View clinical trials related to Vitamin D Deficiency.
Filter by:This is a prospective, randomized, non-blinded interventional study that will investigate the effect of a vitamin D supplement on HbA1c in patients with uncontrolled type 2 diabetes mellitus (DM) and vitamin D deficiency. The goal is to investigate whether correcting vitamin D deficiency will alter the HbA1c level in patients with type 2 DM and lower than normal vitamin D level. My hypothesis is that correcting vitamin D deficiency decreases HbA1c levels in patients with type 2 DM and vitamin D deficiency.
This is a randomized, placebo-controlled trial of vitamin D supplementation with 20mcg cholecalciferol (to achieve a total intake of 25mcg/day), with or without 500mg calcium to assess vitamin D requirements in lactating women and to ascertain whether vitamin D supplementation at levels sufficient to achieve defined thresholds of maternal serum 25-hydroxyvitamin D will increase the vitamin D content of maternal milk. The study will also report serum 25-hydroxyvitamin D in maternal-cord dyads over a 12-month period and describe the relationship between them. Information on maternal iPTH levels, anthropometry, diet and sun exposure will also be reported.
The purpose of this study is to observe changes in iron status and vitamin D status during a 12-24 week supervised training program, specifically males and females between the ages of 30 and 50 years old.
Using a randomized, placebo-controlled trial design in subjects with vitamin D deficiency, the investigators propose to determine if vitamin D treatment improves glycemic control in vitamin D deficient subjects with T2DM. The investigators hypothesize that oral vitamin D treatment will improve glycemic control and ß-cell function in vitamin D deficient AA subjects with T2DM. The investigators further hypothesize that maintaining serum 25(OH)D concentrations above 20 ng/ml with oral supplementation of vitamin D will have additional glycemic control effects.
The assumption has been that 1,25(OH)2D is solely responsible for calcium absorption. That has been one of the presumed causes of hyperparathyroidism in chronic kidney disease (CKD) (low 1,25(OH)2D leads to decreased calcium absorption, which increases parathyroid hormone release in compensation). Replacing 1,25 D directly has been the goal with using 1,25D or its analogues in CKD. There is very little data concerning use of native vitamin D or 25(OH)D in CKD, although autocrine functions in extrarenal tissues would use 25(OH)D. The latest KDIGO guidelines do recognize the autocrine role of vitamin D, but have no data on outcomes or doses or optimal levels to guide them and so have made a blanket recommendation to treat 25D levels in CKD by general healthy population guidelines. 1. This project focuses on an outcome (calcium absorption) that may be impacted by optimizing 25D status in renal patients. The investigators will assume for this project that a level of 25D > 32 ng/ml is optimal in CKD patients as in a healthy population. 2. A secondary outcome is to quantify calcium absorption in CKD patients with and without vitamin D repletion and to quantify systemic 1,25D levels. This may clarify the roles 25D and 1,25D play in calcium absorption.
Many adolescents with acute lymphoblastic leukemia (ALL) have been found to have low bone density by the end of treatment. This can lead to long-term suffering in survivors due to poor bone health. Vitamin D is known to be associated with bone health and previous research has established that Vitamin D insufficiency is very common at diagnosis of ALL and worsens over the course of treatment. Researchers have also learned that a relationship exists between both Vitamin D and fat tissue and ALL and fat tissue. In adolescents being treated for ALL as well as in early survivors, this randomized study will therefore examine the effect of Vitamin D and calcium supplementation on correcting Vitamin D insufficiency and on improving bone density in the context of changes in body composition and body fat. Bone density will be measured by a radiology exam called qCT (quantitative computed tomography) while body composition and body fat will be measured by a different radiology exam called a DXA (dual energy x-ray absorptiometry scan) . The study will also examine in depth the relationship between these three elements - Vitamin D insufficiency, obesity, and ALL - and their impact on bone density.
The optimal dose of vitamin D needed to optimize beneficial effects on musculoskeletal outcomes remains to be defined. Equally unclear is the impact of vitamin D on fuel metabolism and insulin sensitivity in human subjects. Thus, the overall objective of this proposal is to test the hypothesis that in ambulatory overweight elderly individuals, vitamin D administration at doses higher than currently recommended will: 1. Have a salutary effect on parameters of glucose and fuel metabolism. It will thus decrease indices of insulin resistance, improve lipid profile, and decrease markers of cardiovascular disease including adipokines, inflammatory cytokines, and markers of cell adhesion. 2. Have a superior effect on indices of mineral and musculoskeletal metabolism, including bone remodeling markers, lean mass, and bone mineral density. We will investigate whether this effect is modulated by entry status of vitaminD and PTH as detailed below
This study will look at the effect of 2 treatment regimens that contain vitamin D in a six-month treatment trial of patients with PHPT who are vitamin D deficient. Patients will be assigned randomly to one of 2 regimens, and will be followed with tests of their blood, urine and bones. This study should provide important information on the effect of vitamin D therapy in patients with PHPT. In addition, data from this study will guide physicians as to how best to treat their patients who have PHPT and vitamin D deficiency.
Vitamin D plays a critical role in maintaining bone health, as well as preventing cardiovascular disease, cancer, and various autoimmune diseases, such as diabetes. Vitamin D deficiency is very common in the United States and worldwide, and is now being increasingly recognized and treated. One group in which vitamin D deficiency may be particularly important is patients who have had kidney stones. These patients frequently have elevated levels of calcium in their urine, which is a common and important risk factor for calcium containing kidney stones. Because vitamin D increases absorption of calcium into the blood by the intestines, physicians may be reluctant to prescribe vitamin D therapy to patients with vitamin D deficiency if they also have kidney stones and high amounts of calcium in the urine. They are concerned about the possible risk of increasing the amount of calcium in the urine (and thereby increasing the risk of calcium stones occurring again). However, studies in patients without kidney stones, as well as studies in patients with high calcium levels in the urine, have demonstrated that giving vitamin D is effective and safe and does not increase calcium in the urine. Therefore, the investigators will study the effects of giving vitamin D on the amount of calcium in the urine in patients with a history of kidney stones and elevated calcium in the urine. The investigators will evaluate the safety of giving vitamin D to this particular group of patients.
In cross-sectional and prospective cohort studies, vitamin D deficiency is associated with increased mortality, cardiovascular events including sudden cardiac death and stroke, diabetes, hypertension and impaired function of the immune and musculoskeletal system. The action of vitamin D on the cardiovascular system regulates cardiac function, endothelial and vascular smooth muscle, and, the renin-angiotensin system. Treatment with sufficiently high doses of vitamin D may represent a promising and inexpensive intervention option. To date, there are few data on the effect of cholecalciferol treatment in patients with chronic heart failure. The primary objective of this study is to investigate whether oral vitamin D supplementation improves chronic heart failure (measured with the surrogate parameter of NT-proBNP levels at month 0 and 6).