Neonatal Intracranial Hemorrhage with a Dramatic Outcome Due to Maternal Anti CD36 Antibodies
BloodCenter of Brittany EFS, HLA-HPA Laboratory, BP91614, 35016 Rennes Cedex, France
Héma-Québec, Laboratoire de Référence et des Cellules Souches, Saint-Laurent, QC H4R 2W7, Canada
Author to whom correspondence should be addressed.
Reports 2019, 2(1), 7; https://doi.org/10.3390/reports2010007
Received: 10 January 2019 / Accepted: 1 February 2019 / Published: 5 February 2019
(This article belongs to the Special Issue Case Reports in Pediatrics)
Fetal/neonatal allo-immune thrombocytopenia (FNAIT) results from maternal immunization against fetal platelet-specific antigens (HPA) inherited from the father. Most cases involve HPA located on glycoproteins (GP) IbIX, IaIIa and IIbIIIa. Iso-immunizations can also occur in the absence of expression of membrane proteins, such as GPIIb or GPIIIa in Glanzmann patients. CD36 (also called glycoprotein GPIV) deficiency is observed in 3 to 5% of Asian and African populations. We report here the case of a 41-year-old Canadian woman originated from Africa, who delivered a male dead new-born at 39 weeks of gestation. A massive intracranial haemorrhage was identified as being the obvious cause of death. No platelet antibody against GPIbIX, IaIIa, and IIbIIIa was identified by the gold-standard Monoclonal Antibody-specific Immobilization of Platelet Antigens (MAIPA) assay. Surprisingly, anti CD36 iso-antibodies were identified in the maternal serum with a new bead-based multiplex assay. The CD36 gene was sequenced for both parents, and a mutation was identified on Exon 10 of the mother’s CD36 gene, which was absent for the father: NM_000072.3:c.975T>G inducing a STOP codon at position 325 of the mature protein. The absence of CD36 expression on the mother’s platelets was confirmed by flow cytometry.