{"title":"Special series on platelet transfusion","authors":"Pilar Solves Alcaina","doi":"10.21037/aob-2021-04","DOIUrl":"https://doi.org/10.21037/aob-2021-04","url":null,"abstract":"","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44773834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Richard C Godby, Jori E. May, Jose L. Lima, Nirupama Singh, M. Marques
{"title":"Congenital and acquired disorders of primary hemostasis","authors":"Richard C Godby, Jori E. May, Jose L. Lima, Nirupama Singh, M. Marques","doi":"10.21037/aob-21-77","DOIUrl":"https://doi.org/10.21037/aob-21-77","url":null,"abstract":"","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44946492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lymphocyte response and recovery to radiation therapy alone","authors":"G. Swanson, K. Hammonds, S. Jhavar","doi":"10.21037/aob-21-74","DOIUrl":"https://doi.org/10.21037/aob-21-74","url":null,"abstract":"","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42337196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ling Wei, Y. Liew, Brett Wilson, Ai-jun Huang, J. Wen, Zhen Wang, G. Luo, Y. Ji
Background: Common alloantibodies leading to severe hemolytic disease of the fetus and newborn (HDFN) could vary among different ethnic groups. The MNS blood group hybrid glycophorin GP.Mur distributes with a high frequency in the regions of Southeast Asia. Alloantibodies against GP.Mur (anti-‘Mi a ’) often present as mixture of antibodies against several low frequency antigens. In this study, we first described a case of severe HDFN in Guangzhou, China, which was caused by alloantibodies of anti-E in combination with specificities to the GP.Mur including Mi a , Mur and Hil. Methods: Blood samples from the newborn boy and parents have been subjected to antibody screening and identification analysis followed by GYP*Mur genotyping. The direct antiglobulin test (DAT) and the eluate technique were also performed for the newborn. Results: The mother was group B, CCDee, Mur−, the father was group B, ccDEE, Mur+, and the newborn was group B, CcDEe, Mur+. Genotyping results showed the mother was absent for GYP*Mur , while the father and the newborn carried heterozygous GYP*Mur allele. DAT test of the newborn was strongly positive with anti-IgG. Anti-E and anti-‘Mi a ’ were detected in the maternal serum and the newborn’s eluate, whereas anti-E alone was detected in the newborn’s serum. The anti-‘Mi a ’ specificity was further identified as combination of anti-Mi a , anti-Mur and anti-Hil. Conclusions: Because alloantibodies to GP.Mur could cause severe HDFN, it is highly recommended to include GP.Mur red cells in antibody screening cells to avoid miss detection of the alloantibodies in the populations of Southeast Asia.
{"title":"Severe hemolytic disease of a newborn due to anti-E combined with anti-Mia, anti-Mur and anti-Hil","authors":"Ling Wei, Y. Liew, Brett Wilson, Ai-jun Huang, J. Wen, Zhen Wang, G. Luo, Y. Ji","doi":"10.21037/aob-21-35","DOIUrl":"https://doi.org/10.21037/aob-21-35","url":null,"abstract":"Background: Common alloantibodies leading to severe hemolytic disease of the fetus and newborn (HDFN) could vary among different ethnic groups. The MNS blood group hybrid glycophorin GP.Mur distributes with a high frequency in the regions of Southeast Asia. Alloantibodies against GP.Mur (anti-‘Mi a ’) often present as mixture of antibodies against several low frequency antigens. In this study, we first described a case of severe HDFN in Guangzhou, China, which was caused by alloantibodies of anti-E in combination with specificities to the GP.Mur including Mi a , Mur and Hil. Methods: Blood samples from the newborn boy and parents have been subjected to antibody screening and identification analysis followed by GYP*Mur genotyping. The direct antiglobulin test (DAT) and the eluate technique were also performed for the newborn. Results: The mother was group B, CCDee, Mur−, the father was group B, ccDEE, Mur+, and the newborn was group B, CcDEe, Mur+. Genotyping results showed the mother was absent for GYP*Mur , while the father and the newborn carried heterozygous GYP*Mur allele. DAT test of the newborn was strongly positive with anti-IgG. Anti-E and anti-‘Mi a ’ were detected in the maternal serum and the newborn’s eluate, whereas anti-E alone was detected in the newborn’s serum. The anti-‘Mi a ’ specificity was further identified as combination of anti-Mi a , anti-Mur and anti-Hil. Conclusions: Because alloantibodies to GP.Mur could cause severe HDFN, it is highly recommended to include GP.Mur red cells in antibody screening cells to avoid miss detection of the alloantibodies in the populations of Southeast Asia.","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46770079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The MNS blood group system, International Society of Blood Transfusion (ISBT) 002, is second after the ABO system. GYPA and GYPB genes encode MNS blood group antigens carried on glycophorin A (GPA), glycophorin B (GPB), or on variant glycophorins. A third