Placental Complement Activation in Fetal and Neonatal Alloimmune Thrombocytopenia: An Observational Study

Autor: Leendert Porcelijn, Leendert A. Trouw, Dick Oepkes, Gestur Vidarsson, Hans J. Baelde, Enrico Lopriore, Marie-Louise P. van der Hoorn, Kyra L. Dijkstra, Carin van der Keur, C. Ellen van der Schoot, Dian Winkelhorst, Thijs W de Vos, Peter G. J. Nikkels, Masja de Haas, Rick Kapur, Lotte E van der Meeren, Michael Eikmans, Rianne D M van Bergen, Manon Bos
Přispěvatelé: Clinical Haematology, AII - Inflammatory diseases
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Male
Placenta
placental dysfunction
030204 cardiovascular system & hematology
fetal growth restriction
0302 clinical medicine
Pregnancy
Biology (General)
Complement Activation
Spectroscopy
030219 obstetrics & reproductive medicine
biology
Obstetrics
Communication
Immunoglobulins
Intravenous
General Medicine
Computer Science Applications
Chemistry
medicine.anatomical_structure
Neonatal alloimmune thrombocytopenia
Female
Antibody
Adult
medicine.medical_specialty
QH301-705.5
Catalysis
Antibodies
Inorganic Chemistry
03 medical and health sciences
Syncytiotrophoblast
Fetus
Antigen
medicine
Humans
Physical and Theoretical Chemistry
QD1-999
Molecular Biology
Retrospective Studies
placentaldysfunction
business.industry
Organic Chemistry
Histocompatibility Antigens Class I
Infant
Newborn
fetal neonatal alloimmune thrombocytopenia
medicine.disease
alloimmunization during pregnancy
Thrombocytopenia
Neonatal Alloimmune
histopathology placenta
Case-Control Studies
biology.protein
Histopathology
business
classical pathway complement activation
Villitis of unknown etiology
Zdroj: International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 22, Iss 6763, p 6763 (2021)
International journal of molecular sciences, 22(13):6763. Multidisciplinary Digital Publishing Institute (MDPI)
International Journal of Molecular Sciences, 22(13), 1. MDPI AG
International Journal of Molecular Sciences, 22(13). MDPI
ISSN: 1422-0067
1661-6596
Popis: 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.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje