Prevalence of irregular red cell antibody in healthy blood donors attending a tertiary care hospital in North India

Abstract

BACKGROUND:Alloantibodies may be detected in blood donors who have either been transfused previously or female donors with previous obstetric events. These antibodies can occasionally cause severe transfusion reaction, if a large amount of plasma or whole blood is transfused, as in massive transfusions and pediatric patients.AIMS:The present study aims to assess the prevalence of red cell antibodies in healthy blood donors at a tertiary care hospital-based blood bank in India.MATERIALS AND METHODS:A total of 82,153 donor samples were screened for irregular red cell antibodies between January 2012 and December 2015 at the Department of Transfusion Medicine, Indraprastha Apollo Hospitals, New Delhi. Antibody screening was performed by solid phase method using Immucor Capture–R ready screen (pooled cells) on fully automated immunohematology analyzer Galileo Neo (Immucor Inc., Norcross, GA, USA). Positive tests were further confirmed using Capture-R ready screen (4 cell panel). Advanced investigations to identify the antibody/ies were performed on confirmed positive samples. Antibody identification was conducted using various cell panels (Immucor Capture-R Ready-ID, Panocell-10, Ficin Treated). An advanced technique such as adsorption and elution was performed as per requirement.RESULTS:Screening with pooled cells and 4 cell panel was positive in 227 donors (0.27%), 150 of these donors had autoantibodies, 1 had autoantibodies with underlying alloantibody anti-Jka (0.001%), and 76 had alloantibodies (0.09%) alone in their plasma. Anti-M was the most common antibody (43 donors) identified, followed by anti-D (21 donors). Anti-N was detected in 4; anti-Jka, anti-C, and anti-E in two donors each followed by anti-P1 and anti-Leb in 1 donor.CONCLUSION:Antibodies against red cells can be present in healthy donors detection of which is important in providing safe blood to the patient. The prevalence of red blood cell antibody in healthy donors in this study was found to be 0.27%, while the prevalence of alloantibodies was 0.09%. The majority of alloantibodies were anti-M (56.57%) and anti-D (27.63%).

Prevalence of red blood cell antibodies in whole blood donors

“…The higher rate of alloimmunization in females could be attributed to antigenic exposure during pregnancies. Other studies on healthy blood donors showed frequency of alloimmunization from 0.05 to 4.0 per cent 4 5 6 7 8 9 10 11 . In our study, most frequent alloantibodies identified were of MNS blood group system.…”

“…The prevalence of red cell alloantibodies varies in males and females (multiple pregnancies) and individuals with past history of transfusion and/or transplant. Red cell alloantibodies have been found in up to four per cent of blood donors 4 5 6 7 8 9 10 11 . Among patient populations, the prevalence of alloantibodies has been reported to be 2-9 per cent in multitransfused patients and 9-40 per cent in sickle cell anaemia and thalassaemia patients 12 13 14 .…”

Adding further evidence for clinically significant anti-Leb antibody in a voluntary blood donor

“…found these frequencies to be 2.1% and 1.31%, respectively. [ 9 10 ] The prevalence of anti-Le b among our donor population was found to be 0.13%.…”

Dealing with a clinically important anti-M case with cross-reactivity induced by monoclonal typing reagent

“…As it is reminded in the monoclonal typing reagent insert accompanying the anti-M anti-sera, unexpected results may occur from very rare types of antigens. This warning was noted in one of the anti-M reagents we used (10). Some common monoclonal anti-M clones (e.g.2514E6 and M-11H2) extensively cross-react with the low prevalence He antigen (Henshaw, MNS6) (11).…”

“…Some common monoclonal anti-M clones (e.g.2514E6 and M-11H2) extensively cross-react with the low prevalence He antigen (Henshaw, MNS6) (11). Most anti-M reagents detect as well as He (Henschaw) which generally is found in 2.3 percent of the central African population (10). It is produced by DNA exchanging between the glycophorin A (GPA) and glycophorin B (GPB) genes, which are located close together on chromosome 4.…”