gene, GYPE, produce glycophorin E (GPE) but is not expressed. MNS antigens arise from several genetic mechanisms. Single nucleotide variants (SNVs) contribute to the diversity of the MNS system. A new antigen SUMI (MNS50), p.Thr31Pro on GPA has been described in the Japanese population. Unequal crossing-over and gene conversion are the mechanisms forming hybrid glycophorins, usually from parent genes GYPA and GYPB. GYPE also contributes to gene recombination previously only described with GYPA. Recently, however, GYPE was shown to recombine with GYPB to form a GYP(B-E-B) hybrid. A GYP(B-E-B) hybrid allele encodes a mature GP(E-B) molecule expressing a trypsin-resistant M antigen but no S/s. Another novel glycophorin GP.Mot has been described carrying Mi, Mur, MUT, and KIPP antigens. GP.Mot is encoded by a GYP(A-B-A) hybrid allele. Newly reported cases of haemolytic transfusion reaction (HTR) or haemolytic disease of the fetus and newborn (HDFN) due to antibodies to MNS antigens is a constant reminder of the clinical significance of the MNS system. In one HDFN case, anti-U and anti-D were detected in an Indian D–, S–s–U– mother. The S–s– U– phenotype is rare in Asians and Caucasians but it is more commonly found in the African populations. Several types of novel GYPB deletion alleles that drive the S–s–U– phenotype have been recently described. Two large GYPB deletion alleles, over 100 kb, were identified as the predominant alleles in the African population. The use of advanced DNA sequencing techniques and bioinformatic analysis has helped uncover these large gene-deletion variants. Molecular typing platforms used for MNS genotyping are also discussed in this review. In conclusion, this review considers currently recognised MNS antigens and variants, new hybrid alleles and GYPB gene deletion alleles as well as clinical case studies. These new discoveries contribute to our understanding of the complexity of the MNS system to guide decision-making in genetic analysis and transfusion medicine.
MNS血型系统，即国际输血协会(ISBT) 002，是继ABO血型系统之后的第二大血型系统。GYPA和GYPB基因编码携带在糖蛋白A (GPA)、糖蛋白B (GPB)或变体糖蛋白上的MNS血型抗原。第三个基因，GYPE，产生糖蛋白E (GPE)，但不表达。MNS抗原产生于多种遗传机制。单核苷酸变异(snv)有助于MNS系统的多样性。在日本人群中发现了一种新的GPA抗原SUMI (MNS50) p.Thr31Pro。不均匀杂交和基因转换是形成糖蛋白的机制，通常来自亲本基因GYPA和GYPB。GYPE还有助于基因重组，以前仅用GYPA描述。然而，最近，GYPE被证明与GYPB重组形成GYP(B-E-B)杂交种。GYP(B-E-B)杂交等位基因编码成熟的GP(E-B)分子，表达胰蛋白酶抗性M抗原，但不表达S/ S。另一种新型糖蛋白GP。莫特被描述携带Mi、Mur、MUT和KIPP抗原。全科医生。Mot由GYP(a - b - a)杂交等位基因编码。新报道的由MNS抗原抗体引起的溶血性输血反应(HTR)或胎儿和新生儿溶血性疾病(hddn)的病例不断提醒着MNS系统的临床意义。在一例hdf病例中，在一名印度D -， S-s-U -母亲中检测到抗u和抗D。S-s - U -表型在亚洲人和白种人中很少见，但在非洲人群中更为常见。最近已经描述了几种驱动S-s-U表型的新型GYPB缺失等位基因。两个大的GYPB缺失等位基因，超过100 kb，被确定为非洲人群的优势等位基因。使用先进的DNA测序技术和生物信息学分析有助于发现这些大的基因缺失变异。本文还讨论了用于MNS基因分型的分子分型平台。综上所述，本文综述了目前公认的MNS抗原和变异、新的杂交等位基因和GYPB基因缺失等位基因以及临床病例研究。这些新发现有助于我们理解MNS系统的复杂性，以指导遗传分析和输血医学的决策。
{"title":"Glycophorins and the MNS blood group system: a narrative review","authors":"G. Lopez, C. Hyland, R. Flower","doi":"10.21037/AOB-21-9","DOIUrl":"https://doi.org/10.21037/AOB-21-9","url":null,"abstract":"The MNS blood group system, International Society of Blood Transfusion (ISBT) 002, is second after the ABO system. GYPA and GYPB genes encode MNS blood group antigens carried on glycophorin A (GPA), glycophorin B (GPB), or on variant glycophorins. A third gene, GYPE, produce glycophorin E (GPE) but is not expressed. MNS antigens arise from several genetic mechanisms. Single nucleotide variants (SNVs) contribute to the diversity of the MNS system. A new antigen SUMI (MNS50), p.Thr31Pro on GPA has been described in the Japanese population. Unequal crossing-over and gene conversion are the mechanisms forming hybrid glycophorins, usually from parent genes GYPA and GYPB. GYPE also contributes to gene recombination previously only described with GYPA. Recently, however, GYPE was shown to recombine with GYPB to form a GYP(B-E-B) hybrid. A GYP(B-E-B) hybrid allele encodes a mature GP(E-B) molecule expressing a trypsin-resistant M antigen but no S/s. Another novel glycophorin GP.Mot has been described carrying Mi, Mur, MUT, and KIPP antigens. GP.Mot is encoded by a GYP(A-B-A) hybrid allele. Newly reported cases of haemolytic transfusion reaction (HTR) or haemolytic disease of the fetus and newborn (HDFN) due to antibodies to MNS antigens is a constant reminder of the clinical significance of the MNS system. In one HDFN case, anti-U and anti-D were detected in an Indian D–, S–s–U– mother. The S–s– U– phenotype is rare in Asians and Caucasians but it is more commonly found in the African populations. Several types of novel GYPB deletion alleles that drive the S–s–U– phenotype have been recently described. Two large GYPB deletion alleles, over 100 kb, were identified as the predominant alleles in the African population. The use of advanced DNA sequencing techniques and bioinformatic analysis has helped uncover these large gene-deletion variants. Molecular typing platforms used for MNS genotyping are also discussed in this review. In conclusion, this review considers currently recognised MNS antigens and variants, new hybrid alleles