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Effects of pregnancy-induced hypertension on early-onset neonatal thrombocytopenia.

BMC Pregnancy Childbirth

January 2025

Department of Neonatology, Taizhou Hospital of Zhejiang Province affiliated to Wenzhou Medical University, Enze Hospital, Taizhou Enze Medical Center (Group), 1 East Tongyang Road, Tongyu Street, Luqiao, 318050, Zhejiang, China.

Background: Gestational hypertension and preeclampsia are potentially linked to similar pathophysiological processes. Maternal preeclampsia increases the occurrence of early-onset neonatal thrombocytopenia. We hypothesized that maternal gestational hypertension may impact the incident early-onset neonatal thrombocytopenia.

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Background: Although alloimmunization risk of pathogen-reduced (PR) platelets has been studied, the risk has not been reported with PR red blood cells (RBCs).

Study Design And Methods: In a Phase III, randomized, controlled trial (Red Cell Pathogen Inactivation), cardiac or thoracic-aorta surgery patients were randomized to transfusion with amustaline/glutathione PR versus conventional RBCs. Pre-transfusion and Day 28 samples were evaluated for Human leukocyte antigen (HLA) Class I and Class II antibodies at low, medium, and high cutoff values.

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Fetal and neonatal alloimmune thrombocytopenia (FNAIT) results from maternal antibodies targeting fetal platelets during pregnancy, often causing hemorrhagic manifestations detectable antenatally or shortly after birth. We report an atypical form of FNAIT with delayed onset in a healthy, breastfed male infant who developed diffuse petechiae 2 weeks after birth due to severe thrombocytopenia. The mother was shown to be negative for the human platelet antigen-1a (HPA-1a) allele but had anti-HPA-1a IgG antibodies, while the father and newborn were HPA-1a positive, confirming the diagnosis.

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Alloimmunization during pregnancy occurs when a mother produces antibodies against fetal antigens, leading to complications like hemolytic disease of the fetus and newborn (HDFN) and fetal and neonatal alloimmune thrombocytopenia (FNAIT). HDFN involves destruction of fetal red blood cells, potentially causing severe anemia, hydrops fetalis, and fetal death. FNAIT affects fetal platelets and possibly endothelial cells, resulting in risk of intracranial hemorrhage and brain damage.

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Objective: Fetal intracranial hemorrhage (FICH) is a rare and potentially deleterious condition. Fetal alloimmune thrombocytopenia and pathogenic variations in COL4A1/A2 genes are well-recognized causes of FICH. However, pathogenic COL4A1/A2 variations are identified in only 20% of fetuses referred for FICH after excluding other known causes, leaving the majority unexplained and making genetic counseling difficult.

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