RESUMO
BACKGROUND: Vitamin D has significant effects on the immune system and thereby on the pathogenesis of rosacea. However, there is a lack of information on the vitamin D status and vitamin D receptors (VDRs) of patients with rosacea. AIM: To evaluate the role of vitamin D in rosacea susceptibility. METHODS: A case-control study was conducted, enrolling patients with rosacea and healthy controls (HCs). Five VDR gene single nucleotide polymorphisms (SNPs) (Cdx2, FokI, ApaI, BsmI and TaqI) and serum 25-hydroxyvitamin D3 [25(OH)D3 ] levels were compared between patients and HCs. RESULTS: The study enrolled 60 patients (M/F: 14/46) and 60 age- and sex-matched HCs (M/F: 14/46). Age (mean ± SD) was 48 ± 11 years for both groups. The serum 25(OH)D3 levels (median ± interquartile range) were higher in patients with rosacea (12.9 ± 6.8 ng/mL) than in HCs (10.5 ± 3.7 ng/mL) (P < 0.001). Subjects with high serum 25(OH)D3 levels had a 1.36-fold increased risk of rosacea (95% CI 1.17-1.58). Heterozygous and mutant ApaI polymorphisms increased rosacea risk by 5.26-fold (95% CI 1.51-18.35) and 3.69-fold (95% CI 1.19-11.48), respectively, whereas mutant TaqI polymorphisms decreased the risk by 4.69 times (95% CI 1.37-16.67). Heterozygosity for Cdx2 alleles increased rosacea risk, whereas wildtype ApaI and mutant TaqI alleles decreased it. CONCLUSIONS: The present study suggests that an increase in vitamin D levels may contribute to the development of rosacea. ApaI and TaqI polymorphisms, and heterozygous Cdx2, wildtype ApaI and mutant TaqI alleles were significantly associated with rosacea. These results indicate a possible role of vitamin D and VDR pathways in the pathogenesis of rosacea, although causality could not be assessed.
