Scientific articles
Treatment of total/universal/focal alopecia with Vitamin D and matched treatments: three case studies
Dimitrios T. Papadimitriou, Christina Bothou, Eleni Dermitzaki, Alexios Alexopoulos, George Mastorakos
Index
INTRODUCTION: Alopecia areata (AA) is an inflammatory disease with autoimmune, environmental, and hereditary factors that affects the hair follicle, presenting as limited hair loss on the scalp (Focal, AF), total scalp hair loss (Total, AT), or both hair and body hair loss (Universal, AU). There are many treatments, however, there is no 100% effective cure. Vitamin D deficiency in AA/AT/AF patients affects disease severity and duration: histologically speaking, it is inversely proportional to inflammation.
CLINICAL CASES: Three girls with AT (P1), AU (P2) and AF (P3) aged 1 year, 5 years and 5 years, respectively. As for Patients 1 and 2, each individual treatment employed for two years did not yield results. The first step was supplementation with oral cholecalciferol 2000/4000 IU/d, which lasted six months, with no effect recorded. Next, the route of immunomodulation was taken through the use of calcitriol combined with oral paracalcitol. With the use of Calcitriol 0.5 mcg/d, P1 achieved hair regrowth in the first 6 months. After 4 years, she suffered a relapse, with loss of eyebrow hair, which was resolved by doubling the dose of calcitriol to 0.5 mcg x 2/d; the results obtained have been stable for 6 years. Using calcitriol 0.25mcg x 3/d, P2 developed asymptomatic hypercalcemia-hypercalciuria, which were resolved by modifying therapy with the use of paracalcitol 2mcg x 3/d; the patient continued to have mild hypercalciuria. Hair growth was observed after 6 months that only stabilized after 12 months. AF in P3 was completely cured in 3 months using a very high daily dose (8000 IU) of cholecalciferol.
CONCLUSIONS: Vitamin D may have played a key role in the immunomodulation of AT/AU/AF, to be confirmed upon further experimental clinical cases.
©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
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