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Tomoko Nagamine - One of the best experts on this subject based on the ideXlab platform.
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Neonatal alloimmune thrombocytopenia caused by an antibody specific for a newly identified allele of human platelet antigen 7
Transfusion, 2010Co-Authors: Atsuko Taniue, Hiroyuki Ishii, Nobuki Matsuyama, Etsuko Amakishi, Tomoya Hayashi, Rika A Furuta, Yasuo Fukumori, Fumiya Hirayama, Keiji Yoshimura, Tomoko NagamineAbstract:BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) is a Neonatal Disorder characterized by maternal alloimmunization against fetal platelet (PLT) antigens inherited from the father. A healthy 30-year-old Japanese woman (Hit) gave birth to her second child after an uneventful pregnancy. Nine hours after birth, the infant presented with severe petechiae and a PLT count of 6 × 109/L. STUDY DESIGN AND METHODS: To elucidate the maternal cause of NAIT in the infant, serologic and genetic studies, including PLT genotyping and sequence-based analysis, were conducted. Additionally, serologic screening for the new PLT antigen was performed. RESULTS: Serum from the NAIT infant's mother contained antibodies directed against a human PLT antigen (HPA) of the newborn. Using five-cell-lineage flow cytometry, we localized the antigen to a PLT glycoprotein (GP). Subsequent monoclonal antibody immobilization of PLT antigen assay and PLT immunofluorescence inhibition experiments localized the antigen to the GPIIIa subunit of the GPIIb/IIIa complex. GPIIIa localization was confirmed by sequence-based typing studies, which identified a 1297C>T (407proline>serine substitution) mutation on the ninth exon of the GPIIIa gene. This mutation identified the third allele of HPA-7. Anti-Hita reacted with mutated GPIIIa-transfected cells but not with stable transfectants expressing wild-type GPIIIa. Serologic screening for Hita in the Japanese population revealed a phenotypic frequency of approximately 0.0015. CONCLUSIONS: We identified a new third allele of HPA-7, which is characterized by a 1297C>T mutation in the GPIIIa gene. This 1297C>T allele was found in 0.15% of the Japanese population. An antibody against this antigen could be the cause of severe NAIT.
Atsuko Taniue - One of the best experts on this subject based on the ideXlab platform.
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Neonatal alloimmune thrombocytopenia caused by an antibody specific for a newly identified allele of human platelet antigen 7
Transfusion, 2010Co-Authors: Atsuko Taniue, Hiroyuki Ishii, Nobuki Matsuyama, Etsuko Amakishi, Tomoya Hayashi, Rika A Furuta, Yasuo Fukumori, Fumiya Hirayama, Keiji Yoshimura, Tomoko NagamineAbstract:BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) is a Neonatal Disorder characterized by maternal alloimmunization against fetal platelet (PLT) antigens inherited from the father. A healthy 30-year-old Japanese woman (Hit) gave birth to her second child after an uneventful pregnancy. Nine hours after birth, the infant presented with severe petechiae and a PLT count of 6 × 109/L. STUDY DESIGN AND METHODS: To elucidate the maternal cause of NAIT in the infant, serologic and genetic studies, including PLT genotyping and sequence-based analysis, were conducted. Additionally, serologic screening for the new PLT antigen was performed. RESULTS: Serum from the NAIT infant's mother contained antibodies directed against a human PLT antigen (HPA) of the newborn. Using five-cell-lineage flow cytometry, we localized the antigen to a PLT glycoprotein (GP). Subsequent monoclonal antibody immobilization of PLT antigen assay and PLT immunofluorescence inhibition experiments localized the antigen to the GPIIIa subunit of the GPIIb/IIIa complex. GPIIIa localization was confirmed by sequence-based typing studies, which identified a 1297C>T (407proline>serine substitution) mutation on the ninth exon of the GPIIIa gene. This mutation identified the third allele of HPA-7. Anti-Hita reacted with mutated GPIIIa-transfected cells but not with stable transfectants expressing wild-type GPIIIa. Serologic screening for Hita in the Japanese population revealed a phenotypic frequency of approximately 0.0015. CONCLUSIONS: We identified a new third allele of HPA-7, which is characterized by a 1297C>T mutation in the GPIIIa gene. This 1297C>T allele was found in 0.15% of the Japanese population. An antibody against this antigen could be the cause of severe NAIT.
Hanna Wabnitz - One of the best experts on this subject based on the ideXlab platform.
