INTRODUCTION
Alopecia areata (AA) is an organ-specific, T-cell mediated autoimmune disease of anagen-stage hair follicles. A wide range of clinical presentations can occur, from a single patch of hair loss to the complete loss of hair from the scalp (alopecia totalis) or from the whole body (alopecia universalis).1 The disease has long been known to have HLA Class I and II associations and to occur with various autoimmune disorders, such as rheumatoid arthritis (RA), type I diabetes mellitus (DM), vitiligo, and thyroiditis.1,2 The most characteristic histological feature of AA is a perifollicular lymphocytic infiltrate around the anagen hair bulb, comprised predominantly of CD4+ T cells, whereas the few intrafollicular lymphocytes tend to be CD8+ T cells.3 The treatment of AA aims to reduce inflammation and stimulate hair regrowth. Different treatment modalities have been suggested, but none of them is a definitive cure; therefore, there is still a need for new therapeutic alternatives.
Recent researchers have demonstrated that apart from their calcium-related actions, vitamin D and its analogues have potent immunomodulatory activities, and poor vitamin D status has been found to be associated with several autoimmune diseases.4,5 Our previous study demonstrated that 25(OH)D levels were decreased in AA and its levels were inversely correlated with disease severity.6 Recently, vitamin D analogues have been used as topical treatment for psoriasis, and clinical trials for its use in autoimmune diseases are underway.7 This finding suggests that vitamin D deficiency might be an environmental trigger for the induction of autoimmunity, and the administration of vitamin D may perform therapeutic and preventive action in different autoimmune diseases.7,8 On the other hand, it has been demonstrated that vitamin D receptors (VDRs) are strongly expressed in the key structures of hair follicles. The expression of VDRs in keratinocytes is necessary for the maintenance of the normal hair cycle.9 It has also been shown that a lack of VDRs reduces epidermal differentiation and hair follicle growth.10 In addition, the alopecia phenotype has been observed in VDR knockout mice and in patients with hereditary 1,25(OH)2D3-resistant rickets.9,10
For these reasons, we performed this retrospective study to evaluate the efficacy of a topically applied vitamin D analogue, calcipotriol, in AA, as to the best of our knowledge, no previous trials have been done.
SUBJECT AND METHODS
Patients
This retrospective study included 48 patients with mild-to-moderate (S1 or S2 grade) patchy AA treated with calcipotriol cream between September 2012 and December 2014. Data used in this study were collected retrospectively from the treatment charts of the patients followed up at our derma-