الفهرس 
Introduction and Aim of the Work
VitiligoOnly 14 pages are availabe for public view
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Abstract
Vitiligo is a skin disorder with an autoimmune basis. Humoral and cell-mediated immune mechanisms are likely to be involved in melanocyte destruction of vitiligo. Abnormal immune responses and changes in the level of cytokines frequently observed in vitiligo patients suggest that cytokine imbalance may be responsible for development of this autoimmune disease. IL-33, member of the IL-1 family, has been described as an epithelial alarmin defense system. Studies found that IL-33 and ST2 expression is increased in vitiligo skin lesions, and that serum IL-33 expression is raised in patients with vitiligo. Keratinocyte-derived IL-33 may induce melanocyte death by regulating cytokines in the cellular microenvironment. Subjects and Methods : This is a prospective case-control study was conducted on 3 groups of subjects : 30 consecutive patients suffering from active non-segmental vitiligo, 30 consecutive patients with stable non-segmental vitiligo and 30 age- and sex-matched healthy controls were recruited from Mansoura University Hospital Outpatient Clinics of Dermatology. None of the patients had immune-mediated comorbidities, and those participating in the study had to refrain from vitiligo treatment for at least 1 month before the study. All participants were subjected to detailed history taking, complete dermatological examination, and laboratory investigations including assessment of IL-33 by enzyme-linked immunosorbent assay. Clinical assessment of vitiligo lesions was performed to determine the distribution, clinical variant, and extent (VES). Results : The mean age of patients with stable vitiligo, patients with active vitiligo, and control group was 34.77 years, 33.97 years, and 33.67 years, respectively. Each group comprised 18 males (60%) and 12 females (40%). No significant intergroup difference was detected between the mean value for age, sex or occupation. The median age of onset did not differ significantly between active (31.07 years) and stable (28.5 years) cases; while the disease median duration differed significantly between active (1 year) and stable (4 years) cases. The median serum IL-33 level was significantly higher in all vitiligo cases (11.39 pg/ml) when compared to control group (4.61 pg/ml), and the difference was statistically significant. In addition, median serum level of serum IL33 was significantly higher (33.19 pg/ml) in active vitiligo cases when compared to the stable group (5.74 pg/ml), and there was a statistically significant difference between control, stable and active subjects. Comparison of serum IL-33 levels between different clinical types of vitiligo in this study showed no statistically significant difference. There was a weak, statistically non-significant, positive correlation of IL-33 serum levels with extension of vitiligo (VES) and disease activity. The best cut off point for serum IL-33 as a diagnostic index for vitiligo was determined to be ≥ 5.8209 pg∕ml, which was able to predict vitiligo with 71.7% sensitivity and 69% specificity. In addition, the best cut off point for IL-33 as a diagnostic index for discrimination between active and stable vitiligo cases was determined to be ≥ 10.8845 pg∕ml, which was able to predict active vitiligo with 100% sensitivity and 93.3% specificity. Linear regression for prediction of extent and activity of vitiligo revealed that serum IL-33 levels do not have significant regression coefficient. Conclusion : Serum IL-33 levels in patients with vitiligo were significantly increased compared with controls, which imply an involvement of IL-33 in vitiligo development and suggest possible therapeutic potential of targeting this cytokine for vitiligo amelioration. IL-33 levels were also found to be higher in patients with active disease within the last year compared to other patients with stable disease. These data suggest that higher IL-33 can be associated with more clinical complications and disease progression in the vitiligo patients.