Search In this Thesis
   Search In this Thesis  
العنوان
Evolution of some biochemical alterations in neonatal hypoxic Ischemic encephalopathy (Hie) /
الناشر
Mohammad Yousef Ahmed,
المؤلف
Ahmed, Mohammad Yousef.
هيئة الاعداد
باحث / محمد رجب يوسف أحمد
مشرف / محمد طلعت خشبة
مشرف / علي علي شلتوت
مشرف / محمد إبراهيم سليم
الموضوع
Hypoxic­ Ishemic Encephalopathy.
تاريخ النشر
1998.
عدد الصفحات
127 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب الأطفال ، الفترة المحيطة بالولادة وصحة الطفل
تاريخ الإجازة
1/1/1998
مكان الإجازة
جامعة المنصورة - كلية الطب - قسم طب الأطفال
الفهرس
Only 14 pages are availabe for public view

from 152

from 152

Abstract

The subjects of the present study comprised 40 children with RHD, there were selected from the Pediatric Department and Out - Patient Clinic in Mansoura University Hospital from the period of August 1996 to April 1997 . They were divided into 2 main groups : active RHD group; which include 20 children : 13 were males and 7 were females aged 7- 15 years (mean age 11. 2 ± 2.1). This group subdivided into 2 sub- groups: patients with carditis (13 patients) and patients with carditis and arthritis (7 patients) . The chronic non - active RHD group included 20 children, 6 were males and 14 were females aged 7 -15 (mean age 11.3 ± 2.5 ) . Control group comprised from 20 normal children of matched age and sex (mean age 11.2 ± 2.3) .All cases as well as control subjects, were subjected to: - Thorough histroy taking, clinical evaluation . - Laboratory investigations including ESR, CRP, ASO . - Radiological and echocardiographic examination . - Determination ofIL-I a, HLA-DR and ICAM-I . - Our results can be summerized in the following : 1- Intercellular adhesion molecule (ICAM-l) : In our study, we found that there was a significant increse in ICAM-I expression in active RHD comparing with the control group, while there was no significant difference have been found between active and non-active RHD groups. But the activity alone does not reflect any increase in ICAM-I when we compare non-active with active patients. This may be due to the overexpression of ICAM-I from the activated endothelial cells during both the acute and chronic inflammatory process of rheumatic fever. Also we