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The Prevalence of Vitamin D Deficiency and Effects of Vitamin D Supplementation in HIV-1 Infected Patients

2014-08-27 03:45:31 | BioPortfolio

Summary

The purpose of this study is to determine the effect of normalization of vitamin D levels on bone density, immune and adipocyte function in HIV1-seropositive patients.

Description

Vitamin D deficiency is common in, especially black, HIV-seropositive patients. Vitamin D deficiency can be caused by lack of sunlight and/or insufficient vitamin D intake via diet. The HIV infection itself and antiretroviral therapy (ART) may also cause vitamin D deficiency. ART interferes with cytochrome p450 activity and as such might affect vitamin D metabolism.

Vitamin D has several important physiological functions such as 1. regulation of calcium and phosphate homeostasis, 2. immunomodulatory properties and 3. effects on adipocyte differentiation. Low vitamin D levels lead to decreased bone mineralization, eventually resulting in rachitis(children) or osteomalacia (in adults). In addition vitamin D deficiency leads to secondary hyperparathyroidism, which leads to even more bone matrix demineralization. In HIV infected persons the overall prevalence of osteopenia and osteoporoses is 14-84% and 0-45% respectively. Vitamin D has been suggested to play a role in HIV-associated bone disorders. The vitamin D status also affects the host defence in HIV patients; a significantly lower CD4 cell count has been found in patients with 1,25(OH)vitamin D deficiency. Furthermore, the influence of vitamin D on adipocyte differentiation and the effect of HAART on vitamin D levels might be relevant for changes in fat distribution and the development of insulin resistance as is seen days after initiation of HAART.

Vitamin D is metabolized in the body trough cytochrome P450 enzymes. HAART might interact with vitamin D metabolism on basis of CYP3A4, which plays an important role in clearance of most antiretroviral agents and also showed to be a vitamin D 24 and 25-hydroxylase in vitro. We hypothesize that PI’s lead to lower 1a,25(OH)2D3 by suppressing 1a- and 25-hydroxylase activity.

The results of our pilot showed that 25(OH)D deficiency is common among HIV patients. Seen the diversity of functions of vitamin D, we hypothesize that it’s beneficial for the patients to have a normal vitamin D status. Therefore, supplementation of vitamin D is warranted.

In this study we want to investigate if, despite the complex interaction between HAART/ HIV and vitamin D metabolism, supplementation of colecalciferol (2000 IU daily) will lead to normalization of the vitamin D levels. Furthermore, we want to study the effects of normalization of vitamin D levels on bone mineral density, immune and adipocyte function. Therefore we will do a prospective, randomized, double-blind, placebo-controlled vitamin D intervention study in vitamin D deficient HIV1-seropositive patients.

Study Design

Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double-Blind, Primary Purpose: Treatment

Conditions

Vitamin D Deficiency

Intervention

colecalciferol

Location

Radboud University Nijmegen Medical Center
Nijmegen
Netherlands
P.O. BOX 9101

Status

Recruiting

Source

Radboud University

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:45:31-0400

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Medical and Biotech [MESH] Definitions

A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)

A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)

A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)

A nutritional condition produced by a deficiency of VITAMIN A in the diet, characterized by NIGHT BLINDNESS and other ocular manifestations such as dryness of the conjunctiva and later of the cornea (XEROPHTHALMIA). Vitamin A deficiency is a very common problem worldwide, particularly in developing countries as a consequence of famine or shortages of vitamin A-rich foods. In the United States it is found among the urban poor, the elderly, alcoholics, and patients with malabsorption. (From Cecil Textbook of Medicine, 19th ed, p1179)

A nutritional condition produced by a deficiency of VITAMIN B 6 in the diet, characterized by dermatitis, glossitis, cheilosis, and stomatitis. Marked deficiency causes irritability, weakness, depression, dizziness, peripheral neuropathy, and seizures. In infants and children typical manifestations are diarrhea, anemia, and seizures. Deficiency can be caused by certain medications, such as isoniazid.

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