EVALUATION OF PLATELET ANTIGENS INVOLVED IN ALLOIMMUNE THROMBOCYTOPENIA

MATTALONI S; LUJÁN BRAJOVICH M; BIONDI C; TRUCCO BOGGIONE C; RACCA L; COTORRUELO C; MIGONI A; MUFARREGE N; ENSINCK A

Mar del Plata

Congreso; LXIV Reunión científica anual, Sociedad Argentina de Inmunología; 2016

SAIC - SAI - SAFE

In Caucasians, fetal/neonatal alloimmune thrombocytopenia(FNAIT) is most frequently caused by maternal alloimmunizationagainst the human platelet antigen HPA-1a. Previous observationsin immunized pregnant women from our hospital have shown thatanti-HPA-1a is not mainly involved in the FNAIT cases studied.Moreover, the specificity of the alloantibodies found could not bedefined in most of the cases. Considering that our current populationis the result of a complex process of hybridization betweenCaucasians, Native Americans and Africans and that the admixturedegree varies among different social groups, we consider critical toevaluate the distribution of platelet phenotypes in our population.The aim of this study is to analyze phenotype and allele frequenciesof the HPA-1 system in two different groups: patients from apublic hospital [G1] and patients from a private laboratory [G2].Blood samples were obtained from 179 individuals from G1 and156 from G2. HPA typing was performed by molecular strategiesbased on PCR-SSP and PCR-RFLP. For G1, HPA-1 phenotypefrequencies were: HPA-1(a+,b-)=84.9%, HPA-1(a+,b+)=15.1%,HPA-1(a-,b+)=0% while for G2 were: HPA-1(a+,b-)=74.4%, HPA-1(a+,b+)=23.1%, HPA-1(a-,b+)=2.6%. The allele frequency foundfor G1 was: HPA-1A=92.5%, HPA-1B=7.5% while for G2 was HPA-1A=85.9%, HPA-1B=14.1%. Statistically significant differenceswere found for the HPA-1 phenotype distribution between bothgroups (z-test; p=0.009) and for the allele frequency (chi-squaretest with Yates? correction, p=0.0059). These results are consistentwith our previous studies in other blood group systems showingethnic variability in the different social groups analyzed. Thesefindings suggest that variants found in G2 are representative of theCaucasian population. The absence of HPA-1(a-,b+) phenotypein G1 explain why anti-HPA-1a is not responsible for most of theFNAIT in our hospital. We speculate that another, yet unreportedHPA antigen could be involved.