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ABO antibodies are naturally occurring antibodies. The ABO antibodies found in the Group O individuals include anti-A and anti-B. In Group O individuals, it tends to be predominantly immunoglobulins G (IgG), although immunoglobulins M and IgA components are also present. Infants of Group O mothers are at higher risk for hemolytic disease of the fetus and new-born than those born to mothers with Group A or B because IgG readily cross the placenta. At the same time, abnormal high concentration of ABO antibody in mother can lead to destruction of platelets in neonates and leads to development of neonatal alloimmune thrombocytopenia as human platelets carry detectable quantities of A and B blood group antigens on their surface. Proper and early diagnosis combined with treatment with intravenous immunoglobulins or transfusion with compatible platelets, may be from mother, can save the neonate from bleeding episodes.

ObjectiveTo summarize the clinical characteristics and treatment options together with the maternal and neonatal prognoses in women with different degrees of thrombocytopenia of unknown causes during pregnancy.Materials and MethodsOne hundred twenty-nine cases meeting the inclusion and exclusion criteria were retrospectively analyzed. Patients were divided into group A (50*109/L) and group B (50*109/L to 100*109/L) according to the lowest level of platelet count during pregnancy. Patients were divided into those found to have thrombocytopenia in the relatively early, middle, and late stages according to the detection period of maternal thrombocytopenia during pregnancy.ResultsThere were 72 cases in group A, and 57 cases in group B. There existed statistically significant differences in terms of the proportion of primipara, the proportion with a history of thrombocytopenia, and the median length of pregnancy between the two groups (p

ABO antibodies are naturally occurring antibodies. The ABO antibodies found in the Group O individuals include anti-A and anti-B. In Group O individuals, it tends to be predominantly immunoglobulins G (IgG), although immunoglobulins M and IgA components are also present. Infants of Group O mothers are at higher risk for hemolytic disease of the fetus and new-born than those born to mothers with Group A or B because IgG readily cross the placenta. At the same time, abnormal high concentration of ABO antibody in mother can lead to destruction of platelets in neonates and leads to development of neonatal alloimmune thrombocytopenia as human platelets carry detectable quantities of A and B blood group antigens on their surface. Proper and early diagnosis combined with treatment with intravenous immunoglobulins or transfusion with compatible platelets, may be from mother, can save the neonate from bleeding episodes. [ABSTRACT FROM AUTHOR]

Even though Fetal and Neonatal Alloimmune Thrombocytopenia (FNAIT) has been recognized as the main cause of primary hemorrhagic morbidity and mortality in fetuses and newborns, screening programs to detect pregnancies at risk have not yet been implemented in any country. Moreover, in spite of increased concerns about maternal, fetal and neonatal health care in general, this potentially lethal disease is still underdiagnosed. The aim of this report is to highlight the importance of considering FNAIT in fetal and perinatal health-care settings and show the usefulness of molecular tools in early diagnosis of this clinical entity. DNA was extracted from whole blood from parents and newborns; genotyping was performed by in house PCR using sequence-specific primers for typing Human Platelet Antigens (HPA)-1 to -6, -9, and -15, and with commercial HPA-TYPE (BAG HealthCare, Lich, Germany). Anti-HPA antibodies in the maternal serum were detected by the Monoclonal Antibody Solid Phase Platelet antibody Test (MASPAT). Chloroquine-treated platelets were used for the discrimination of platelet-specific antibodies from anti-HLA antibodies. Patients 1 and 2 had severe thrombocytopenia due to incompatibility in HPA-1 and HPA-15, respectively. The third case was a thrombocytopenic neonate with severe bleeding complications other than ICH and in whom differential diagnosis between FNAIT and Von Willebrand congenital disease was necessary; incompatibility in HPA-15 was also demonstrated. Case 4 represents a missed diagnostic opportunity. This is the first report of FNAIT cases confirmed by molecular evidence and anti-HPA antibodies detection in Argentina. This report reinforces the relevance of early diagnosis of this clinical entity. Since the delay in FNAIT diagnosis could lead to severe consequences in the fetus and neonates, strategies to approach maternal, fetal, and perinatal health, as well as prevention policies aimed to reduce fetal and neonatal morbidity and mortality should focus on implementing programs to identify high-risk pregnancies and thus reduce thrombocytopenia-related complications in fetuses and newborns. [ABSTRACT FROM AUTHOR]

Background: Neonatal alloimmune thrombocytopenia is a rare but potentially severe postnatal complication caused by maternal allo‐antibodies against platelet antigens of the newborn. In relatively few cases, immunisation against low‐frequency antigens has been reported. Methods: Platelet antigens of a newborn with severe thrombocytopenia and his family members were investigated by serological and molecular biological methods. A real‐time PCR assay was developed to reliably detect this mutation in pools of DNA from up to seven individuals. Results Serological testing showed positive reactions of maternal plasma with paternal platelets but not with conventional platelet donor panels. Sequencing of the ITGB3 gene revealed a G > A polymorphism in position c.1915 of exon 12 for the father, the newborn and three of four paternal relatives. Screening of samples from a local population of 1575 Caucasian blood donors identified only a single individual with this mutation. Conclusion: This finding of a previously unreported private platelet antigen demonstrates that the identification of the target glycoprotein by MAIPA assay followed by sequencing of the affected gene can be combined with an efficient population screening by real‐time PCR with pooling of DNA samples. [ABSTRACT FROM AUTHOR]

Neonatal alloimmune thrombocytopenia (NAIT) arises from fetomaternal platelet incompatibility that results in transplacental passage of maternal antibodies mostly against fetal human platelet antigens (HPA), whereas NAIT due to anti-human leukocyte antigen (HLA) antibodies is extremely rare. Here, we report a case of Down syndrome (DS) with NAIT that was attributed to HLA antibodies. A boy with DS was delivered at 36 weeks' gestation. His platelet count declined to 13.0 × 109/L, suggestive of NAIT rather than other conditions, including transient abnormal myelopoiesis. Random platelet concentrates and intravenous immunoglobulin administration resolved the thrombocytopenia without clinical complications. Immunoserological investigations detected anti-HLA, but no anti-HPA antibodies in samples from the patient and the mother. HLA typing and cross-matching indicated that anti-HLA antibodies to paternal HLA A31 and B61, which had probably been induced during a prior pregnancy, led to NAIT in this case. Although it is a rare condition, healthcare providers should consider NAIT due to HLA antibodies and be vigilant for subsequent cases in DS. [ABSTRACT FROM AUTHOR]

Background: Neonatal alloimmune thrombocytopenia (NAIT) is defined as an uncommon platelet disorder caused by maternal alloimmunization to human-specific antigens (HPAs) that are paternally inherited, resulting in low fetal/neonatal platelet levels and debilitating effects on the newborn. The incidence of NAIT is 1 in every 1000 live births within the United States; it is the most common cause of severe thrombocytopenia (<30 × 109/L) and intracranial hemorrhage in term newborns.Purpose: The purpose of this article is to discuss the pathophysiology, clinical manifestations, diagnosis, and treatment of NAIT and its implications upon the lifespan of the neonate.Methods: A literature review was conducted using PubMed, CINAHL, and Google Scholar (2014-2019). Search terms included NAIT, neonatal/fetal alloimmune thrombocytopenia, newborn platelets, and intracranial bleeding and NAIT.Results: NAIT can affect first pregnancies and often goes undiagnosed until delivery. Universal screening tools with a focus on HPA-1a typing via noninvasive testing have been successfully trialed and have yielded promising results indicating a 75% reduction in risks associated with NAIT; however, none have been incorporated into practice and prophylactic treatment remains unavailable.Implications For Research: Adopting a universal screening tool and prophylaxis for NAIT would allow for early diagnosis and treatment in utero.Implications For Practice: Many healthcare providers are not familiar with NAIT often focusing on other causes of thrombocytopenia as a potential diagnosis. [ABSTRACT FROM AUTHOR]

Background: Current assays for the detection of (allo)antibodies to platelet antigens are often laborious and widely based on the presence of well-characterized donor platelets., Objectives: To develop an easy-to-perform, sensitive, and specific test for the detection of antibodies against platelet antigens, in particular, glycoprotein (GP) antigens, called "Recombinantly Expressed Tagged SUrface Protein" (RETSUP) assay, which does not require donor platelets., Methods: Twin-Strep-tagged GP complexes were recombinantly expressed in human embryonic kidney 293 cells after stable transfection. These cell lines were used as antigen sources in the RETSUP assay, combining cell-based and enzyme-linked immunosorbent assay-based assay procedures. The assay performance was tested with recombinant antibodies, anti-human platelet antigen (HPA) reference plasmas, and anti-HPA patient sera., Results: Human embryonic kidney 293 cell lines stably expressing either Twin-Strep-labeled GPIa/IIa, GPIIb/IIIa, GPIb/IX, or GPIb/IX/V complexes or GPV as well as the distinct HPA-1, HPA-3, and HPA-5 epitopes were successfully generated. Applying the generated GP-expressing cell lines, the developed RETSUP assay proved very sensitive and specific with recombinant antibodies targeting different GPs and human plasma/serum samples. The results of the test were not affected by the GP carrying the Twin-Strep-tag or by using freshly harvested or cryopreserved cells., Conclusion: The RETSUP assay is an easy-to-perform, sensitive, and specific assay for the detection of plasma/serum antibodies to platelet GP, with performance comparable to or better than those of current state-of-the-art assays in antiplatelet antibody diagnostics. Owing to the recombinant nature of the target antigens, it can be easily adapted to detect antibodies in other antibody-mediated diseases., Competing Interests: Declaration of competing interests There are no competing interests to disclose., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

The aim. Mechanisms underlying the development of neonatal alloimmune thrombocytopenia (NAIT) in in Russia have been studied. Materials and methods. Genetic polymorphisms of human platelet alloantigens (HPA) -1, -2, -3, -4, -5, and -15 were evaluated in 27 families having the newborns with NAIT. NAIT was diagnosed according to the following criteria: (1) newborn with thrombocytopenia; (2) mother with no thrombocytopenia and no increase of platelet associated IgG, (3) presence of antibodies reacting with paternal platelets in maternal plasma / serum. HPA genotyping revealed incompatibilities in 23 out of 27 tested families. In these 23 families HPA-1 conflicts were detected in 16 ones (70%). In 8 cases mothers were homozygous carriers of rare HPA-1b allele and in another 8 cases - of HPA-1a allele which cased incompatibilities with fetal HPA-1a and HPA-1b respectively. In 5 out of 23 families (22%) there were incompatibilities with fetal HPA-15 (HPA-15a, n=2 and HPA-15b, n=3), in 1 family - with HPA-5b (4%), and in 1 family - with HPA-3b (4%) alloantigens. In conclusion the main causes of NAIT in Russia were HPA-1a and -1b conflicts and HPA-15 conflicts were the second frequent ones.

Alloimmunization against platelet antigens causes complications in transfusion settings as platelet transfusion refractoriness and post-transfusion purpura, as well as in pregnancy, causing fetal/neonatal alloimmune thrombocytopenia. Strategies for the laboratory investigations depend on a repertoire of serological and molecular assays and are often dependent on timing and objective. Technical improvements have led to a number of sophisticated methods for alloantigen typing and alloantibody identifications during the last decade; however, some traditional methods are still beneficial. The laboratory investigations should ensure that the causative antibody specificities are identified as soon as possible to support the correct diagnosis and guide the selection of compatible platelets if needed. [ABSTRACT FROM AUTHOR]

