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      Vitamin D deficiency in alopecia areata

      1 , 1 , 1
      British Journal of Dermatology
      Wiley

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          Abstract

          Alopecia areata (AA) is a T cell-mediated autoimmune disease that causes inflammation around anagen-stage hair follicles. Insufficient levels of vitamin D have been implicated in a variety of autoimmune diseases. Previous reports have described the effects of vitamin D on hair follicles.

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          Vitamin D and autoimmunity: new aetiological and therapeutic considerations.

          Vitamin D is frequently prescribed by rheumatologists to prevent and treat osteoporosis. Several observations have shown that vitamin D inhibits proinflammatory processes by suppressing the enhanced activity of immune cells that take part in the autoimmune reaction. Moreover, recent evidence strongly suggests that vitamin D supplementation may be therapeutically beneficial, particularly for Th1-mediated autoimmune disorders. Some reports imply that vitamin D may even be preventive in certain disorders such as multiple sclerosis and diabetes type 1. It seems that vitamin D has crossed the boundaries of calcium metabolism and has become a significant factor in a number of physiological functions, specifically as a biological inhibitor of inflammatory hyperactivity.
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            Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease.

            Most humans depend on sun exposure to satisfy their requirements for vitamin D. Solar ultraviolet B photons are absorbed by 7-dehydrocholesterol in the skin, leading to its transformation to previtamin D3, which is rapidly converted to vitamin D3. Season, latitude, time of day, skin pigmentation, aging, sunscreen use, and glass all influence the cutaneous production of vitamin D3. Once formed, vitamin D3 is metabolized in the liver to 25-hydroxyvitamin D3 and then in the kidney to its biologically active form, 1,25-dihydroxyvitamin D3. Vitamin D deficiency is an unrecognized epidemic among both children and adults in the United States. Vitamin D deficiency not only causes rickets among children but also precipitates and exacerbates osteoporosis among adults and causes the painful bone disease osteomalacia. Vitamin D deficiency has been associated with increased risks of deadly cancers, cardiovascular disease, multiple sclerosis, rheumatoid arthritis, and type 1 diabetes mellitus. Maintaining blood concentrations of 25-hydroxyvitamin D above 80 nmol/L (approximately 30 ng/mL) not only is important for maximizing intestinal calcium absorption but also may be important for providing the extrarenal 1alpha-hydroxylase that is present in most tissues to produce 1,25-dihydroxyvitamin D3. Although chronic excessive exposure to sunlight increases the risk of nonmelanoma skin cancer, the avoidance of all direct sun exposure increases the risk of vitamin D deficiency, which can have serious consequences. Monitoring serum 25-hydroxyvitamin D concentrations yearly should help reveal vitamin D deficiencies. Sensible sun exposure (usually 5-10 min of exposure of the arms and legs or the hands, arms, and face, 2 or 3 times per week) and increased dietary and supplemental vitamin D intakes are reasonable approaches to guarantee vitamin D sufficiency.
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              Vitamin D3: a helpful immuno-modulator.

              The active metabolite of vitamin D, 1α, 25-dihydroxyvitamin D3 [1,25(OH)(2) D3], is involved in calcium and phosphate metabolism and exerts a large number of biological effects. Vitamin D3 inhibits parathyroid hormone secretion, adaptive immunity and cell proliferation, and at the same time promotes insulin secretion, innate immunity and stimulates cellular differentiation. The role of vitamin D3 in immunoregulation has led to the concept of a dual function as both as an important secosteroid hormone for the regulation of body calcium homeostasis and as an essential organic compound that has been shown to have a crucial effect on the immune responses. Altered levels of vitamin D3 have been associated, by recent observational studies, with a higher susceptibility of immune-mediated disorders and inflammatory diseases. This review reports the new developments with specific reference to the metabolic and signalling mechanisms associated with the complex immune-regulatory effects of vitamin D3 on immune cells. © 2011 The Authors. Immunology © 2011 Blackwell Publishing Ltd.
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                Author and article information

                Journal
                British Journal of Dermatology
                Br J Dermatol
                Wiley
                00070963
                June 2014
                June 2014
                June 19 2014
                : 170
                : 6
                : 1299-1304
                Affiliations
                [1 ]Dermatology Department; Şişli Etfal Training and Research Hospital; Halaskargazi Cad. 34371 Şişli-Istanbul Turkey
                Article
                10.1111/bjd.12980
                24655364
                3adee94e-1b1c-4ee1-8cf0-63f74f3fcafc
                © 2014

                http://doi.wiley.com/10.1002/tdm_license_1.1

                Product
                Self URI (article page): http://doi.wiley.com/10.1111/bjd.12980

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