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Distribution of ABO, RhD Blood Group among Secondary School Students at Bishops Girls Secondary School Rushere Kiruhura Southwestern Uganda

Benjamin Nuwareeba, Antony Atuhaire, Esau Mawejje and Emmanuel Ifeanyi Obeagu

Department of Medical Laboratory Science, Kampala International University, Uganda.

^*Corresponding author: Emmanuel Ifeanyi Obeagu

Department of Medical Laboratory Science, Kampala International University, Uganda, emmanuelobeagu@yahoo.com, ORCID: 0000-0002-4538-0161                        

ABSRACT

ABO and Rhesus blood group antigens are inherited genetic markers in human blood. Haemoglobin is an efficient transporter of oxygen from the lungs to the tissues and carbon dioxide from tissues to the lungs for exhalation. The study was to determine the distribution of ABO and Rhesus blood groups among secondary school female students. The blood samples of 107 secondary school students at Bishops girls’ Secondary School Rushere kiruhura Southwestern Uganda between July to August, 2023 were collected and their haemoglobin genotypes were determined using HemoTypeSC™ rapid test kit and ABO and Rhesus blood groups were determined by a standard tube method. Results. The frequencies of ABO blood groups among the study population were 20 (18.5%), 24 (22.5%), 06 (5.4%) and 57 (53.6%) for blood group A, B, AB, and O respectively. Also, the distribution of Rhesus (D) positive and Rhesus (D) negative were reported as 98 (91.6%) and 9 (8.4%) each. There was no association between ABO, Rhesus (D) and Hb genotypes observed. Data revealed that Rhesus (D) positive students were statistically higher in number compared to the Rhesus (D) negative students (p=0.000).  The sequence of ABO distribution among the rural population in southwestern Uganda is; O > A > B > AB. The frequency of Rhesus (D) negative is very low among secondary school students at Bishops’ Girls Secondary School Rushere Kiruhura Southwestern Uganda

Keywords: blood groups, ABO blood group, Rh group, Haemolytic Disease of the Newborn

INTRODUCTION

The ABO blood is widely credited to have been discovered by the Austrian scientist Karl Landsteiner who found three different types in 1900. He was awarded the noble prize in physiology/medicine in 1930 for his work [1-3]. ABO blood groups are based on antigen that are located on red blood cells (RBC) membrane and are coded by alleles on different loci on a chromosome [4]. Individuals are classified into four major ABO blood groups namely; A, B, AB and O depending on the antigen present on their RBC surface [5]. RhD (D or RH1), originally identified in 1939, was the first clinically important blood group to be found following the discovery of ABO 39 years earlier. A phenotypic relationship between D and an antigen on human red cells detected by antibodies made in rabbits immunized with rhesus monkey red cells, led to D being inappropriately named the Rhesus antigen. A vestige of that term remains in Rh, the name of the blood group system that contains D [6]. The Rh blood group system was discovered in 1940 by Karl Landsteiner and Weiner. It consists of D, d, C, c, E and e blood group antigens [7]. The D antigen is highly considered in blood banking and transfusion medicine, and on this antigenic basis, individuals are typed as either RhD positive or negative [8-10].

The Rhesus (Rh) antigen is found on the surface of human red blood cell (RBC) membrane and the Rh blood group system is located on the short arm of chromosome number 1 (1p34/1-1p36). It is the most polymorphic and immunogenic blood group system in humans. This system has great importance in transfusion medicine because of its role in developing HDFN, HTR, and autoimmune hemolytic anemia. Of the 61 antigens present in the Rh blood group system, five antigens (CDEce) have clinical significance [10] with the ABO system and the Rhesus (Rh) system remaining the most clinically significant blood group antigens on the red cell membrane. If the mother is RhD-negative and the fetus RhD positive, she has a potential capacity to form antibodies if exposed to fetal antigens, a process known as RhD sensitization [11-13].

RhD variants are classified for practical purposes into 3 groups: partial D, weak D, and Del alleles. Partial D variants are characterized by mutations in the extracellular domains leading to altered epitopes, and people with these variants may develop anti-D when exposed to wild-type D antigen from transfusion or during pregnancy. Women who have partial D variants and have developed anti-D are at risk for HDFN. In contrast with partial D, weak D variants have a reduced number of qualitatively normal D antigens resulting from mutations within the intracellular or transmembrane regions of RhD. RBCs with Del alleles express low quantities of D antigen but type as D-negative on routine testing [14].

The weak D variant results from a single point mutation in the transmembranous or intracellular region of the RHD gene and is reflected by reduced quantities of the normal D antigen. The partial D variant is as a result of mutation in the extracellular regions and replacement of RhD exons by the RHCE counterparts, leading to an altered or new epitopes. Individuals with partial D contain normal number of the D antigens but with a reduced quantity of D-specific epitopes on the RhD proteins. The DEL D variant expresses very low quantities of the RhD antigen [13].

In white Europeans and Americans, the D-negative phenotype is caused by the complete deletion of the RHD gene. In Africans, the D-negative phenotype is due to the formation of RHD-CE-D hybrid gene RHD pseudogene: a premature termination codon and with the presence of an extra 37 base pair duplication. The Del phenotype, which is the result of mutations in the RHD gene exons, is found in 10% to 30% of Asians [14].

HDFN is an important cause of neonatal morbidity and death. To reduce the incidence of HDFN and mortality among fetuses and neonates, anti-D immunoglobulin has been tested in clinical trials 1960s. Anti-D immunoglobulin has been used to prevent postpartum disease in RhD-negative women, and has greatly reduced HDFN-related morbidity as well as fetal and neonatal mortality [14].

CONCLUSION

The sequence of ABO distribution among the rural population in southwestern Uganda is; O > A > B > AB. The frequency of Rhesus (D) negative is very low among secondary school students at Bishops’ Girls Secondary School Rushere Kiruhura Southwestern Uganda

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