Background and objectives: To detect HPA‐15 alloantibodies, we previously developed a human platelet antigen 15 (HPA‐15)‐expressing cell line‐based modified rapid monoclonal antibody immobilization of platelet antigen (CL‐MR‐MAIPA) assay. In this study, the protocol was modified for easier performance by introducing the mixed‐passive haemagglutination (MPHA) principle. Material and methods: In total, 20 samples that tested negative for HPA alloantibodies and eight that tested positive for HPA‐15 alloantibodies (two and six positive for HPA‐15a and HPA‐15b antibodies, respectively) by CL‐MR‐MAIPA assay were used in this study. HPA‐15 cell lines were incubated with serum/plasma and then solubilized. The lysate was transferred to a round‐bottom well, which was coated with anti‐human CD109 monoclonal antibodies. After incubation and repeated washings, sheep red blood cells, coated with anti‐human IgG, were added to the wells. Haemagglutination was assessed the next day. Results: The proposed cell line‐based immune complex capture‐dependent mixed‐passive haemagglutination (CL‐IC‐MPHA) assay consisted of four steps, but required only 2 h to perform, except for overnight incubation for haemagglutination. Two HPA‐15a alloantibody samples were reactive only for HPA‐15a cells, and six HPA‐15b alloantibody samples were reactive only for HPA‐15b cells with the CL‐IC‐MPHA assay. The 20 samples that tested negative for HPA alloantibodies did not react with HPA‐15a or HPA‐15b cells. These data indicated that the CL‐IC‐MPHA assay was highly specific and sensitive. Unfortunately, the CL‐IC‐MPHA assay's analytic sensitivity was twofold to eightfold lower than that of the CL‐MR‐MAIPA assay. Conclusion: A novel, easy‐to‐perform protocol was successfully developed to detect HPA‐15 alloantibodies with high specificity and sensitivity. [ABSTRACT FROM AUTHOR]

At birth, severe thrombocytopenia without context of infection should mainly suggest neonatal alloimmune thrombocytopenia (NAIT), especially in case of a platelet count below 20 GL−1. We report two cases of severe neonatal thrombocytopenia, first suspected as being NAIT. Both had a platelet count below 20 GL−1 with platelet clumps. The absence of alloantibodies and failure of platelet transfusion and intravenous immunoglobulins to improve the platelet count led to question the diagnosis and to evoke inherited bleeding disorders. Measurements of Von Willebrand factor (VWF) levels showed a marked reduction of VWF:RCo and a normal VWF:Ag, suggesting a type 2B Von Willebrand disease (VWD2B). Ristocetin-induced platelet aggregation could not be performed because of the very low platelet count. In the first case, after sequencing VWF exon 28, a heterozygous p.Leu1460Pro mutation was found consistent with VWD2B. In the second case, the genetic analysis of VWF exon 28 identified a homozygous mutation: p.Pro1337Leu confirming type VWD2B and also the p.Arg854Gln homozygous mutation in exon 20 confirming type 2N (ratio FVIII/VWF:Ag

Abstract Background Neonatal alloimmune thrombocytopenia (NAIT), caused by maternal antibodies raised against alloantigens carried on foetal platelets, is a very common haematological abnormality in newborns worldwide. However, baseline data on NAIT in China are lacking. Therefore, this study seeks to explore the incidence of alloantibody against the human platelet antigen (HPA) in pregnant women and its associations with NAIT in China. Methods A multicentre, prospective cohort study design will be used, and 55,497 pregnant women will be recruited for the first screening of the anti-HPA antibody at 12 to 28 weeks of gestational age. Subjects who are positive in the first screening for the anti-HPA antibody will be included in the exposure group. Re-tests of the antibody titre, antigen-specificity and genotyping of HPA and HLA will be conducted during admission. A ratio of 1:1 paired individuals with the same ethnicity and parity but testing negative for the anti-HPA antibody will be randomly selected to be included in the non-exposure group. NAIT will be diagnosed in the newborns on day one of the birth. The HPA of the neonates in the exposure group will also be genotyped by sequencing. Associations of maternal HLA with the occurrence of the anti-HPA antibody and correlation of the severity of NAIT with the titre of the anti-HPA antibody will be further analysed. Discussion The study is expected to provide baseline data on NAIT in China. Besides, we hope to find out a population who expresses particular HLA molecules has significant higher risk of HPA alloimmunization in Chinese individuals. We also hope to find a Chinese-specific cut-off antibody titre for the prediction of the severity of NAIT and to provide a means to evaluate the necessity of antenatal treatment. Trial registration ClinicalTrials.gov: NCT02934906 (date registered: 13.10.2016).

Background: The human platelet alloantigens (HPA) HPA-1a and HPA-5b are located on glycoproteins on the platelet surface and are the most relevant to cause neonatal alloimmune thrombocytopenia (NAIT). The antigens are defined by single nucleotide polymorphisms (SNPs) in the glycoprotein genes, and the antigen status can be determined by genotyping the SNPs. However, genotyping is time-consuming and costly depending on the method and sample throughput. Here, we tested the reliability of the evanescence wave based fluorescence (EVA) biosensor technology for the rapid phenotyping of the HPA-1a and HPA-5b antigens on blood donor samples in two laboratories. Methods: HPA-1a and HPA-5b phenotyping was performed on EDTA blood samples from 336 blood donors (Lyon: 216 donors; Mannheim: 120 donors) using EVA typing assays and the biosensor system (Davos Diagnostics, Davos, Switzerland). For genotyping, validated PCR-SSP and TaqMan-PCR methods were used. Results: HPA-1a phenotyping was positive for all samples with HPA-1aa (n = 244; EVA value 807 ± 167 U/s) and HPA-1ab (n = 82; 542 ± 110 U/s) genotypes. All samples (n = 10) with negative EVA values (<10 U/s) had the HPA-1bb genotype. HPA-5b phenotyping was negative for all HPA-5aa genotypes (n = 267) and positive for the HPA-5ab (n = 66; 83 ± 22 U/s) and HPA-5bb (n = 3; 118 ± 25 U/s) genotypes. EVA values from heterozygotes were significantly lower compared to HPA-1a or HPA-5b homozygotes. A strong correlation of the EVA values with the platelet count in the blood samples was observed. Conclusion: EVA is a reliable method for rapid phenotyping of the clinically relevant HPA-1a and HPA-5b platelet antigens. All phenotyping results were 100% concordant with the HPA-1 or HPA-5 genotype. The test can be performed from only 10 µl of fresh or frozen blood samples within less than 15 min time-to-result. [ABSTRACT FROM AUTHOR]

Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a rare but potentially very serious bleeding condition affecting the fetus/newborn. The vast majority (>80%) of FNAIT cases among Caucasians, and the most serious one, are caused by maternal antibodies to the human platelet antigen 1a (HPA‐1a). The clinical consequences of FNAIT span a continuum from no symptoms to intracranial haemorrhage (ICH) and intrauterine death. The incidence of FNAIT‐associated ICH has been estimated to be around 1 in 10 000 newborns. For many reasons, FNAIT has not been considered for prophylactic efforts similar to those that have been used for the prevention of HDFN, caused by antibodies against RhD: first, HPA‐1a typing kits are not well suited to the workflow in immunohaematology laboratories; secondly, the costs associated with HPA‐1a typing of all pregnant women have been a hindrance; thirdly, there is no international consensus regarding the optimal antenatal management of HPA‐1a‐immunized women identified in a screening programme; fourthly, it has generally been believed that immunization against HPA‐1a mostly takes place during the first incompatible pregnancy, and finally, there is yet no medicinal product available that can prevent HPA‐1a‐immunization in the same way as anti‐D can prevent RhD immunization. Implementation of HPA‐1a typing of all pregnant women has been discussed by the health authorities in several European countries. The abovementioned five hindrances for FNAIT screening and the Wilson and Jungner criteria for screening programmes will be discussed in the light of recent advances within FNAIT research. [ABSTRACT FROM AUTHOR]

