Mette Kjaer1,2, Gerald Bertrand3, Tamam Bakchoul4,5, Edwin Massey6, Jillian M Baker7, Lani Lieberman8, Susano Tanael9, Andreas Greinacher5, Michael F Murphy10, Donald M Arnold11, Shoma Baidya12, James Bussel13, Heather Hume14, Cécile Kaplan15, Dick Oepkes16, Greg Ryan17, Helen Savoia18, Nadine Shehata9,19,20, Jens Kjeldsen-Kragh1,21. 1. Department of Laboratory Medicine, Diagnostic Clinic, University Hospital of North Norway, Tromsø, Norway. 2. Finnmark Hospital Trust, Finnmark, Norway. 3. Platelet Immunology Department, French Blood Services of Brittany, Rennes, France. 4. Center for Clinical Transfusion Medicine, University of Tuebingen, Tuebingen, Germany. 5. Institute of Immunology and Transfusion Medicine, University Hospital Greifswald, Greifswald, Germany. 6. NHS Blood and Transplant, Bristol, UK. 7. Hospital for Sick Children, St. Michael's Hospital, Toronto, ON, Canada. 8. University Health Network, University of Toronto, Toronto, ON, Canada. 9. Center for Innovation, Canadian Blood Services, Toronto, ON, Canada. 10. NHS Blood and Transplant, Oxford University Hospitals and University of Oxford, Oxford, UK. 11. Division of Hematology and Thromboembolism, McMaster University, Hamilton, ON, Canada. 12. Australian Red Cross Blood Service, Brisbane, QLD, Australia. 13. Weill Cornell Medicine, New York, NY, USA. 14. Division of Hematology-Oncology, Centre Hospitalier Universitaire Sainte-Justine, University of Montreal, Montreal, QC, Canada. 15. Institut National de la Transfusion Sanguine, Paris, France. 16. Department of Obstetrics, Leiden University Medical Center, Leiden, The Netherlands. 17. Fetal Medicine Unit, Mount Sinai Hospital, Toronto, ON, Canada. 18. Royal Children's Hospital, Melbourne, VIC, Australia. 19. Department of Medicine, Mount Sinai Hospital, Toronto, ON, Canada. 20. Department of Obstetric Medicine, Mount Sinai Hospital, Toronto, ON, Canada. 21. Department of Clinical Immunology and Transfusion Medicine, Regional and University Laboratories Region Skåne, Lund, Sweden.
Abstract
BACKGROUND AND OBJECTIVES: In Caucasians, fetal/neonatal alloimmune thrombocytopenia (FNAIT) is most commonly due to maternal HPA-1a antibodies. HPA-1a typing followed by screening for anti-HPA-1a antibodies in HPA-1bb women may identify first pregnancies at risk. Our goal was to review results from previous published studies to examine whether the maternal antibody level to HPA-1a could be used to identify high-risk pregnancies. MATERIALS AND METHODS: The studies included were categorized by recruitment strategies: screening of unselected pregnancies or samples analyzed from known or suspected FNAIT patients. RESULTS: Three prospective studies reported results from screening programmes, and 10 retrospective studies focused on suspected cases of FNAIT. In 8 studies samples for antibody measurement, performed by the monoclonal antibody immobilization of platelet antigen (MAIPA) assay, and samples for determining fetal/neonatal platelet count were collected simultaneously. In these 8 studies, the maternal antibody level correlated with the risk of severe thrombocytopenia. The prospective studies reported high negative predictive values (88-95%), which would allow for the use of maternal anti-HPA-1a antibody level as a predictive tool in a screening setting, in order to identify cases at low risk for FNAIT. However, due to low positive predictive values reported in prospective as well as retrospective studies (54-97%), the maternal antibody level is less suited for the final diagnosis and for guiding antenatal treatment. CONCLUSION: HPA-1a antibody level has the potential to predict the severity of FNAIT.
BACKGROUND AND OBJECTIVES: In Caucasians, fetal/neonatal alloimmune thrombocytopenia (FNAIT) is most commonly due to maternal HPA-1a antibodies. HPA-1a typing followed by screening for anti-HPA-1a antibodies in HPA-1bb women may identify first pregnancies at risk. Our goal was to review results from previous published studies to examine whether the maternal antibody level to HPA-1a could be used to identify high-risk pregnancies. MATERIALS AND METHODS: The studies included were categorized by recruitment strategies: screening of unselected pregnancies or samples analyzed from known or suspected FNAIT patients. RESULTS: Three prospective studies reported results from screening programmes, and 10 retrospective studies focused on suspected cases of FNAIT. In 8 studies samples for antibody measurement, performed by the monoclonal antibody immobilization of platelet antigen (MAIPA) assay, and samples for determining fetal/neonatal platelet count were collected simultaneously. In these 8 studies, the maternal antibody level correlated with the risk of severe thrombocytopenia. The prospective studies reported high negative predictive values (88-95%), which would allow for the use of maternal anti-HPA-1a antibody level as a predictive tool in a screening setting, in order to identify cases at low risk for FNAIT. However, due to low positive predictive values reported in prospective as well as retrospective studies (54-97%), the maternal antibody level is less suited for the final diagnosis and for guiding antenatal treatment. CONCLUSION: HPA-1a antibody level has the potential to predict the severity of FNAIT.
Authors: Jens Kjeldsen-Kragh; Dean A Fergusson; Mette Kjaer; Lani Lieberman; Andreas Greinacher; Michael F Murphy; James Bussel; Tamam Bakchoul; Stacy Corke; Gérald Bertrand; Dick Oepkes; Jillian M Baker; Heather Hume; Edwin Massey; Cecile Kaplan; Donald M Arnold; Shoma Baidya; Greg Ryan; Helen F Savoia; Denise Landry; Nadine Shehata Journal: Blood Adv Date: 2020-07-28