The HPA-15 (Gov) alloantigen is a biallelic co-dominant system on human platelets, and its allele HPA-15a and HPA-15b differ by an A-->C single nucleotide polymorphism at nucleotide 2108 of the coding sequence resulting in a Tyr682Ser substitution in the mature CD109 glycoprotein. Employing the polymerase chain reaction-restriction fragment length polymorphism technique, we determined the HPA-15 gene frequencies among 276 subjects of distinct Brazilian ethnic groups including, 15 Caucasians, 15 African Brazilians, 15 Orientals, 106 Amazon Xikrin Indians, 31 Amazon Gavioes Indians and 94 blood donors. The calculated HPA-15a and HPA-15b allele frequencies found in Caucasians (0.53/0.47), African Brazilians (0.57/0.43), Orientals (0.57/0.43) and Brazilian blood donors (0.52/0.48) did not differ significantly. However, the HPA-15a and HPA-15b gene frequencies of Xikrin Indians (0.78/0.22) were significantly different from that of all other groups (P < 0.01). The HPA-15a/a, HPA-15a/b and HPA-15b/b genotype frequencies observed in Gavioes Indians were significantly different from those seen in African Brazilians (P = 0.04) and blood donors (P = 0.017). The present data showed that the distribution of the HPA-15 (Gov) system alleles observed among the Brazilian population is quite similar to the distributions already reported among Asian, Canadian and European populations. Moreover, the data indicated differences in the frequency of the HPA-15 system between Amazon Indians and other distinct Brazilian ethnic groups suggesting that Amerindians would be at higher risk of HPA-15 alloimmunization in the need of receiving blood components collected from blood donors of other ethnic groups.

Background: KELnull (K₀) persons can produce clinically significant anti-KEL5 antibody after transfusion and/or pregnancy, requiring K₀ blood transfusion when indicated. 37 K₀ alleles have been reported in studies over different populations, but none in Amerindian-Caucasian descendants from South America. The aim of this study was to identify the molecular basis of K₀ phenotype in Brazilians. Methods: We investigated three K₀ samples from different Brazilian blood banks (Recife, Manaus, and Vila Velha) in women with anti-KEL5. KEL antigen typing was performed by serologic techniques, and the K₀ status was confirmed by flow cytometry. PCR-RFLP and DNA sequencing of the KEL coding and exon-intron regions were also performed. Results: RBCs of the 3 patients were phenotyped as KEL:-1,-2,-3,-4,-7. The 3 patients had the same KEL*02/02 genotype and were negative for KEL*02.03 and KEL*02.06 alleles. The Recife K₀ patient was homozygous for IVS16 + 1g>a mutation(KEL*02N.31 allele). The flow cytometry with anti-KEL1, anti-KEL2, anti-KEL3, anti-KEL4, and anti-CD238 confirmed the K₀ phenotype. In addition, we found the c.1042C>T mutation (KEL*02N.04 allele) in both the Manaus K₀ and the Vila Velha K₀ patients. Conclusion: This report represents the first study of K₀ molecular basis performed in Amerindian-Caucasian descendants from South America.

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tration. It can be proposed that a relapsing TTP known as rituximab-responsive should be retreated in emergency. The rapidity of the rituximab effect is supported by its ability to clear from the blood within a few hours a significant number of B cells, which is correlated to B-cell depletion within marrow and lymph nodes. 3 From undetectable ADAMTS13 at her third episode, a progressive increase was observed under rituximab. Despite the reported correlation between a persistent deficiency in ADAMTS13 and the risk of relapse, this is still a subject of controversy. 4 Thus, the absence of relapse under rituximab maintenance could be explained or not by this. Although plasma levels of rituximab are low or undetectable 4 months after its infusion, a 6-month frequency administration could be enough to achieve the long-term B-cell depletion necessary to maintain the remission. 5 Safety issues concerning a prolonged administration of rituximab should be outlined, but few data exist. 1 Early front-line therapy with rituximab for relapsing TTP patients previously responsive to the same drug could be a therapeutic option. For those who achieve remission, a rituximab maintenance schedule could also be considered, ideally within clinical trials, because our experience with this one patient is not enough to be raised as a solid recommendation.