Fetal/neonatal alloimmune thrombocytopenia (FNAIT) is a severe bleeding disorder which can result in intracranial haemorrhage (ICH), leading to death or neurological sequelae. In Caucasians, maternal anti‐HPA‐1a antibodies (abs) are responsible for the majority of FNAIT cases. However, the correlation between fetal platelet counts and risk of bleeding is loose. ICH was also observed in FNAIT cases with platelet counts within reference ranges. These observations question the exclusive role of thrombocytopenia in ICH. Recently, we observed stronger binding of anti‐HPA‐1a antibodies from mothers with ICH‐positive (+ICH) FNAIT to endothelial cell‐derived αvβ3 when compared to anti‐HPA‐1a from ‐ICH. Differential absorption experiments demonstrated that anti‐HPA‐1a is not a single antibody entity. Sera from immunized women may contain three different subspecificities: anti‐β3, anti‐αIIbβ3 and anti‐αvβ3. Anti‐β3 appears to be the dominant subtype of anti‐HPA‐1a. However, anti‐αvβ3 was only found in +ICH sera, and only the anti‐αvβ3, but not anti‐β3 subtype, induced apoptosis and disturbed tube formation of endothelial cells in vitro. Therefore, we believe that this anti‐HPA‐1a subtype plays a significant role in the development of ICH. Together with other subtypes, anti‐αvβ3 may trigger bleeding in a threshold model of FNAIT/ICH, where bleeding occurs if yet undefined levels of anti‐endothelial (loss of integrity) and/or antiplatelet (low platelet count) activities are achieved. Thus, defining anti‐HPA‐1a subtypes may have significant potential in the prediction of ICH. With upcoming nation‐wide screening programmes, detection of anti‐HPA‐1a subtypes could prove helpful to allocate treatment to appropriate (at‐risk) cases, especially in countries with restricted resources. [ABSTRACT FROM AUTHOR]

The immune response against platelets is a complex process involving many aspects of the innate and adaptive immune system. Immune destruction of platelets and megakaryocytes and the thrombocytopenia that ensues can cause different clinically significant haematological disorders such as foetal and neonatal alloimmune thrombocytopenia (FNAIT), transfusion‐induced platelet refractoriness or immune thrombocytopenia (ITP). These conditions are frequently difficult to manage so an understanding of the biological nature of these adverse conditions is critical for an understanding of how to potentially reduce them. Superimposed on these immune platelet attack mechanisms are the immune characteristics of the platelets themselves. This paper will give an overview of how the immune system recognizes platelet antigens and mounts efficient effector mechanism to mediate thrombocytopenia. It will also present evidence to suggest that platelets also play a role in stimulating these responses and suppressing them: a scenario where the ‘prey’ can become the ‘predator’. [ABSTRACT FROM AUTHOR]

Background In fetal and neonatal alloimmune thrombocytopenia (FNAIT), maternal alloantibodies directed against paternally-derived platelet antigens are transported across the placenta to the fetus, where they may cause thrombocytopenia. The most serious complication of FNAIT is an intracranial hemorrhage (ICH), which may cause death or life-long disability of the child. Apart from alloantibody-mediated platelet destruction, the clinical outcome in FNAIT may be affected by properties of neonatal platelets and possible functional effects on platelets caused by maternal alloantibodies. Methods and results The function of umbilical cord blood platelets was compared with adult platelets in two assays, impedance aggregometry (Multiplate) and rotational thromboelastometry (Rotem). Both revealed a decreased in vitro neonatal platelet function compared to adult platelets. Consistent with this finding, activation using TRAP revealed less pronounced changes in the expression of CD62P, PAC-1, CD41 and CD42a in umbilical cord blood platelets compared to adult platelets. Furthermore, a monoclonal anti-HPA-1a antibody, derived from an immunized mother of two children with FNAIT, blocked fibrinogen binding to resting and activated umbilical cord blood and adult HPA-1aa and HPA-1ab platelets, interfered with platelet activation by TRAP, and impaired the function of umbilical cord blood HPA-1aa platelets in rotational thromboelastometry. Discussion and conclusions Reduced fibrinogen binding in the presence of anti-HPA-1a antibodies may disturb the neonatal hemostatic balance, characterized by poorly responsive platelets. This effect may operate in parallel to platelet destruction and contribute to the clinical outcome in FNAIT. [ABSTRACT FROM AUTHOR]

