Objectives:The aim of this study was to verify the possibility of performing prophylactic Rh genotype-matching in Brazilian patients with sickle cell disease (SCD) and identify the genotypes that are lacking or insufficient in our donor cohort.Background: Rh alloimmunisation is still a challenge in transfused patients with SCD. Rh genotype-matching may mitigate Rh alloimmunisation. Methods/Materials:We examined the transfusion requests for antigen-matched donor units in SCD patients with Rh variants and compared the Rh altered alleles in the patients to the Rh allele frequency in a selected donor population. For each patient and donor, RBC antigen genotyping was performed using HEA, RHD and RHCE BeadChip arrays. Sequencing was used to clarify inconclusive results. Twenty-one patients and 956 Brazilian blood donors were genotyped.Results: According to our matching strategies, 47·6% of patients filled most of their unit requests, but 52·4% of patients had insufficient donors to fill their annual transfusion needs. We found different combinations of RHCE variant alleles in patients and donors, but the most frequent genotypes that are lacking or insufficient in our donor cohort are those associated with the lack of hr B and hr S high prevalence antigens and those co-inherited with altered RHD alleles. Conclusion:Our study shows that the provision of compatible blood with Rh genotype-matching in Brazilian patients with SCD can be feasible but challenging and, efficient strategies of recruitment of African-Brazilian donors must be developed.

False-positive and false-negative reactions exist for serological and molecular antigen typing methods. If the predicted phenotype is inconsistent with the patient`s known antibodies or serological phenotype, the discrepancy must be investigated. False-negative and false-positive results are clinically problematic in blood donors and patients. In this study, we investigated discrepant results between serology and molecular testing in patients and blood donors that occurred in daily molecular laboratory practice over a two year-period. SCD patients represented a large percentage of our cases of discrepancies but we also observed a high prevalence of discrepancies between phenotypes and genotypes in blood donors. The main reasons that led to discrepancies were recent transfusions and limitations of phenotyping. Discrepancies classified as false positive phenotype/ true negative genotype and false negative phenotype/true positive genotype occurred mainly in patients with recent transfusions and individuals with RH variants while those classified as true negative phenotype/false positive genotype involved null phenotypes due to silent genes. Despite the limitations of molecular methods currently employed, we found more false-negative and false-positive phenotypes than genotypes demonstrating that genotyping is more efficient to define the blood types, especially in transfusion dependent patients.