Abstract

IntroductionHemolytic reactions are adverse complications associated with red blood cell transfusion. These reactions are associated with clinically important erythrocyte antigens, such as those of Duffy blood Meny (2010). Individuals with the Duffy null phenotype Fy (a−b−) are more likely to develop an alloimmunization reaction, resulting in an incompatibility with all available red blood cell units, thus increasing the risk of complications from their underlying disease Höher et al. (2018). Hence, it is important to determine the prevalence of the Fy (a−b−) phenotype in blood donors in our population and to create a database to ensure safe transfusion in patients with this phenotype. Moreover, we intend to establish whether there is any relationship between individuals with this phenotype and the sickle cell trait. We conducted this study to measure the prevalence of the Fy (a-b-) phenotype in our blood donors. Materials and methodsThis prospective, descriptive study included black blood donors visiting the blood bank of a tertiary care university hospital between January 2019 and July 2019. We used Fitzpatrick classification phototype VI and self-identification to select donors in the study. The presence of the Duffy antigens Fya and Fyb was determined by the Coombs test using monoclonal antibodies. To establish the presence of hemoglobin S (HbS) and sickle cell traits, a hemoglobin electrophoresis test was performed. ResultsWe included 166 patients in the study. Seventy-nine donors were identified as having Fy (a-b-). The prevalence of the Fy (a−b−) phenotype was 48 %. Sickle cell trait hemoglobinopathy was found in 6 blood donors (8%). ConclusionThis information is relevant for the implementation of a database of blood donors to guarantee the safety of transfusion in patients with a Fitzpatrick skin type 6at our institution. Moreover, it may provide information of interest to other blood banks in case donors with this phenotype are needed. No significant association was found between the donor Fy (a−b−) phenotype and the sickle cell trait.

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