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the use of ivig in fetal and Neonatal alloimmune thrombocytopenia principles and mechanisms
Transfusion and Apheresis Science, 2020Co-Authors: Hanna Wabnitz, Ramsha Khan, Alan H LazarusAbstract:Abstract Fetal and Neonatal alloimmune thrombocytopenia (FNAIT) is a rare Neonatal Disorder that is caused by alloimmunization against platelet antigens during pregnancy. Although rare, affecting only 1 in 1000 live births, it can cause intracranial hemorrhage and other bleeding complications that can lead to miscarriage, stillbirth and life-long neurological complications. One of the gold-standard therapies for at risk pregnancies is the administration of IVIg. Although IVIg has been used in a variety of different Disorders for over 40 years, its exact mechanism of action is still unknown. In FNAIT, the majority of its therapeutic effect is thought the be mediated through the Neonatal Fc receptor, however other mechanisms cannot be excluded. Due to safety, supply and other concerns that are associated with IVIg use, alternative therapies that could replace IVIg are additionally being investigated. This includes the possibility of a prophylaxis regimen for FNAIT, similarly to what has been successfully used in hemolytic disease of the fetus and newborn for over 50 years.
Hassan M Yaish - One of the best experts on this subject based on the ideXlab platform.
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thrombocytopenia in late preterm and term neonates after perinatal asphyxia
Transfusion, 2015Co-Authors: Robert D Christensen, Vickie L Baer, Hassan M YaishAbstract:Background A recent NHLBI conference concluded that platelet (PLT) transfusions of neonates must become more evidence based. One Neonatal Disorder for which transfusions are given is a poorly defined entity, the “thrombocytopenia of perinatal asphyxia.” To expand the evidence base for this entity, we performed a multicentered, retrospective analysis of neonates with perinatal asphyxia. Study Design and Methods We analyzed records of term and late preterm neonates with perinatal asphyxia defined by a cord blood pH of not more than 6.99 and/or base deficit of at least 16 mmol/L. From these we identified neonates with at least two PLT counts of fewer than 150 × 109/L in the first week of life and described the severity, nadir, and duration of the thrombocytopenia. Results Thrombocytopenia occurred in 31% (117/375) of neonates with asphyxia versus 5% of matched nonasphyxiated controls admitted to a Neonatal intensive care unit (p < 0.0001). Twenty-one of the 117 asphyxiated neonates were excluded from the remaining analysis due to disseminated intravascular coagulation or extracorporeal membrane oxygenation. Nadir PLT counts of the remaining 96 were on Day 3 (75 × 109/L; 90% confidence interval, 35.7 × 109-128.6 × 109/L) and normalized by Days 19 to 21. PLT counts after asphyxia roughly correlated inversely with elevated nucleated red blood cell count (NRBC) counts at birth. Thirty of the 96 received at least one PLT transfusion, all given prophylactically, none for bleeding. Conclusions We maintain that the thrombocytopenia of perinatal asphyxia is an authentic entity. Its association with elevated NRBC counts suggests that hypoxia is involved in the pathogenesis. Because PLT counts are only moderately low, the condition is transient, and bleeding problems seem rare, we speculate that PLT transfusions should not be needed for most neonates with this condition.
Nobuki Matsuyama - One of the best experts on this subject based on the ideXlab platform.
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Neonatal alloimmune thrombocytopenia caused by an antibody specific for a newly identified allele of human platelet antigen 7
Transfusion, 2010Co-Authors: Atsuko Taniue, Hiroyuki Ishii, Nobuki Matsuyama, Etsuko Amakishi, Tomoya Hayashi, Rika A Furuta, Yasuo Fukumori, Fumiya Hirayama, Keiji Yoshimura, Tomoko NagamineAbstract:BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) is a Neonatal Disorder characterized by maternal alloimmunization against fetal platelet (PLT) antigens inherited from the father. A healthy 30-year-old Japanese woman (Hit) gave birth to her second child after an uneventful pregnancy. Nine hours after birth, the infant presented with severe petechiae and a PLT count of 6 × 109/L. STUDY DESIGN AND METHODS: To elucidate the maternal cause of NAIT in the infant, serologic and genetic studies, including PLT genotyping and sequence-based analysis, were conducted. Additionally, serologic screening for the new PLT antigen was performed. RESULTS: Serum from the NAIT infant's mother contained antibodies directed against a human PLT antigen (HPA) of the newborn. Using five-cell-lineage flow cytometry, we localized the antigen to a PLT glycoprotein (GP). Subsequent monoclonal antibody immobilization of PLT antigen assay and PLT immunofluorescence inhibition experiments localized the antigen to the GPIIIa subunit of the GPIIb/IIIa complex. GPIIIa localization was confirmed by sequence-based typing studies, which identified a 1297C>T (407proline>serine substitution) mutation on the ninth exon of the GPIIIa gene. This mutation identified the third allele of HPA-7. Anti-Hita reacted with mutated GPIIIa-transfected cells but not with stable transfectants expressing wild-type GPIIIa. Serologic screening for Hita in the Japanese population revealed a phenotypic frequency of approximately 0.0015. CONCLUSIONS: We identified a new third allele of HPA-7, which is characterized by a 1297C>T mutation in the GPIIIa gene. This 1297C>T allele was found in 0.15% of the Japanese population. An antibody against this antigen could be the cause of severe NAIT.
