01561nas a2200205 4500000000100000008004100001260005600042653001200098653001100110653001200121653002600133653001400159100001600173700001600189245003800205300001100243490000800254520107900262022001401341 2012 d c2012 JunbLippincott Williams & WilkinsaHagerstown10aAnimals10aHumans10aleprosy10aReceptors, Calcitriol10aVitamin D1 aLuʼoʼng K1 aNguyên LTH00aRole of the vitamin D in leprosy. a471-820 v3433 a
There is an evidence of abnormal metabolism in the vitamin D endocrine system of patients with leprosy. Bone deformities usually occur in patients with leprosy. Genetic factors, such as the vitamin D receptor, the major histocompatibility complex region, chromosome 20, human toll-like receptors, the natural resistance-associated macrophage protein 1, the nucleotide-binding oligomerization domain containing 2, phosphate-regulating gene with homologies to endopeptidase on the X chromosome and the tyrosine kinase growth factor receptor-ErbB-2, contribute to both vitamin D status and leprosy. The role of vitamin D in leprosy has been demonstrated by its effects on Bacillus Calmette-Guérin vaccination, vascular endothelial growth factor, prostaglandins, reactive oxygen species, reactive nitrogen intermediates, matrix metalloproteinases, antiphospholipid syndrome and the nerve growth factor. Vitamin D plays a definite role in leprosy. Vitamin D, itself, may effect on leprosy through the vitamin D receptors or may influence leprosy through indirect effects.
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