Abstract

Pigmentary dilution is observed in patients with homocystinuria. Therefore, it is possible that an increase of local homocysteine (Hcy) interferes with normal melanogenesis and plays a role in the pathogenesis of vitiligo. Vitamin B12 and folic acid, levels of which are decreased in vitiligo, are important cofactors in the metabolism of Hcy. Consequently, a nutritional deficiency in either of these two vitamins will result in an increase in homocysteine in the circulation, a finding that we expect to find in vitiligo. To determine the level of Hcy in the blood of patients with vitiligo as a first step in revealing if it has any relationship with the pathogenesis of vitiligo and consequently if this will have an impact on the treatment of vitiligo. Twenty-six patients of both sexes with vitiligo (age range 20-50 years, mean 31.4 +/- 8.09) and 26 age-matched healthy controls were included in the study. After excluding factors that may affect serum Hcy levels, blood samples from patients and controls were obtained for homocysteine determination by enzyme immunoassay. The mean serum level of Hcy was significantly higher in patients with vitiligo than in controls (21.61 +/- 13.28 vs. 13.1 +/- 4.88 micromol L(-1); P < 0.001). The Hcy level was significantly higher in male patients than in female patients (28.67 +/- 15.95 vs. 15.56 +/- 6.2 micromol L(-1); P < 0.001) and in male controls compared with female controls (15.07 +/- 4.61 vs. 12.05 +/- 4.82 micromol L(-1); P < 0.001). The homocysteine level was related to the activity of vitiligo and was significantly higher in patients with progressive disease than in controls (25.4 +/- 14.99 vs. 13.1 +/- 4.88 micromol L(-1); P < 0.001). No significant difference in Hcy levels was found between either untreated vitiligo patients (22.77 +/- 13.36 micromol L(-1)) or patients receiving ultraviolet therapy (20.45 +/- 13.73 micromol L(-1)) and the total patient group (21.62 +/- 13.28 micromol L(-1)). An elevated homocysteine level may be a precipitating factor for vitiligo in predisposed individuals. In view of the biological role of vitamin B(12) and folic acid in Hcy metabolism, we present our recommendations regarding the investigation and treatment of this common disease.

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