and GYPB gene deletion alleles as well as clinical case studies. These new discoveries contribute to our understanding of the complexity of the MNS system to guide decision-making in genetic analysis and transfusion medicine.","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44426707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fetal and neonatal immune thrombocytopenia caused by maternal alloantibodies and isoantibodies in Caucasian and Asian populations: a narrative review","authors":"Xiuzhang Xu, Yongshui Fu, V. Kiefel, S. Santoso","doi":"10.21037/aob-21-47","DOIUrl":"https://doi.org/10.21037/aob-21-47","url":null,"abstract":"","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41539023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Convalescent plasma special series","authors":"M. Franchini","doi":"10.21037/aob-2021-02","DOIUrl":"https://doi.org/10.21037/aob-2021-02","url":null,"abstract":"","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46108556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: This narrative review aims to describe the clinical and laboratory approach to patients with platelet transfusion refractoriness (PTR) from CD36 immunization. Background: The most common cause of PTR is non-immune and within the immune-mediated causes, antibodies against CD36 are rare but clinically significant. CD36 deficiency is more common in African, African American, Chinese and Japanese populations. Immune-mediated PTR from CD36 antibodies almost exclusively affects individuals with type I deficiency, affecting both platelets and monocytes. Methods: We describe a general approach to identify and manage patients with CD36 immunization as the cause of PTR. An overview of cases reported in the literature with emphasis in the clinical characteristics and outcomes is presented. Conclusions: Approaching patients systematically, with post-transfusion counts, antibody screening and confirmatory testing to identify the antigen(s) involved is key in selecting the platelet units that are most likely to provide an adequate transfusion yield. Due to the high frequency of CD36 in the general population, CD36 negative platelet units are not readily available, and procurement of these units relies on related donors or units from reference blood banks around the world. Even when CD36 negative platelet units are available, other immune and non-immune mediated causes of PTR can be present simultaneously making platelet transfusions of little clinical utility. Additional interventions to increase transfusion yield such as administration of polyvalent immunoglobulin and addition of immunosuppression have also been described. The management of patients with PTR from CD36 antibodies remains challenging despite wider access to testing and antigen negative platelet units.
{"title":"CD36 immunization causing platelet transfusion refractoriness: narrative review","authors":"Mia J. Sullivan, J. P. Botero","doi":"10.21037/aob-21-36","DOIUrl":"https://doi.org/10.21037/aob-21-36","url":null,"abstract":"Objective: This narrative review aims to describe the clinical and laboratory approach to patients with platelet transfusion refractoriness (PTR) from CD36 immunization. Background: The most common cause of PTR is non-immune and within the immune-mediated causes, antibodies against CD36 are rare but clinically significant. CD36 deficiency is more common in African, African American, Chinese and Japanese populations. Immune-mediated PTR from CD36 antibodies almost exclusively affects individuals with type I deficiency, affecting both platelets and monocytes. Methods: We describe a general approach to identify and manage patients with CD36 immunization as the cause of PTR. An overview of cases reported in the literature with emphasis in the clinical characteristics and outcomes is presented. Conclusions: Approaching patients systematically, with post-transfusion counts, antibody screening and confirmatory testing to identify the antigen(s) involved is key in selecting the platelet units that are most likely to provide an adequate transfusion yield. Due to the high frequency of CD36 in the general population, CD36 negative platelet units are not readily available, and procurement of these units relies on related donors or units from reference blood banks around the world. Even when CD36 negative platelet units are available, other immune and non-immune mediated causes of PTR can be present simultaneously making platelet transfusions of little clinical utility. Additional interventions to increase transfusion yield such as administration of polyvalent immunoglobulin and addition of immunosuppression have also been described. The management of patients with PTR from CD36 antibodies remains challenging despite wider access to testing and antigen negative platelet units.","PeriodicalId":72211,"journal":{"name":"Annals of blood","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43457744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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