Vitiligo is a pigmentary disorder that affects 0.38-1.13% of the population in different regions of the world. The pathogenesis of vitiligo is still unknown, but genetic and immunological factors have an important role in the origin of vitiligo .Human leukocyte antigen (HLA) molecules perform a crucial function in the regulation of the immune response.
Subjects and Methods: One hundred subjects were included in this study, 50 patients with vitiligo and 50 normal subjects as a control group. Patients and controls were selected from the attendants of the dermatology and venereology clinic, Benha University Hospital. HLA Class I and II polymorphism HLA-A, B, C, DR and DQ typing was carried out in all patients and controls for class I antigens and on B-enriched suspensions, obtained by resetting with sheep’s red blood cells for class II antigens. The antigenic frequencies of class I and class II from patients and controls were compared. Z-test was used to calculate the P. values. The strength of the association was estimated by relative risk according to Woolf’s formula.
Results: When all the vitiligo patients are compared to controls a significantly increased frequency of HLA-A1(50% versus 20% RR=4), A19 (34% versus 8%, RR=5.926), B16 (16% versus 4%, RR=4.571), CW4 (34% versus 6%, RR=3.5),CW6 (50% versus 30%, RR=2.041), DR4 (42% versus16%, RR=3.812), DR7 (50% versus 10%, RR=8.2) DQ3 (50% versus 30%, RR=2.333) and a significantly decreased frequency of CW3 (26% versus 46%, RR=0.412) and DQ1 (34% versus 56%, RR=0.400) are found Frequencies of CW3 (RR=0.412) and DQ1 (RR=0.400) were significantly decreased. The familial form of vitiligo was associated with a significant increase in HLA-A19 (RR=18.39), A28 (RR=5.1), B16 (RR=10.66), B27 (RR=10.66), B48 (RR=10.66), CW2 (RR=5.1) and DQ3 (RR=5.24). The non-familial form of vitiligo was associated with significant increase in HLA-A1 (RR=5.22) and CW6 (RR=5.24), DR13 (RR=3.97) compared to controls (Table 3). Both familial and non-familial forms of vitiligo was associated with significant increase in HLA-A19, HLA-CW4, DR4 and DR7 compared to controls
Conclusion: The significance of HLA phenotype in the pathogenesis of vitiligo remains to be elucidated. Overall, our results indicate that specific MHC-linked genetic variation contributes to risk of vitiligo. HLA associations with vitiligo contribute evidence that the disease has an autoimmune component to its pathogenesis. The apparent difference in HLA phenotype suggests a different genetic background of familial and no familial vitiligo. Further investigations for other vitiligo-risk factors are necessary. It is known that genetic variation may affect response of patients to medications (pharmacogenetics). So, more studies are needed to assess the effects of HLA phenotypes on response of patients to the different treatment modalities of vitiligo.
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