SUPEROXIDE DISMUTASE 1 AND 2 GENE POLYMORPHISM IN TURKISH VITILIGO PATIENTS
Tuna A1, Ozturk G1, Gerceker TB1, Karaca E2,*, Onay H2, Guvenc SM2, Cogulu O2
*Corresponding Author: Emin Karaca, M.D., Associacte Professor, Department of Dermatology and Venerology, Faculty of Medicine, Ege University, Kazım Dirik mah, Izmir, Turkey. Tel: +90-232-3903961-+90-532-2579285. Fax: +90-232- 3903971. E-mail: karacaemin@gmail.com
page: 67

RESULTS

A total of 101 vitiligo patients; 58 women, (57.4%) and 43 men (42.6%) were enrolled in the study. The mean age was 37.4 ± 15.2; range 7-68 years. The control group consisted of 99 healthy volunteers; 50 women (50.5%) and 49 men (49.5%), with a mean age of 36.6 ± 12.6, range 18-69. In terms of age and gender, no statistical difference existed between the groups. The median duration of vitiligo was 9.0 years (range 1–35 years). A family history of vitiligo was noted in firstdegree relatives of 23 patients (22.7%). With regard to vitiligo type, 46 patients were focal (45.5%), 25 acrofacial (24.7%), 21 generalized (20.7%), four segmental (3.9%), three universal (2.9%) and two patients were classified as mixed (1.9%). Results can be seen in Table 1. The comorbidities in vitiligo patients were as follows: Hashimoto’s thyroiditis 12 patients (11.8%), DM 11 patients (10.8%), pernicious anemia two patients (1.9%). When considering the distribution of the comor-bidities between the vitiligo and the control group (p = 0.431), no statistical difference was revealed. Similarly, when genotypes of SOD1 35 AA and AC were compared between groups (Table 2), the distribution rate was considered insignificant. There was no statistical difference for genotype and allele frequency between the groups (p = 0.21) (Table 3). However, when the patient cohort and control group were compared for the presence of the SOD2 Ala9Val (C/T) polymorphism, the distribution of the genotypes [p = 0.047, odds ratio (OR) = 2.075, 95% confidence interval (95% CI) = 1.008-4.272] was considered significant. The genotype distribution in vitiligo and the control group was as follows: CC 25.7%, CT 36.6%, TT 37.6%; CC 35.3%, CT 40.4%, TT 24.2%) (Table 2). In the TT genotype, relative risk for the development of vitiligo was found to have increased 2-fold. The T allelic frequency was determined as 76.2% in the patient cohort, with 62.67% for the control group, while C allelic frequency was 23.8% in the patients compared to 37.4% for the control group. There was no significant difference for allele frequency (p = 0.46) (Table 2). More common alleles of both polymorphisms were considered as reference alleles. Logistic regression analysis showed no significant association between SOD1 35 A/C polymorphism (AA vs. AC: OR = 0.380, 95% CI: 0.072-2.005, p = 0.271) and SOD2 Ala9Val (C/T) polymorphism (CC vs. CT: OR = 1.75, 95% CI: 0.889-3.446, p = 0.106). However, a significant association between cases and controls in the SOD2 Ala9Val (C/T) polymorphism (CC vs. TT: OR = 2.158, 95% CI: 1.044-4.462, p = 0.038) (Table 3) was seen. Analysis also confirmed that the presence of the T allele of SOD2 Ala9Val (C/T) polymorphism increased the risk of vitiligo significantly (OR = 0.792, 95% CI: 0.648-0.968, p = 0.022) (Table 3).



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