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Trying to clarify the issue, in 2013, Samochocki et al. [66] carried out a study in which 20 out of 95 patients were selected for vitamin D supplementation (2000?IU of oral cholecalciferol daily); 25(OH)D mean concentrations were very low, between 4 and 15?ng/mL. After supplementation both mean objective SCORAD and SCORAD index were significantly lower than before. Similarly, after supplementation, all SCORAD parameters, except lichenification, were significantly decreased. After 3 months of PDK4 supplementation most patients' vitamin D levels switched from selleck screening library (n = 12). Before heliotherapy, 17 of 23 patients had vitamin D deficiency; after 2 weeks of therapy, only 4 patients remained deficient. Of note, a positive correlation find more was evidenced between the increase in vitamin D levels and the decrease in the SCORAD index in March but not in January. The same authors carried out a later study [69] on 18 patients with AD. Of these, 16 were vitamin D deficient and underwent 15 sessions of narrowband UVB. This therapy resulted in a significant increase in serum vitamin D levels. Moreover, a significant decrease in mean SCORAD was recorded. 10.3. Topical Therapy Certain observations further aimed at clarifying the role of topical vitamin D analogues. Evidence shows that topical application of the 1,25-dihydroxyvitamin D analogue is able to elicit an AD-like eruption in mice [70]. This reaction has been clarified to be not a simple irritant contact dermatitis, but rather a VDR- and thymic stromal lymphopoietin-dependent process [71, 72]. 11. Conclusions Epidemiological and clinical evidences indicate a beneficial role for vitamin D in AD. These observations are supported by basic research data showing that vitamin D acts on many different immune cell functions.