ORCID Profile
0000-0001-9044-8009
Current Organisation
RMIT University
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Publisher: Wiley
Date: 14-09-2022
DOI: 10.1111/VOX.13351
Abstract: Sickle cell disease (SCD) patients are commonly treated with red blood cell (RBC) transfusion. Pretransfusion tests commonly involve limited serological antibody testing. RBC alloimmunization to RBC antigens is a frequently encountered complication seen in chronically transfused patients. Genetic factors such as the human leukocyte antigen (HLA) are known to influence and regulate immune responses. HLAs are highly polymorphic and play an essential role in regulating immune responses, including RBC alloimmunization. The aim of this study was to conduct a systematic review and meta-analysis to evaluate the association between HLA Class II allelic polymorphisms with the possible risk of developing RBC alloantibodies. Four databases were systematically searched for relevant studies between the years 2000 and 2021 following the PRISMA guidelines. Four articles met the eligibility and quality criterion, and three alleles, HLA-DRB1*04, HLA-DRB1*15 and HLA-DQB1*03, that were found to be potentially associated with an increased risk in alloantibody formation were included. The primary outcome measure was alloimmunization by RBC antigen exposure in multiply transfused SCD patients. The total estimate of alloimmunization of the SCD patients was 2.33 (95% CI, 1.58-3.44), demonstrating susceptibility to RBC alloantibody formation. Heterogeneity between the studies was insignificant, suggesting the differences associated with random s ling errors. The results showed that SCD patients carry an increased risk of producing RBC alloantibodies. A strategy to prevent RBC alloimmunization is genotyping for genetically susceptible SCD patients receiving multiple transfusions. Early identification of genetic variants that can potentially increase the risk of RBC alloimmunization could aid in the screening process and selection of phenotypically matched RBC units.
Publisher: Elsevier BV
Date: 04-2022
DOI: 10.1016/J.TMRV.2022.01.001
Abstract: Human platelet antigen (HPA) genotyping is performed in a number of clinical scenarios, including characterization of immune-mediated thrombocytopenia and provision of HPA-matched platelets. Current gold-standard methods for HPA genotyping utilize single nucleotide variant (SNV) based approaches. This review aims to ascertain if next generation sequencing (NGS) has reasonable grounds to replace SNV-based genotyping for HPA systems. A systematic review was conducted following a comprehensive literature search in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis guidelines. Studies were subjected to screening based on a defined set of inclusion/exclusion criteria. Study quality, characteristics and results were extracted and a meta-analysis was performed to assess the concordance of HPA genotyping results between NGS and the SNV-based comparators for HPA-1,-2,-3,-4,-5,-15. In total, 3374 potentially eligible articles were identified, only 6 of which were included in the meta-analysis. The pooled proportion agreement for the overall concordance of the 6 included studies was shown to be 0.998, 95%CI [0.995, 0.999], P < .001. The discrepancies between HPA genotypes obtained by the two platforms were due to allele dropout in real-time PCR, thus discordant results were in favor of NGS over SNV-based comparators. Currently available platforms for NGS are not without their limitations, including high upfront and ongoing costs, data management and storage, accurate variant calling and availability of appropriately trained staff. Despite the high level of concordance between NGS and current gold-standard methods, these significant challenges mean that NGS is currently not viable as a stand-alone technique for HPA typing.
Publisher: Elsevier BV
Date: 10-2023
Publisher: Informa UK Limited
Date: 11-2021
DOI: 10.2147/IDR.S342259
Publisher: Informa UK Limited
Date: 11-2021
DOI: 10.2147/IJGM.S340283
Publisher: American Society of Hematology
Date: 23-12-2019
DOI: 10.1182/BLOODADVANCES.2019000640
Abstract: Ibrutinib but not zanubrutinib induces shedding of GPIb-IX complex in an ADAM17-dependent manner GPIX has not been shown previously. Ibrutinib, but not zanubrutinib, induces shedding of integrin αIIbβ3 by an unknown sheddase.
Publisher: Elsevier BV
Date: 04-2021
Publisher: Informa UK Limited
Date: 12-2021
DOI: 10.2147/PGPM.S342625
Publisher: Informa UK Limited
Date: 04-2022
DOI: 10.2147/IDR.S355395
No related grants have been discovered for Denise Jackson.