View clinical trials related to Hypoparathyroidism.
Filter by:The purpose is to perform a one-year study designed to assess whether treatment of hypovitaminosis D increases intestinal absorption of calcium, subsequent retention of calcium within bone, decreases bone turnover, and favorably impacts upon skeletal muscle mass, functional status, measures of physical function and quality of life. I hypothesize that treatment of hypovitaminosis D results in improved intestinal calcium absorption, greater retention of calcium within the bone reservoir and improved physical function, quality of life and muscle mass.
This study has three primary purposes: to assess parathyroid function after parathyroid transplantation in infants with Complete DiGeorge syndrome; to assess immune function development after transplantation; and, to assess safety and tolerability of the procedures. This is a Phase 1, single site, open, non-randomized clinical protocol. Enrollment is closed and study intervention is complete for all enrolled subjects; but subjects continue for observation and follow-up. Subjects under 2 years old with complete DiGeorge syndrome (atypical or typical) received thymus transplantation. Subjects received pre-transplant immune suppression with rabbit anti-human-thymocyte-globulin. Subjects with hypoparathyroidism and an eligible parental donor received thymus and parental parathyroid transplantation. A primary hypothesis: Thymus/Parathyroid transplant subjects will need less calcium and/or calcitriol supplementation at 1 year post-transplant as compared to historical controls.
Whereas much information is known about the properties of bone in primary hyperparathyroidism, a disorder of parathyroid hormone (PTH) excess, virtually nothing is known about the skeleton in hypoparathyroidism, a disorder in which PTH is absent. The purpose of this research project is to test the hypothesis that the skeleton in hypoparathyroidism is abnormal in its metabolic, densitometric, geometric, biomechanical and microarchitectural features. We will also test the hypothesis that the skeleton is dependent upon PTH for normal structure and function. Using non-invasive approaches as well as direct analysis of bone itself, the human hypoparathyroid skeleton will be thoroughly characterized. With each patient serving as his/her own control, we will determine how, to what extent, and in what ways the administration of PTH restores skeletal dynamics and structure to the hypoparathyroid skeleton. In this way, we will identify those structural and dynamic elements of the skeleton that are influenced by or dependent upon PTH. Methods to be utilized include dual energy X-ray absorptiometry, quantitative central and peripheral computed tomography, geometry and size quantification, histomorphometry by standard and microCT methods, finite element analysis, biochemical bone markers, quantitative back scattered electron imaging, and Fourier Transform Infrared Spectroscopy. This research project will extend our knowledge of the skeletal effects of PTH to its deficient range and thus complete our understanding of PTH action on bone gained by our many years of studying PTH overexpression in primary hyperparathyroidism. This investigation may also provide insight into the means by which PTH helps to restore the skeleton when it is used to treat osteoporosis.
This study will explore the regulation of fibroblast growth factor-23 (FGF-23). It is a hormone recently identified as a regulator of the blood levels of phosphorus and vitamin D, both of which are essential for overall health and especially important for bone health. The parathyroid hormone (PTH) regulates phosphorus and calcium, but people with hypoparathyroidism or pseudohypoparathyroidism do not have sufficient PTH action. There are genetic diseases that influence FGF-23, causing abnormal metabolism of phosphorus and vitamin D, thus affecting the bones. Also, there are rare tumors that may cause overproduction of FGF-23 causing debilitating bone disease. Patients ages 18 and older who have low PTH levels, or are resistant to PTH action, and take calcitriol and calcium supplements, who are not pregnant, and who do not have kidney disorders may be eligible for this study. During the 4-day study, patients will be provided with a controlled diet that has a lower than usual phosphorus content. On day 1, patients will be admitted to the NIH Clinic Center and undergo blood and urine tests to measure calcium, phosphorus, vitamin D, and FGF-23. They will continue with their regular medicine for hypoparathyroidism. On that day and throughout the study, patients will fast from 10:00 p.m. to 8:00 a.m. the following day. On day 2, patients will continue fasting until 4:00 p.m. A tube will be placed in the vein of each arm: one for drawing blood and the other for infusing calcium. Just one intravenous (IV) line will be used on the other days. Patients will receive calcium chloride for 8 hours, at a dose carefully monitored by a machine. The purpose is to bring the blood calcium level to the high normal range or just above. Blood and urine samples will be collected periodically, to check for effects of calcium chloride on FGF-23 and PTH. On days 3 and 4, patients will not take calcitriol and calcium but will receive injections of PTH, under the skin, two times each day. On day 3, blood and urine samples will be again be collected for analysis. On day 4, patients will receive one dose of calcitriol by IV. The total amount of blood drawn during this study will be about 5 ounces.
OBJECTIVES: I. Identify latent hypoparathyroidism in normocalcemic adult survivors with repaired conotruncal cardiac defects, by evaluating parathyroid gland secretory function after induced hypocalcemia. II. Determine the relationship of parathyroid hormone secretion to microdeletions in the same region of chromosome 22q11 as found in patients with DiGeorge anomaly.
This study has been important in establishing synthetic human parathyroid hormone 1-34 (PTH) as a beneficial treatment for hypoparathyroidism, superior to conventional therapy with calcium and calcitriol. Providing synthetic human parathyroid hormone 1-34 (PTH) to patients who are unresponsive to conventional therapy has enabled severe cases of hypoparathyroidism to be managed effectively with the investigational drug, PTH. The primary goals of this study are to (1) provide long-term PTH therapy to patients who do not respond to conventional therapy; (2) understand the long-term effect of therapeutic PTH replacement on kidney function and bone mineral density; (3) study and track linear growth and bone accrual in children with hypoparathyroidism. (4) determine if subjects reach a normal level of peak bone mass and if the timing of this is comparable to normal age-matched healthy controls.