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C Kaplan - One of the best experts on this subject based on the ideXlab platform.
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prediction of ivig treatment efficiency in fetal Neonatal Alloimmune Thrombocytopenia
Blood, 2014Co-Authors: Gerald Bertrand, Rachel Petermann, C KaplanAbstract:To the editor: Fetal/Neonatal Alloimmune Thrombocytopenia resulting from specific maternal immunization against human platelet antigens (HPAs) is the most frequent cause of severe isolated Thrombocytopenia (platelet counts <50 × 109/L) in maternity wards, and its most destructive consequence is
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Neonatal Alloimmune Thrombocytopenia
Haematologica, 2008Co-Authors: C KaplanAbstract:Neonatal Alloimmune Thrombocytopenia is the commonest cause of early onset isolated Thrombocytopenia in an otherwise healthy neonate.[1][1] This syndrome is comparable to hemolytic disease of the newborn, although it frequently affects the first infant. The Thrombocytopenia results from maternal
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hpa 13bw Neonatal Alloimmune Thrombocytopenia and low frequency alloantigens case report and review of the literature
Transfusion, 2007Co-Authors: Gerald Bertrand, Frederic Bianchi, Marie Alexandre, J Quesne, Christophe Chenet, Corinne Martageix, Vincent Jallu, C KaplanAbstract:BACKGROUND: Fetal-Neonatal Alloimmune Thrombocytopenia (FNAIT) linked to rare or private antigens is not a rare event. STUDY DESIGN AND METHODS: Such a case discovered during the follow-up of a second child with jaundice with mild Thrombocytopenia is reported here. Platelet (PLT) genotyping was performed by polymerase chain reaction (PCR)–sequence-specific primers method and PCR-restriction fragment length polymorphism (RFLP) analysis. Serologic investigation was done with the monoclonal antibody–specific immobilization of PLT antigens technique. Glycoprotein Ia–specific amplification and sequencing were performed for the polymorphism 807 (exon 7). RESULTS: The mother was found to be HPA-13aaw, and the father HPA-13abw. A maternal alloantibody directed against HPA-13bw has been characterized, leading to the diagnosis of Neonatal Alloimmune Thrombocytopenia. CONCLUSION: This report provides further evidence that NAIT associated with low-frequency antigens is not restricted to single families. Therefore, laboratory investigation of a suspected case should be carried out in a specialist laboratory well experienced in optimal testing to propose appropriate management for the index case and subsequent pregnancies.
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anti hpa 3a induces severe Neonatal Alloimmune Thrombocytopenia
The Journal of Pediatrics, 2001Co-Authors: Julia Gladebender, Janice G. Mcfarland, C Kaplan, Leendert Porcelijn, James B. BusselAbstract:Abstract Objective: Fetal and Neonatal Alloimmune Thrombocytopenia (AIT) caused by feto-maternal incompatibility at the HPA-1a (PLA-1) locus is well characterized. Alloimmunization and disease caused by HPA-3a is rare. Study design: We conducted a retrospective analysis of all known cases of AIT caused by HPA-3a incompatibility identified at 3 major reference laboratories from 1986 to 1996. Platelet antigen typing and antibody specificity were determined by serologic evaluation. In some cases confirmatory genotyping was performed. Results: Fourteen cases of anti-HPA-3a-induced AIT in 11 families were identified. Five patients had a previous affected sibling, and 2 cases were firstborn children. All patients had severe Thrombocytopenia at birth (platelet count
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Severe Neonatal Alloimmune Thrombocytopenia due to Anti-HPA-3a
Vox Sanguinis, 1998Co-Authors: Françoise Boehlen, C Kaplan, P. De MoerlooseAbstract:Background and Objectives: Neonatal Alloimmune Thrombocytopenia is usually attributable to HPA-la antibodies. We report a case of parental platelet antigen incompatibility associated with a severe Neonatal Thrombocytopenia secondary to alloimmunization to HPA-3a. Materials and Methods: Platelet antibodies were detected by the monoclonal antibody-specific immobilization of platelet antigens, genotyping of the platelets by PCR, and HLA typing by serologic procedures and PCR. Results: Genotyping of maternal and paternal platelets confirmed the incompatibility in the HPA-3a system. It is noteworthy that the mother is of the HLA type DRB3*0101, is ABO-incompatible with her husband, and also has HLA class I antibodies. Conclusion: Severe Neonatal Thrombocytopenia associated with HPA-3a alloimmunization is infrequent and all the factors mentioned above could have played a role in the severity of the disease.
Karin J Blakemore - One of the best experts on this subject based on the ideXlab platform.
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Chronic villitis in untreated Neonatal Alloimmune Thrombocytopenia: an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy.
American journal of obstetrics and gynecology, 2020Co-Authors: Janyne Althaus, Thomas S. Kickler, Edward G Weir, Frederic B Askin, Karin J BlakemoreAbstract:The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated Neonatal Alloimmune Thrombocytopenia and correlate pathological findings with clinical outcomes. Placentas from 14 Neonatal Alloimmune Thrombocytopenia-affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P < .05 was considered significant. Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin-treated pregnancies (P = .005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. Chronic villitis is frequently manifest in Neonatal Alloimmune Thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of Neonatal Alloimmune Thrombocytopenia.
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chronic villitis in untreated Neonatal Alloimmune Thrombocytopenia an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy
American Journal of Obstetrics and Gynecology, 2005Co-Authors: Janyne Althaus, Thomas S. Kickler, Edward G Weir, Frederic B Askin, Karin J BlakemoreAbstract:Objective The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated Neonatal Alloimmune Thrombocytopenia and correlate pathological findings with clinical outcomes. Study design Placentas from 14 Neonatal Alloimmune Thrombocytopenia–affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P Results Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin–treated pregnancies ( P =.005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. Conclusion Chronic villitis is frequently manifest in Neonatal Alloimmune Thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of Neonatal Alloimmune Thrombocytopenia.
Janyne Althaus - One of the best experts on this subject based on the ideXlab platform.
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Chronic villitis in untreated Neonatal Alloimmune Thrombocytopenia: an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy.
American journal of obstetrics and gynecology, 2020Co-Authors: Janyne Althaus, Thomas S. Kickler, Edward G Weir, Frederic B Askin, Karin J BlakemoreAbstract:The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated Neonatal Alloimmune Thrombocytopenia and correlate pathological findings with clinical outcomes. Placentas from 14 Neonatal Alloimmune Thrombocytopenia-affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P < .05 was considered significant. Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin-treated pregnancies (P = .005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. Chronic villitis is frequently manifest in Neonatal Alloimmune Thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of Neonatal Alloimmune Thrombocytopenia.
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chronic villitis in untreated Neonatal Alloimmune Thrombocytopenia an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy
American Journal of Obstetrics and Gynecology, 2005Co-Authors: Janyne Althaus, Thomas S. Kickler, Edward G Weir, Frederic B Askin, Karin J BlakemoreAbstract:Objective The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated Neonatal Alloimmune Thrombocytopenia and correlate pathological findings with clinical outcomes. Study design Placentas from 14 Neonatal Alloimmune Thrombocytopenia–affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P Results Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin–treated pregnancies ( P =.005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. Conclusion Chronic villitis is frequently manifest in Neonatal Alloimmune Thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of Neonatal Alloimmune Thrombocytopenia.
Bjørn Skogen - One of the best experts on this subject based on the ideXlab platform.
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the development of severe Neonatal Alloimmune Thrombocytopenia due to anti hpa 1a antibodies is correlated to maternal abo genotypes
Clinical & Developmental Immunology, 2012Co-Authors: Bjørn Skogen, Maria Therese Ahlen, Anne Husebekk, Mette Kjaer Killie, Jens Kjeldsenkragh, Martin L OlssonAbstract:Background. Maternal alloantibodies against HPA-1a can cross placenta, opsonize foetal platelets, and induce Neonatal Alloimmune Thrombocytopenia (NAIT). In a study of 100, 448 pregnant women in Norway during 1995–2004, 10.6% of HPA-1a negative women had detectable anti-HPA-1a antibodies. Design and Methods. A possible correlation between the maternal ABO blood group phenotype, or underlying genotype, and severe Thrombocytopenia in the newborn was investigated. Results. We observed that immunized women with blood group O had a lower risk of having a child with severe NAIT than women with group A; 20% with blood group O gave birth to children with severe NAIT, compared to 47% among the blood group A mothers (relative risk 0.43; 95% CI 0.25–0.75). Conclusion. The risk of severe Neonatal Alloimmune Thrombocytopenia due to anti-HPA-1a antibodies is correlated to maternal ABO types, and this study indicates that the observation is due to genetic properties on the maternal side.
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The cellular immunobiology associated with fetal and Neonatal Alloimmune Thrombocytopenia
Transfusion and Apheresis Science, 2011Co-Authors: Tor B. Stuge, Bjørn Skogen, Maria Therese Ahlen, Anne Husebekk, Stanislaw J. Urbaniak, Hagop BessosAbstract:Abstract Fetal and Neonatal Alloimmune Thrombocytopenia (FNAIT) is caused by maternal antibodies that cross the placenta in connection with pregnancy and destroy fetal platelets. Recently, maternal T cell responses associated with FNAIT have been studied at the clonal level. These T cell clones recognize an integrin β3 epitope, which is anchored to the HLA-DRB3∗0101 -encoded MHC molecule DR52a. The same MHC allele is strongly associated with FNAIT. As the production of pathological antibodies reactive with fetal platelets is likely dependent on these T cell responses, there exists a potential for preventing FNAIT by targeting these T cells.
Thomas S. Kickler - One of the best experts on this subject based on the ideXlab platform.
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Chronic villitis in untreated Neonatal Alloimmune Thrombocytopenia: an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy.
American journal of obstetrics and gynecology, 2020Co-Authors: Janyne Althaus, Thomas S. Kickler, Edward G Weir, Frederic B Askin, Karin J BlakemoreAbstract:The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated Neonatal Alloimmune Thrombocytopenia and correlate pathological findings with clinical outcomes. Placentas from 14 Neonatal Alloimmune Thrombocytopenia-affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P < .05 was considered significant. Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin-treated pregnancies (P = .005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. Chronic villitis is frequently manifest in Neonatal Alloimmune Thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of Neonatal Alloimmune Thrombocytopenia.
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Neonatal Alloimmune Thrombocytopenia due to anti-HPA-5b (Bra).
Immunohematology American Red Cross, 2020Co-Authors: Sally A. Campbell-lee, Deirdre Desantis-parsons, R. Sue Shirey, Thomas S. KicklerAbstract:: Neonatal Alloimmune Thrombocytopenia (NAIT) results from maternal immunization against fetal platelet antigens and can occur during the first pregnancy. The most common complications of NAIT are Neonatal Thrombocytopenia, intracerebral hemorrhage, and fetal death. Most cases of NAIT in Caucasians are caused by anti-HPA-1a (PlA1). Anti-HPA-5b (Bra) accounts for only 4.3 percent of all NAIT cases. NAIT due to anti-HPA-5b is thought to be milder and have fewer complications than NAIT caused by anti-HPA-1a because of the lower number of HPA-5b antigenic sites per platelet. This report describes a severe case of NAIT due to anti-HPA-5b that was treated by intrauterine platelet transfusion.
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chronic villitis in untreated Neonatal Alloimmune Thrombocytopenia an etiology for severe early intrauterine growth restriction and the effect of intravenous immunoglobulin therapy
American Journal of Obstetrics and Gynecology, 2005Co-Authors: Janyne Althaus, Thomas S. Kickler, Edward G Weir, Frederic B Askin, Karin J BlakemoreAbstract:Objective The objective of the study was to examine placental histopathology in intravenous immunoglobulin-treated and untreated Neonatal Alloimmune Thrombocytopenia and correlate pathological findings with clinical outcomes. Study design Placentas from 14 Neonatal Alloimmune Thrombocytopenia–affected pregnancies were identified. Maternal antepartum treatment with intravenous immunoglobulin and pregnancy outcomes were abstracted from medical records. Placental histopathology and clinical outcomes were compared between intravenous immunoglobulin and no intravenous immunoglobulin treatment groups using Fisher's exact test. One subject, treated only after an intracranial hemorrhage (ICH) was diagnosed, was excluded from the analysis. P Results Untreated pregnancies demonstrated a lymphoplasmacytic chronic villitis not seen in the intravenous immunoglobulin–treated pregnancies ( P =.005). Intrauterine growth restriction and intrauterine fetal demise occurred as frequently as ICH in the untreated group. No ICH, intrauterine growth restriction, or intrauterine fetal demises occurred in the treated group, although the P value was not significant. Conclusion Chronic villitis is frequently manifest in Neonatal Alloimmune Thrombocytopenia, with intravenous immunoglobulin alleviating this inflammatory immunologic response. We suspect a more universal role for the maternal antibody, such as fetal endothelial cell damage, in the sequelae of Neonatal Alloimmune Thrombocytopenia.
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Neonatal Alloimmune Thrombocytopenia.
Clinics in Laboratory Medicine, 1992Co-Authors: Thomas S. KicklerAbstract:Neonatal Alloimmune Thrombocytopenia is caused by the transplacental passage of maternal antibodies directed against platelet-specific antigens. Because complications from bleeding may result, prompt institution of therapy may be necessary. Accurate diagnosis by serologic techniques permits appropriate therapy to be administered both prenatally and postnatally.
