1. Poster Title Weak D Types in the Egyptian Population Eiman Hussein, MD 1 and Jun Teruya, MD, DSc 2 Clinical Pathology, Division of Transfusion Medicine / Blood Banking, Cairo University, Cairo, Egypt 1 Pathology & Immunology, Pediatrics, and Medicine Baylor College of Medicine and Texas Children’s Hospital Houston, Texas, USA 2 Numerous studies have been addressing RHD alleles in Caucasians, Africans, and Asians, but none have been conducted among the Middle Eastern population. Approximately 6% of Egyptians are Rh negative. More than 50 different molecular weak D types have been described. Their frequency varies among different populations. Patients with weak D types 1, 2, 3, 4.0 and 4.1 are not sensitized when exposed to D antigen. They can be safely considered D positive, saving some D negative units and doses of Rh immune globulin prophylaxis. These phenotypes represent more than 90% of all weak D types in Caucasians. Usually transfusion of 200 mL or more of D positive red blood cells (RBC) causes allo anti D production in 75-80% of Rh negative recipients within 2-5 months. More recent data pointed toward an inverse correlation between the number of transfused units and the probability of antibody formation, bringing transfusion of weak D into focus. This issue has been debated recently, as there are not enough cases in literature to give conclusive evidence. OBJECTIVES The aim of this study was to determine the frequency of various weak D types among Egyptians. This was performed in an attempt to propose a cost effective, standard transfusion policy related to D variant testing and administration of Rh immune globulin. It was also conducted to help assess the risk of anti D development in Rh negative patients receiving RBC units for which weak D was not tested.  A total of 1,113 Rh negative blood samples from Egyptian donors and patients were studied for weak D expression.  Samples that were weakly agglutinated by tube method or that reacted only by indirect antiglobulin test (IAT) were classified D variants.  Routine D typing was performed by monoclonal blended anti D reagents containing IgG and IgM (Diamed, Cressier sur Morat, Switzerland).  D variants were further tested by PCR with sequence specific priming (BAGene PCR-SSP), designed to detect types 1, 2, 3, 4.0/4.1, 4.2, 5, 11, 15, and 17.  We also studied the probability of anti D development in 52 Rh negative children with beta thalassemia, receiving Rh negative RBC units for which weak D was not tested. RESULTS CONCLUSION REFERENCES 1. METHODS  A total of 50 out of 1,113 Rh negative samples (4.5%) were classified D variants.  Molecular typing of the 50 weak D variants revealed that 16 were weak D type 4.2 (32%), 8 were weak D type 4.0/4.1 (16%) and 1 sample was weak D type 15 (2%). (Table)  The remaining 25 (50%) samples probably constituted partial D or other rare weak D types.  Eight of 1,113 cases (0.7%) were weak D type 4.0/4.1, which can be considered Rh positive for transfusion and pregnancy.  Transfusion of Rh negative RBC units that were not tested for weak D, caused alloimmunization in 33 out of the 52 (63.5%) multitransfused thalassemia patients. Their mean age was 15.0 ± 3.5 years, and they received a mean of 247.7 ± 44.8 RBC units (212 – 298 units) in 10.2 ± 2.2 years with a range of 7 – 13 years. Table: Prevalence of D variants in Egyptian population INTRODUCTION RHD variantNO. (%) of samples Weak D type 4.216 (32%) Weak D type 4.0/4.18 (16%) Weak D type 151 (2%) Partial or other rare weak D25 (50%)  In Egyptian population, most D variants with weak expression were partial D, resembling black individuals.  A higher incidence of weak D types 4.2 and 4.0/4.1 was noted in Egyptians when compared to Caucasians.  Since only a small number of Rh negative cases can be considered Rh positive, routine molecular screening for D variants among Egyptian patients may not be cost effective.  The high incidence of anti D in our group of transfusion dependent thalassemia patients, underscores the importance of IAT in the D typing of Egyptian donors. 1.Peng CT,Shih MC, Liu TC. Molecular basis for RHD negative phenotypes in Chinese. Int J Mol Med 2003;11:515-21. 2.Felgel WA. Blood group genotyping in Germany. Transfusion 2007;47:47S-53S. 3. Wang D, Lane C, Quillen K. Prevalence of Rh D variants, confirmed by molecular genotyping, in a multiethnic prenatal population. Am J Clin Pathol 2010;134:438-42.