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العنوان
Serum Interleukins 2 and 10 in Juvenile Systemic Lupus Erythematosus :
المؤلف
Abo-Ali, Amera Sobhi.
هيئة الاعداد
باحث / اميرة صبحي ابو علي
مشرف / ماهر احمد عبد الحافظ
مشرف / امل سعيد البنداري سعد
مشرف / هند حسن عبد النبي
مشرف / لا يوجد
الموضوع
Pediatric.
تاريخ النشر
2020.
عدد الصفحات
106 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب الأطفال ، الفترة المحيطة بالولادة وصحة الطفل
تاريخ الإجازة
20/1/2021
مكان الإجازة
جامعة طنطا - كلية الطب - الاطفال
الفهرس
Only 14 pages are availabe for public view

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Abstract

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by dysregulation of the immune system, involving the hyperactivity of T- and B-lymphocytes, the production of auto-antibodies, and the formation of immune complexes causing organ damage by deposition in host tissues. The clinical manifestations of the disease, which are remarkably diverse, include fever, erythematous rash, polyarthralgia and arthritis, polyserositis, anemia, and thrombocytopenia along with renal, neurological and cardiac abnormalities, such as pericarditis, myocarditis and endocarditis. Rates of organ involvement are higher in children. The pathogenesis of SLE is complex and multifactorial; it involves environmental, hormonal, drug induced and immunological factors in a genetically predisposed individual. Both innate and adaptive immunity contribute to tissue damage. Cytokines play an important and diverse role in the pathogenesis of SLE and their balance determines disease activity. Cytokines produced by CD4+ helper T (Th)lymphocytes are thought to regulate the function of the immune system, and they are functionally grouped into Th1and Th2 cytokines. The former includes interleukin (IL)-2 which induce cellular immunity, and the latter include IL-10 which stimulate antibody production and induce humoral immunity. An overproduction of Th2 cytokines, which resulted in B-cell hyperactivity, has been demonstrated in patients with SLE. However, it has also been reported that the abnormality of Th1 cytokines is involved in the pathogenesis of SLE. Thus, defective regulation of both Th1 and Th2 cytokines expression has been suggested to participate in promoting or inhibiting SLE. The objective of this work was to measure the serum level of cytokines (IL-2, IL-10) in children with SLE and evaluate their relation to disease activity. This study was done at Pediatric Nephrology unit, Pediatric Department, Tanta University Hospital, during the period from May 2018 to May 2020. The study included the following three groups: G 1: Included 30active j-SLE patients (SLEDAI < 4). G 2: Included 30 inactive j-SLE patients (SLEDAI ≥ 4) . G 3: Included 30healthy children of matched age and sex. All these subjects were subjected to the following: 1. Full history taking: including personal, family, present and past history. 2. Clinical Evaluation: - General, regional and systemic examination as body weight, height, and vital signs such as heart rate and blood pressure. Depend on assessment the clinical manifestations using SLEDAI index. 3. Investigations: - CBC. - ESR, CRP. - Serum creatinine, blood urea. - 24-hour urinary protein . - Serum C3, C4. - Serum antinuclear antibodies (ANA) & anti-DNA (using ELISA). - Renal biopsy with histo pathological examination in cases with renal affection. - Serum interleukin 2 (IL-2) and interleukin 10 (IL-10) levels were measured by an enzyme linked immunosorbent assay (ELISA) kit. The results of the present study revealed that: There was significant increase of SBP and DBP in Active patients with j-SLE as compared to Inactive patients with j-SLE and Controls. Females-to-male ratio of the groups was (5:1). Hemoglobin, Platelets and TLC levels were significantly decreased in patients with active disease with mean (9.82 ± 1.50 gm / dl), (149.87 ± 57.8) and (3.06 ± 0.74) respectively when compared to patients with inactive disease with mean (11.33 ± 1.12 gm / dl), (286.87 ± 84.80) and ( 7.73 ± 2.60) respectively. There was significant increase between SLE patients with active disease and SLE patients with inactive disease as regard 1sthr and 2ndhr ESR (p value = 0.001*). CRP levels were significantly higher in patients with active disease when compared to patients with inactive disease (P value = 0.001*). Creatinine had no significant difference between Active and Inactive groups (P value =0.892). Blood urea was significantly higher in patients with active disease when compared to patients with inactive disease (P value = 0.003*). Serum albumin levels were significantly decreased in patients with active disease with mean (3.13 ± 0.67 gm/ dl) when compared to patients with inactive disease with mean (3.78 ± 0.34 gm/ dl). We found significant increase between SLE patients with active disease and SLE patients with inactive disease as regard 24hr protein in urine (p value = 0.001*). The serum levels of C3 and C4 were found to be significantly reduced in patients with active disease as compared to patients with inactive disease. ANA level was significantly higher in patients with active disease {+ve 29(96.7%)}when compared to patients with inactive disease{+ve 20(66.7%)} and anti-ds-DNA level was significantly higher in patients with active disease{+ve 28(93.3%)} when compared to patients with inactive disease{+ve 13(43.3%)}. SLEDAI score was significantly increased between patients with active disease with Median(13). LN classes III and IV were the most dominant features in renal biopsy (GI 40% and 13.3% for each respectively) and (GII 33.3% and 13.3% for each respectively).