Thesis (Ph.D.) - Cairo University - Faculty of Medicine - Department of Clinical and Chemical Pathology

Background: Primary immune thrombocytopenia (ITP) is an autoimmune bleeding disorder that affects both children and adults (Hoffbrand et al. 2016). It results from both accelerated destruction and sub-optimal production of platelets (Cines et al. 2009). Initial studies demonstrated a plasma-derived destructive effect, later identified as an anti-platelet antibody (Harrington et al. 1951). Anti- platelet antibodies are usually formed against the human platelet antigen (HPA) system. The HPA systems are derived from the single base pair substitution in the encoding genes of platelet membrane glycoproteins (GP). The GP variants resulting from amino acid substitutions are involved in the rate of alloimmunization to platelet-specific antigens. Subsequently, the alloimmunization can induce fetal and neonatal alloimmune thrombocytopenia (FNAIT) (Mueller- Eckhardt 1986), post-transfusion purpura (PTP), or platelet transfusion refractoriness (PTR) (von dem Borne and Décary 1990). HPA systems are also associated with organ transplantation rejection (Kekomäki et al. 2001) and cardiovascular disease (Ardissino et al. 1999) and are frequently assessed in general population studies. Therefore, accurate donor compatibility for platelet transfusions is extremely important.

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