Table of Contents:

Zinc

Zinc acts by regulation of gene expression and also acts as a cofactor for superoxide dismutase. Adequate cellular levels of zinc are also needed to prevent cellular apoptosis. Decreased zinc levels activate caspase leading to cell death [87, 88]. In a study by Shameer et al., vitiligo patients were found to have 21.6 % lower level of serum zinc in comparison to controls [88]. Yaghoobi et al. carried out a randomized trial with 35 patients of vitiligo receiving topical corticosteroids with or without oral zinc sulfate supplementation in a dose of 220 mg, two capsules per day in teenager and adults, and 10 mg/kg of capsule or syrup for children. At 4 months, response to treatment was higher in the group receiving oral zinc supplementation [89].

Zinc supplementation has shown good results on concomitant treatment with topical corticosteroids, but further studies are needed. The only limiting adverse effect is gastrointestinal irritation with oral zinc therapy [89].

Minocycline

Minocycline is an antibiotic with anti-inflammatory and antioxidant property. In a study by Parsad et al., daily treatment with minocycline (100 mg once daily). After 4 weeks of treatment, minocycline was effective in halting the progression of vitiligo both during and after therapy [90]. Further research, however, is needed to elucidate the efficacy of minocycline therapy in vitiligo.

Vitamin D

Many studies have identified a possible correlation between low vitamin D levels and autoimmunity. A study done by Silverberg and Silverberg showed very low levels (<15 ng/ml) of 25-hydroxy vitamin D levels in patients with vitiligo vulgaris [91]. It has also been shown in a study by Sehrawat et al. that levels of 25-hydroxy vitamin D were found to increase significantly following increase in the cumulative dose of NBUVB [92]. A study conducted by Finamor et al. has showed that daily oral supplementation with 35,000 IU of vitamin D for 6 months showed significant repigmentation in 14 out of 16 vitiligo patients [93].

 
Source
< Prev   CONTENTS   Source   Next >