD

The purpose of this study is to determine if a reduction in the enzyme 1-hydroxylase, which activates Vitamin D, is the cause of overactivity of the parathyroid glands (called secondary hyperparathyroidism - normal blood calcium and elevated parathyroid hormone) in a selected group of young patients with normal kidney function.

Vitamin D, an essential nutrient, is produced by the skin after sunlight shines on it. Vitamin D must then be activated by both the liver and the kidneys to perform its function of maintaining strong bones and helping to prevent heart disease, infection, diabetes and cancer. Reduced kidney activation of Vitamin D occurs with advanced age and with all kidney diseases. We have identified a small group of patients who appear to have reduced ability of the kidneys to activate vitamin D, even though they are young and do not have chronic kidney disease. In these patients, we are comparing the ability of their kidneys to activate Vitamin D to that of healthy controls. To stimulate the kidneys to activate Vitamin D, we are giving parathyroid hormone intravenously over 8 hours and collecting blood and urine at baseline, 4 and 8 hours. This type of parathyroid infusion does not cause side effects. The gene that controls this activation is also being studied (by a simple blood test) to look for abnormalities. We are now actively recruiting healthy controls for this study.

Suspected Deficient Activation of Vitamin D in Patients With Secondary Hyperparathyroidism

Clinical and Molecular Characterization of Suspected Partial 25-hydroxyvitamin D-1-alpha-hydroxylase Deficiency

1,25-D was measured at baseline, 4 and 8 hours after PTH infusion

CYP27B1 gene (the gene for 25-hydroxyvitamin D-1-alpha hydroxylase) was sequenced for all in patient group and compared with published control data

University of Maryland, Baltimore

Associate Professor of Medicine

Controls

patients with secondary hyperparathyroidism

Patient Group

Total

Age, Categorical

Age, Continuous

Sex: Female, Male

United States

Region of Enrollment

The null hypothesis is that there is no statistical difference between patients and controls at baseline

The null hypothesis is that there is no statistical difference between patients and controls at 4 hours

The null hypothesis is that there is no statistical difference between patients and controls at 8 hrs

Baseline

4 hours

8 hours

"patients" with secondary hyperparathyroidism

Group 1

Controls without secondary hyperparathyroidism

The final analysis was made on participants with glomerular filtration rate (GFR) of 70 and above since \<70, 1,25-D production decreases. After study completion, it was noted that one participant in each group (patient and control) had GFR\<70 so these two participants were excluded from final analysis.

The Level of Activated Vitamin D (1,25-dihydroxyvitamin D) After Parathyroid Hormone Infusion at Baseline, 4 and 8 Hours

patients with idiopathic secondary hyperparathyroidism

Patients

All patients were sequenced and compared to published control data. Controls were not sequenced for cost reasons

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