Topical Calcipotriol Therapy for Mild-to-Moderate Alopecia Areata: A Retrospective Study
June 2015 | Volume 14 | Issue 6 | Original Article | 616 | Copyright © June 2015
Asli Aksu Çerman MD, Sezgi Sarıkaya Solak MD, İlknur Altunay MD, and Nihal Asli Küçükünal MD
Şişli Hamidiye Etfal Training and Research Hospital, Dermatology Department, Istanbul, Turkey
BACKGROUND: Alopecia areata (AA) is considered a T-cell mediated autoimmune disease characterized by patchy loss of hair from scalp and other body parts with no definitive treatment. Calcipotriol is a vitamin D analogue and a potent immunomodulatuary molecule. In recent studies, low serum vitamin D levels have been observed in patients with AA and various autoimmune diseases. Previous reports have also described the effects of vitamin D on hair follicles.
OBJECTIVE : The aim of the study was to evaluate the efficacy and safety of topical calcipotriol for the treatment of mild-to-moderate patchy AA.
METHOD: Forty-eight patients with mild-to-moderate AA were enrolled in the retrospective, 12-week trial. Calcipotriol cream was applied to the affected areas twice a day. Severity of Alopecia Tool (SALT) score and hair regrowth rate were calculated at baseline and at 3, 6, 9, and 12 weeks.
RESULTS: At week 12, the total response was achieved in 69.2% of patients. When the mean SALT score of patients at week 12 was compared to that of patients at baseline, the value at week 12 was significantly lower (P
= 0.001). A regrowth score (RGS) ≥ 3 (hair regrowth of ≥ 50%) was observed in 75% of patients, whereas a RGS ≥ 4 (hair regrowth of ≥ 75%) was observed in 62.5% of patients and the complete regrowth rate (hair regrowth= 100%) was 27.1%.
CONCLUSION: Calcipotriol may serve as a safe and effective treatment option in mild-to-moderate patchy AA, and calls for more extensive controlled studies with this treatment. J Drugs Dermatol
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
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-