Abstract
Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a disease that causes thrombocytopenia and a risk of bleeding in the (unborn) child that result from maternal alloantibodies directed against fetal, paternally inherited, human platelet antigens (HPA). It is hypothesized that these alloantibodies can also bind to the placenta, causing placental damage. This study aims to explore signs of antibody-mediated placental damage in FNAIT. We performed a retrospective study that included pregnant women, their newborns, and placentas. It comprised 23 FNAIT cases, of which nine were newly diagnosed (14 samples) and 14 were antenatally treated with intravenous immune globulins (IVIg) (21 samples), and 20 controls, of which 10 had anti-HLA-class I antibodies. Clinical information was collected from medical records. Placental samples were stained for complement activation markers (C1q, C4d, SC5b-9, and mannose-binding lectin) using immunohistochemistry. Histopathology was examined according to the Amsterdam criteria. A higher degree of C4d deposition was present in the newly diagnosed FNAIT cases (10/14 samples), as compared to the IVIg-treated FNAIT cases (2/21 samples, p = 0.002) and anti-HLA-negative controls (3/20 samples, p = 0.006). A histopathological examination showed delayed maturation in four (44%) placentas in the newly diagnosed FNAIT cases, five (36%) in the IVIg-treated FNAIT cases, and one in the controls (NS). C4d deposition at the syncytiotrophoblast was present in combination with low-grade villitis of unknown etiology in three newly diagnosed FNAIT cases that were born SGA. We conclude that a higher degree of classical pathway-induced complement activation is present in placentas from pregnancies with untreated FNAIT. This may affect placental function and fetal growth.
Highlights
Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is the leading cause of thrombocytopenia and bleeding tendency in otherwise healthy and term-born infants
intracranial hemorrhage (ICH) was observed in one of the intravenous immune globulins (IVIg)-treated FNAIT cases (Group 2); this ICH was detected by ultrasound at weeks’ gestation, while the IVIg treatment was planned to start at weeks
Placental weight was below the 10th percentile in four (44%) newly diagnosed FNAIT cases, one (7%) FNAIT IVIg-treated case, and none of the controls (p = 0.022)
Summary
Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is the leading cause of thrombocytopenia and bleeding tendency in otherwise healthy and term-born infants. FNAIT is caused by maternal alloantibodies directed against paternally inherited human platelet antigens (HPA) [1]. Immunoglobulin G (IgG) class alloantibodies cross the placenta and bind to fetal platelets, resulting in thrombocytopenia and risk of bleeding. Bleeding complications in FNAIT are often caused by HPA-1a specific alloantibodies and vary from minor skin bleeding to severe intracranial hemorrhage (ICH), leading to lifelong neurological impairment or death [2]. Administration of intravenous immune globulins (IVIg) to the mother during pregnancy can prevent the hemorrhagic complications due to FNAIT [3]. Since FNAIT is predominantly diagnosed after birth, prenatal treatment can usually only be administered in subsequent pregnancies
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