Shamee Shastry1, Sudha Bhat. 1. Kasturba Medical College, Manipal University, Manipal, Karnataka, India. shameegirish@gmail.com
Abstract
BACKGROUND: The heterogeneity of A and B alleles results in weak variants of these antigens. Subgroups of A differ from each other quantitatively and qualitatively. The expected frequencies of A₁ and A₂ subtypes will be in Hardy-Weinberg equilibrium for the Mendelian inheritance of the allelic A₁ and A₂ genes. The frequency of A subgroups in the population from south India is not known. The aim of our study was to study the frequency of A subtypes and the prevalence of anti-A₁ antibody among this population. METHODS: Over a period of 3 years, patients' blood group was typed using a standard tube technique. Anti-A₁ lectin studies were done for all patients with groups A and AB. Based on serological reactivity the samples were classified into A₁/A₁B, A₂/A₂B and weak A subgroups. The prevalence of A subgroups was determined. The significance of differences in proportions was analysed using the chi-square test. RESULTS: A total of 40,113 patients' samples were typed for ABO, Rh group and A subgroups in our blood bank attached to a tertiary care hospital. Among 10,325 group A samples, 98.14% classified as A₁, 1.07% as A₂, and 0.01% as weak A; the remaining group A samples were from neonates and reacted poorly with anti A₁-lectin. The majority of AB samples (n=2,667) were of A₁B type (89.28%). However, the proportion of A₂B (8.99%) among AB samples was significantly higher than that of A(2) in group A samples (p < 0.0001). The prevalence of anti-A(1) antibodies among A₂ and A₂B samples was 1.8% and 3.75%, respectively, and none of them showed reactivity at 37°C. CONCLUSION: The results of our study show a significantly higher proportion of A₂B subtypes than A₂ subgroups. A similar imbalance is seen in blacks and Japanese. The incidence of anti-A₁ antibodies is also higher among A₂B patients.
BACKGROUND: The heterogeneity of A and B alleles results in weak variants of these antigens. Subgroups of A differ from each other quantitatively and qualitatively. The expected frequencies of A₁ and A₂ subtypes will be in Hardy-Weinberg equilibrium for the Mendelian inheritance of the allelic A₁ and A₂ genes. The frequency of A subgroups in the population from south India is not known. The aim of our study was to study the frequency of A subtypes and the prevalence of anti-A₁ antibody among this population. METHODS: Over a period of 3 years, patients' blood group was typed using a standard tube technique. Anti-A₁ lectin studies were done for all patients with groups A and AB. Based on serological reactivity the samples were classified into A₁/A₁B, A₂/A₂B and weak A subgroups. The prevalence of A subgroups was determined. The significance of differences in proportions was analysed using the chi-square test. RESULTS: A total of 40,113 patients' samples were typed for ABO, Rh group and A subgroups in our blood bank attached to a tertiary care hospital. Among 10,325 group A samples, 98.14% classified as A₁, 1.07% as A₂, and 0.01% as weak A; the remaining group A samples were from neonates and reacted poorly with anti A₁-lectin. The majority of AB samples (n=2,667) were of A₁B type (89.28%). However, the proportion of A₂B (8.99%) among AB samples was significantly higher than that of A(2) in group A samples (p < 0.0001). The prevalence of anti-A(1) antibodies among A₂ and A₂B samples was 1.8% and 3.75%, respectively, and none of them showed reactivity at 37°C. CONCLUSION: The results of our study show a significantly higher proportion of A₂B subtypes than A₂ subgroups. A similar imbalance is seen in blacks and Japanese. The incidence of anti-A₁ antibodies is also higher among A₂B patients.
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