vitamin D status

In IBD, the immune system-mediated attack is against the gas­trointestinal tract. T cells that preferentially produced the Th1 cytokines (IL-2, IFN-gamma, and tumor necrosis factor alpha) were shown to transfer Crohn’s disease-like symptoms to naive mice, and the production of Th1 cytokines is as­sociated with IBD among humans subjects. In convention­al animal facilities, IL-10 KO mice develop enterocolitis within 9­12 wk of life. Approximately 30% of IL-10 KO mice die af­ter the development of severe anemia and weight loss. Vitamin D deficiency accelerated the development of IBD symptoms among IL-10 KO mice.

In the clinical practice, vitamin D deficiency is common among patients with Crohn’s disease, even when the disease is in re­mission. It is unclear why vitamin D deficiency oc­curs more frequently in IBD; it is probably attributable to the combined effects of low vitamin D intake, malabsorption of many nutrients including vitamin D, and decreased outdoor ac­tivities in climates that are not optimal for vitamin D synthesis in the skin. The standard treatments for patients with IBD include short-term high-dose and long-term low-dose prednisone ther­apy. Prednisone and other corticosteroid thera­pies result in decreased bone mineral density, which increases the risks for vertebral fractures. Vitamin D deficiency has been linked to bone loss among patients with IBD, and bone loss is a problem for up to 50% of patients with IBD. A placebo-controlled study showed that calcium and vitamin D supplementation were effective for preventing bone loss among patients with Crohn’s disease. The hor- monally active form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], is known to increase bone mineralization when administered to experimental animals and human sub­jects. Therefore, vitamin D and/or 1,25(OH)2D3 supple­mentation is warranted for patients with IBD, to maintain bone mineral density and to normalize circulating vitamin D concen­trations.

Vitamin D and infectious diseases

On the basis of the ability of 1,25(OH)2D3 to suppress the de­velopment of various autoimmune diseases and to prolong al- lograft survival, 1,25(OH)2D3 has been recognised as an im­munosuppressive hormone. However, 1,25(OH)2D3 has been shown to have no effect on the susceptibility of mice to infections with Herpes simplex virus or Candida albicans. The doses of 1,25(OH)2D3 chosen were the same doses that had been shown previously to prolong allograft survival. Surprisingly, little is known about the effect of vita­min D status on the ability of the host to fight infections. There is an interesting but mechanistically unsubstantiated link be­tween vitamin D deficiency and cases of tuberculosis. Experimentally, vitamin D deficiency and host resistance to in­fectious diseases have not been studied extensively. One ex­periment in VDR KO mice showed that VDR KO mice exhibited increased granulomatous inflammation (slightly more severe infection) during Schistosoma mansoni infection, compared with WT mice. Little is known about the role of vitamin D and 1,25(OH)2D3 in regulating immune responses to infectious diseases. What is known is somewhat paradoxical, on the ba­sis of the ability of this nutrient/hormone to suppress autoim­mune diseases and prolong transplant survival. Need medication you can’t afford? Buy cialis professional