الفهرس 
Title : The impact of Fc gamma receptor IIIa and IIIa gene polymorphisms on the therapeutic response to rituximab in Egyptian adult immune thrombocytopenic purpura patients
ContentsOnly 14 pages are availabe for public view
 |  | from | 239 |  |  |
| | | from | 239 | | |
Abstract
Background: Immune thrombocytopenic purpura (ITP) is a common bleeding disorder. It occurs due to production of antibodies (the immunoglobulin G (IgG) type) against platelet by the immune system or under production of platelet by the bone marrow. (Schwartz RS, 2007). First line treatment options include corticosteroids and intravenous immunoglobulin (IV Ig). Patients who fail to respond to steroid (steroid resistant) or who relapse (steroid dependant) face the options of treatment with second line drug therapy or splenectomy. One of the second line drug therapies is the anti CD-20 monoclonal antibody rituximab. (provan et al, 2010). Rituximab is one of the chimeric monoclonal antibodies (mAbs). The major mechanism of action of rituximab is the antibody-dependent cellular cytotoxicity (ADCC). Fc gamma receptors (FcÞR) on human white blood cells are an integral part of the ADCC pathway. (Alderson KL and Sondel PM, 2011). Differential response to therapeutic mAbs has been reported to correlate with specific polymorphisms in two of FcÞR genes: FcÞRIIa (H131R) and FcÞRIIIa (V158F) in some diseases. (James D etal, 2013). The aim of the work: is to clarify the effect of Fc gamma receptor IIa, IIIa gene polymorphisms on therapeutic response to rituximab in ITP patients