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
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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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