الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Primary ITP presents as isolated thrombocytopenia (platelet count ˂ 100 ×109/L) in the absence of other causes or disorders that may be associated with thrombocytopenia, or as a secondary disorder, most commonly associated with autoimmune disease, lymphoproliferative disorders or chronic infections. Primary ITP in children is usually self-limited, with approximately 80% of cases resolving within 6-12 months. Bleeding is the most clinical manifestation of ITP. The pathogenesis of ITP involves loss of tolerance of glycoproteins expressed on platelets and megakaryocytes. Epitope spreading may explain the fact that many patients have antibodies against more than one glycoprotein. Anti-platelet glycoprotein antibodies cause thrombocytopenia through two mechanisms: 1) reducing the survival of circulating platelets, 2) and inhibiting production of new platelets by bone marrow megakaryocytes. Cellular immunity play a central role in thrombocytopenia. Alterations in T cell subsets and decreased numbers and activity of regulatory T cells are common. Cytotoxic T cells may also mediate toxicity against platelets and megakaryocytes. Treatment strategy include first line therapy as corticosteroids, IVIG, anti-Rh (D), and second line therapy as anti-CD20 (rituximab), thrombopoietin receptors agonist and splenectomy. So, the present study aimed to evaluate the therapeutic response of a high dose dexamethasone in a series of Egyptian children with chronic ITP. The study started with 31 children but actually done on 27 patients comprising 12 males (44.4 %) and 15 females (55.6 %). However, three patients was excluded due to diagnosis of SLE and one patient with HCV during re-evaluation. Also one child was withdrawn from the study due to acquired diabetes and hypertension with 26 patients completing the treatment course.