At birth, severe thrombocytopenia without context of infection should mainly suggest neonatal alloimmune thrombocytopenia (NAIT), especially in case of a platelet count below 20 GL−1. We report two cases of severe neonatal thrombocytopenia, first suspected as being NAIT. Both had a platelet count below 20 GL−1with platelet clumps. The absence of alloantibodies and failure of platelet transfusion and intravenous immunoglobulins to improve the platelet count led to question the diagnosis and to evoke inherited bleeding disorders. Measurements of Von Willebrand factor (VWF) levels showed a marked reduction of VWF:RCo and a normal VWF:Ag, suggesting a type 2B Von Willebrand disease (VWD2B). Ristocetin-induced platelet aggregation could not be performed because of the very low platelet count. In the first case, after sequencingVWFexon 28, a heterozygous p.Leu1460Pro mutation was found consistent with VWD2B. In the second case, the genetic analysis ofVWFexon 28 identified a homozygous mutation: p.Pro1337Leu confirming type VWD2B and also the p.Arg854Gln homozygous mutation in exon 20 confirming type 2N (ratio FVIII/VWF:Ag <0.5). The two cases underline that, even if NAIT remains the most common diagnosis in severe neonatal thrombocytopenia, it should be challenged in the absence of documented incompatibility, chronic evolution, or treatment failure. Diagnosis of VWD2B should be considered in early thrombocytopenia, even without familial history. In the cases presented, genotyping confirmed the subtype of VWD and helped to guide the therapeutic management of bleeding episodes. [ABSTRACT FROM AUTHOR]

Problem Fetal and neonatal alloimmune thrombocytopenia is an alloimmune disorder resulting from platelet opsonization by maternal antibodies that destroy fetal platelets. As there is no antenatal screening or immunization to prevent sensitization, selection of high-risk population or the prevention of antenatal sensitization is significantly limited. Method of study (i) A case report of ante- and postnatal management of a woman with paternal homozygosity for human platelet antigen-1( HPA) incompatibility. (ii) A retrospective case-control study of 11 confirmed FNAIT patients, 8 possible- FNAIT women, and 10 women with confirmed ITP. Result Antenatal screening, prevention of maternal sensitization by serial monitoring and immunosuppression with prednisone and intravenous immunoglobulin G ( IVIG) infusion resulted in two successful pregnancies without sensitization. Conclusion Screening for couples at risk and prednisone and/or IVIG treatment is an option for women with paternal homozygosity for offending HPA antigen to prevent antenatal sensitization. HPA incompatibility is associated with increased Th1 immunity and NK cell cytotoxicity. [ABSTRACT FROM AUTHOR]

Platelet products have been increasingly used for more than 50 years. Platelet transfusion is effective for correcting bleeding caused by thrombocytopenia and platelet function defects. In this review, we will outline research on platelet transfusion in China including platelet biosafety, cryopreservation of platelets, the assessment of the effectiveness of platelet transfusion, the causes of platelet transfusion refractoriness including immunization against CD36, and neonatal alloimmune thrombocytopenia. [ABSTRACT FROM AUTHOR]

Neonatal alloimmune thrombocytopenia (NAIT) may lead to serious complications, including perinatal intracranial hemorrhage and death. Mothers with a history of previously affected pregnancies should receive antenatal treatment with intravenous immunoglobulin (IVIG), which can be associated with toxicities including thrombosis. An infant born to a mother treated with IVIG and steroids was diagnosed with an inferior vena cava thrombus shortly after birth, was anticoagulated and recovered. Thus, this side effect can be seen, and should be considered, in infants of NAIT-affected pregnancies treated with IVIG. [ABSTRACT FROM AUTHOR]