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dc.contributor.authorWibowo, Heri-
dc.contributor.authorNurrahmah, Sheila-
dc.contributor.authorGantini, Ria Syafitri Evi-
dc.date.accessioned2024-12-12T06:36:29Z-
dc.date.available2024-12-12T06:36:29Z-
dc.date.issued2024-06-
dc.identifier.issn2252-8083-
dc.identifier.urihttp://localhost:8080/xmlui/handle/123456789/8821-
dc.description.abstractBACKGROUND Hemolytic disease of the fetus and newborn (HDFN) is a type of anemia in the fetus or newborn, characterized by anemia, jaundice, hyperbilirubinemia, and brain damage. IgG is the only antibody that can cross the placenta. The IgG subtypes have a different ability to destroy red blood cells (RBCs). IgG1 and IgG3 can bind to Fc-phagocyte cell receptors and cause hemolysis, while IgG3 has more ability than IgG1. This study aimed to identify the antibody IgG subtype contributing to clinical manifestation differences in HDFN. METHODS This study used blood and umbilical cord blood samples from 30 pairs of mother-baby. The samples were grouped into control (not jaundice/normal bilirubin levels) and jaundice/hyperbilirubinemia groups. A self-developed IgG subtype enzymelinked immunosorbent assay protocol was performed on maternal samples, resulting in optical density. Statistical analysis was performed using SPSS software version 23. RESULTS Blood type was associated with total bilirubin expression (p = 0.005). IgG1 anti-A, IgG3 anti-A, IgG4 anti-A, IgG1 anti-B, IgG3 anti-B, and IgG4 anti-B significantly affected hyperbilirubinemia in newborns (p = 0.041, 0.013, 0.017, 0.028, 0.001, and 0.007, respectively). CONCLUSIONS IgG1 and IgG3 were more significant in causing clinical problems. IgG4 suppressed IgG activation, resulting in no destruction of the infant’s RBCs.en_US
dc.language.isoen_USen_US
dc.publisherMedical Journal of Indonesiaen_US
dc.relation.ispartofseriesBasic Medical Research;70-74-
dc.subjectABO incompatibilityen_US
dc.subjecthemolytic disease of newbornen_US
dc.subjectimmunoglobulin Gen_US
dc.titleMaternal IgG in hemolytic disease of the fetus and newborn-ABO incompatibilityen_US
dc.typeArticleen_US
Appears in Collections:VOL 33 NO 2 (2024)

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