الفهرس 
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Abstract
Systemic lupus erythematosus is an autoimmune disorder in which the body‟s immune system mistakenly attacks healthy tissue in many parts of the body. It affects many body systems involving skin, joints, kidney, blood vessels and nerves. Multiple factors are linked with development of SLE as genetic, immunoregulatory, hormonal and environmental factors. Juvenile systemic lupus erythematosus is an uncommon disorder with an incidence rate of approximately 0.3-0.9 per 100,000. Females are commonly affected with mean of age between 11-12 years. Cytokines play a promoting role in the maturation, activation and differentiation of a variety of immune cells involved in the immune regulation of SLE. Common initial and chronic complaints include fever, malaise, joint pain, muscle pain, fatigue. Because these symptoms are so often seen in association with other diseases, these symptoms and signs are not part of the diagnostic criteria for SLE. When occurring in conjunction with other signs and symptoms however, they are considered suggestive. Arthritis, skin rash, photosensitivity and nephritis are the most common clinical presentation in SLE. For diagnosis of SLE, many laboratory tests as CBC, urine analysis, renal functions, ESR, CRP and ANA must be done. Systemic lupus erythematosus disease activity index (SLEDAI) can be used for assessment of disease activity in SLE patients. Interleukin 33, which was identified as a member of the IL-1 family, is now recognized to have a key role in innate and adaptive immunity, contributing to tissue homeostasis and responses to environmental stresses. The discovery of IL-33 was preceded by the finding of its unique receptor suppression of tumorigenicity 2 (ST2; also known as IL-1R1, IL-33R), which was identified as a marker that is selectively expressed by T-helper 2 (TH2) cells but not TH1 cells. It was reported that ST2 protein was identified in the serum of SLE, rheumatoid arthritis and other rheumatic disease patients. However, information regarding the role of the IL-33/ST2 signaling pathway in SLE is still limited. The aim of this study was to estimate the serum levels of interleukin-33 in JSLE patients in comparison to healthy controls and to correlate its level with clinical & laboratory findings and with disease activity. This clinical study included subjects divided into the following two groups: - group I: 25 patients with JSLE. group II: 25 healthy age and sex matched individuals who served as a control group. All JSLE patients in this study had been subjected to complete history taking, clinical examination, laboratory investigations including complete blood count, complete urine analysis, 24 hrs. urine collection for proteinuria, ESR, CRP, liver and renal function tests , ANA, levels of anti-dsDNA antibodies, complements c3 and c4 by ELISA, renal biopsy when indicated and radiological investigations such as pelvic abdominal ultrasound & chest X-Ray. The following results were obtained: 1. Age of JSLE patients ranged from 6 years to 16 years with a mean of 13.64 years ± 2.48 (SD) and the incidence was higher in females than males. 2. There was a significant increase in serum IL-33 levels in JSLE patients than control group indicating that IL-33 may play a role in pathogenesis of SLE. 3. There was a significant elevation of the serum IL-33 levels in patients affected with lupus nephritis class III, IV compared to patients who did not undergo renal biopsy indicating that IL-33 may play a role in kidney damage and inflammation. 4. There was a significant positive correlation between IL-33 and serum creatinine, blood urea nitrogen, CRP, 24 hrs urine proteinuria and SLEDAI indicating that IL-33 may have a role in active phase of SLE. 5. There was a significant negative correlation between IL-33 with C3 serum levels and C4 serum levels indicating that IL-33 may play a role during disease activity.