الفهرس 
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Abstract
SUMMARY
Vitiligo is defined as an acquired pigmentary anomaly of the skin, predominantly asymptomatic, which does not cause direct physical impairment, manifested by circumscribed depigmented macules and patches due to the disappearance of pigment cells from the epidermis. The prevalence of vitiligo is increasing and involves up to 1–4% of the world population of all races.
Numerous studies have revealed the variety of stigmatization, defined as a process in which skin appearance is negatively judged and persons who are affected experience absence of acceptance because of their visible symptoms: distress, anxiety experienced by patients with vitiligo, patients are often glared at or even avoided for fear of infection of their skin patches or for disgust. Patients have various degrees of emotional disturbances, including low mood, loss of pleasure, poor body image, poor self‐care, low self‐esteem, and high stress.
Throughout the centuries, vitiligo was one of the most important diseases causing discrimination and segregation in certain cultures and was referred to as sweta kusth, meaning white leprosy. In addition, patients had the same mental abuse as leper and affected individuals were unable to find jobs or get married, based upon ancient religious beliefs.
Theories for the cause of vitiligo identify three mechanisms: autoimmune, auto cytotoxic, and neural. The autoimmune hypothesis focuses on genetic data and vitiligo’s association with other autoimmune diseases. The autocytotoxic hypothesis identifies that cytotoxic substance to melanin synthesis present in melanocytes leading to cell death. The neural theory talking about the relation between segmental vitiligo and the neurons beside melanocytes.
The basis of the autoimmune hypothesis based on studies that showed an association between vitiligo and other autoimmune diseases.
IL-33 is a cytokine, encoded by the IL-33 gene, which is a member of the IL-1 family that drives the production of T-helper-2 (Th-2) associated cytokines.
There is a positive correlation between serum IL-33 levels and disease activity, but there is no correlation with the clinical type of vitiligo. This explains a possible systemic role of IL-33 in the pathogenesis of vitiligo.
Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine central to many autoimmune diseases. Inhibition of TNF-alpha has proven to be an effective therapy for patients with inflammatory disorders including psoriasis, generalized progressive vitiligo, psoriatic arthritis, rheumatoid arthritis and ankylosing spondylitis.
This study aimed to estimate the level of IL-33 and TNF-alpha in lesional tissues of patients with vitiligo in comparison with healthy controls.
This is a case control study that was conducted on out-patients attending Beni-Suef University Hospital, 30 patients with vitiligo and 30 healthy controls, Tissue samples was be collected by punch biopsy (4mm) in diameter from Lesion (vitiliginous areas) of the patients and normal skin from the healthy controls.
The main results of the study revealed that:
Patient’s ages ranged from 20 to 50 years old with an average of 32.87 ±10.9 with no statistically significant difference between cases and controls. Of the studied patients with vitiligo; 10 cases were males and 20 were females without a statistically significant difference between cases and controls.
Fifty percent of biopsies were from back area, 16.7% from upper limb and 33.3% from lower limb.
Level of Interlukien-33 in patients with vitiligo was significantly higher as compared with normal healthy controls where the mean values were (129.71 vs. 33.92) in patients with vitiligo and normal healthy controls respectively; (p-value <0.001).
Level of Interlukien-33 in vitiligo lesions had no significant differences in relation to different skin types; (p-values> 0.05).
Level of Tumor Necrosis Factor-α was significantly lowest among studied lesional Vitiligo Skin Type (V) as compared with other skin types; (p-values≤ 0.05). However; no detected significant differences between other skin types.
In conclusion Serum IL-33 levels in patients with vitiligo were significantly increased compared with healthy controls. IL-33 could be considered a reliable marker for increasing disease severity, Tumour necrosis factor (TNF‐α), a proinflammatory cytokine central to many autoimmune diseases, has been implicated in the depigmentation process in vitiligo.
Based on results we recommend for repeating the present study on large geographical scale and larger sample size to emphasize our conclusion.