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العنوان
LABORATORY EVALUATION OF CLINICAL UTILITY OF SERUM INTERLEUKIN- 8
IN THALASSEMIC PATIENTS /
المؤلف
Ghabbour، EngyMakram Nassif.
هيئة الاعداد
باحث / انجي مكرم نصيف غبور
مشرف / شهيرة مرسي الشافعي
مشرف / هناء حسن محمود الدش
مناقش / هناء حسن محمود الدش
الموضوع
Qrmak
تاريخ النشر
2019
عدد الصفحات
127 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
8/2/2019
مكان الإجازة
جامعة الفيوم - كلية الطب - قسم الباثولوجيا الاكلينيكية
الفهرس
Only 14 pages are availabe for public view

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from 127

Abstract

The thalassemias are a group of inherited disorders in which globin chain synthesis is impaired. -thalassemia, a haemoglobinopathy that results in the precipitation of denatured excess α-globin chain in the membrane, is characterized by erythrocytes with significantly reduced life span (Yuan et al., 1992).
Reduced red blood cells (RBC) deformability has also been described in thalassemia and such a change could result in a greater opportunity for macrophagic attack, either prolonged contact between damaged RBCs and the macrophage, or chronic blood transfusion-induced alloimmunization (Salsas et al., 1997).
Several immunologic defects can be found in patients with -thalassemia, among which the impairment of neutrophil phagocytic and killing functions is of the utmost importance (Uguccioni et al., 1993).
Interleukin-8 is an important component of the pro-inflammatory response (Friedland et al., 1991).
Recently, attention has been directed to the role of cytokines, since the polypeptides that are released by activated monocytes and macrophages can mediate a wide variety of biological effects (Bazi et al., 2017).
Interleukin-8 is an important chemotactic and activating peptide for neutrophils and can be detected in the circulation. This cytokine can be produced by a variety of cell types, including large granular lymphocytes, macrophage, endothelial cells, fibroblasts, and synovial cells (Standiford et al., 2017).
Therefore, changes of IL-8 synthesis, reflected in plasma levels, may be relevant to the pathophysiology of -thalassemia