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Husebekk A.,University of Tromso | El Ekiaby M.,Shabrawishi Blood Transfusion Center | Gorgy G.,Shabrawishi Blood Transfusion Center | Killie M.K.,University of Tromso | And 6 more authors.
Transfusion and Apheresis Science | Year: 2012

Background and objectives: Foetal and neonatal alloimmune thrombocytopenia (FNAIT) is studied mainly in Caucasian populations. Severe thrombocytopenia (<50×109/L) gives risk of haemorrhage and the most feared complication is intracranial haemorrhage (ICH). In Caucasian populations anti-human platelet antigen (HPA)-1a antibodies are the cause of FNAIT in >80% of the cases. The aims of this project were to study the gene frequencies of HPA-1-5 and 15 alleles in an Egyptian population (Arabic), and to determine the frequency of HPA-1a and -5b immunisations in a cohort of Egyptian pregnant women. Materials and methods: Altogether 6974 pregnant women were included in the study. Genotyping was performed by polymerase chain reaction and antibodies were detected by flow cytometry and enzyme-linked immunosorbent assay. HPA-1-5 and 15 alleles were studied in 367 individuals. Results: The HPA genotypes differed from genotypes published from different Caucasian and Chinese (Han) populations in HPA-1, -2, -3, and -5 systems with significant higher frequency of HPA-1b, -2b and -5b. The rate of HPA-1a alloimmunisation was found comparable to Caucasian populations. Severe thrombocytopenia was found in two newborns. No bleeding complication was reported. Anti-HPA-5b antibodies were detected in 4.4% of the pregnant women. Clinical consequences of these antibodies were not studied. Conclusion: The HPA-1bb and -5bb genotypes are more frequent in the Egyptian Arabic population studied compared to Caucasian populations. FNAIT due to anti-HPA-1a and -5b antibodies must be suspected in cases of neonatal thrombocytopenia. Further large prospective studies are needed to increase the knowledge of clinical complications related to HPA alloantibodies in populations with different genetic backgrounds. © 2012 Elsevier Ltd. Source

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