الفهرس 
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Abstract
Childhood immune thrombocytopenic purpura is a well-known disorder with autoimmune processes leading to destruction of platelets. In most of the cases bleeding symptoms are minor and the disease resolves spontaneously after weeks to months. Nevertheless, in some patients the disease lasts more than 6 to 12 months taking a chronic course. In literature the percentage of severe and even fatal haemorrhage varies around 1% and is associated with platelet counts <10 x 109/L.Treatment with IVIG or steroids leads to increased platelet counts. The mechanism of action of this therapy in ITP is not fully understood. For IVIG, besides blockage of the reticulo-endothelial system via Fc-receptors, there are different mechanisms discussed, including the interference with apoptotic processes in platelets.In our prospective study we evaluated laboratory parameters that reflect immune activation, platelet activation and caspase activation in platelets by comparing a series of 30 child with newly diagnosed ITP I 16 child (9 males &7 females) received IVIG and 14 child(7 males&7 females) received Methyl prednisolone toa group of 10 children with chemotherapy induced thrombocytopenia and10 healthy controls children then assess response to either intravenous immunoglobulin or high-dose methylprednisolone. Our results indicate that activation of a caspase dependent cell death pathway in platelets is associated with the active phase of childhood ITP. Amazingly, caspase activation decreases to levels that are detected in normal controls when children respond to IVIG or methylprednisolone treatment but more with IVIG, while the level of anti-apoptotic BCL2 increase with treatment with IVIG and decrease with methylprednisolone.