Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease with intermittent flares and debilitating effects on the patient’s quality of life. It is the most common skin disorder in children, affecting approximately 15% to 20% worldwide. Atopic dermatitis is clinically distinguished by pruritus, eczematous plaques, and a defective epidermal barrier. The pathology of AD is not entirely understood. It involves a complex interplay of dysfunctions of immune response, genetic and environmental factors. Currently, the conventional AD treatments include immune modulatory agents, such as topical and/or oral steroids and topical calcineurin inhibitors. The control of patients with AD may be difficult to be achieved in some patients; this suggests the presence of some other associated factors. The findings obtained in both clinical and observational studies revealed that the deficiency of vitamin D (Vit D) may be a factor to be considered in the pathophysiology of AD.

Vitamin D3 correlate well with synthesis of proteins that are necessary for skin barrier function, these mechanisms suggest a role of 1,25-dihydroxyvitamin D in modulating AD severity. Many researches have investigated difference between 25-dihydroxyvitamin D 25(OH) D levels in AD pediatric patients and matched healthy control. A meta-analysis of these studies found a mean deference of −16 nmol/L in pediatric AD patients compared to healthy control. There is growing interest in the possible role of vit D deficiency in the development of AD. The aggravation of AD in winter, especially in higher-latitude countries, where serum 25(OH)D levels tend to be predominantly low in this season, has been documented. In addition, genetic polymorphisms of the Vit D receptor have been identified as contributor to the development of AD.

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