{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T14:20:16Z","timestamp":1792592416017,"version":"4.5.0"},"reference-count":23,"publisher":"American Academy of Pediatrics (AAP)","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,1,1]]},"abstract":"<jats:p>OBJECTIVE. Direct antibody titer\u2013positive, blood group A or B neonates who are born to group O mothers may be at risk for hemolysis and hyperbilirubinemia. Immunoglobulin G1 and immunoglobulin G3 subclasses are associated with increased hemolysis relative to immunoglobulin G2 and immunoglobulin G4. We investigated whether identification of immunoglobulin G subclass 1 or 3 may be predictive of hemolysis and hyperbilirubinemia.<\/jats:p><jats:p>METHODS. Direct antibody titer-positive, blood group A and B neonates born to group O mothers were tested for the presence of immunoglobulin G subclasses 1 and 3 in umbilical cord blood by using a commercially available gel testing technology. By inference, neonates in whom neither immunoglobulin G1 nor immunoglobulin G3 were detected were designated immunoglobulin G2 and\/or 4. Mandatory plasma total bilirubin was measured at discharge, and additional measurements performed as clinically indicated. Hyperbilirubinemia was defined as any plasma total bilirubin value &amp;gt;95th percentile for hour of life. Blood carboxyhemoglobin and total hemoglobin concentrations were also measured on the predischarge sample. Measured carboxyhemoglobin, expressed as percentage of total hemoglobin, was corrected for ambient carbon monoxide to derive \u201ccorrected carboxyhemoglobin,\u201d a sensitive index of heme catabolism. The corrected carboxyhemoglobin\/total hemoglobin ratio was calculated to correct for any differences in total hemoglobin mass between groups.<\/jats:p><jats:p>RESULTS. Eighty-two infants were studied, 18 of whom were designated as immunoglobulin G1, 0 as immunoglobulin G3, and 64 as immunoglobulin G2 and\/or 4. The incidence of plasma total bilirubin &amp;gt;95th percentile was similar between the subgroupings. Corrected carboxyhemoglobin values and corrected carboxyhemoglobin\/total hemoglobin ratio were also similar between the subgroupings.<\/jats:p><jats:p>CONCLUSIONS. Immunoglobulin G1 was found in 22% of direct antibody titer\u2013positive, group A and B neonates who were born to group O mothers, whereas immunoglobulin G3 was rare. Hemolysis and hyperbilirubinemia could not be predicted by this gel technique that enabled identification of these immunoglobulin G subclasses.<\/jats:p>","DOI":"10.1542\/peds.2008-2617","type":"journal-article","created":{"date-parts":[[2008,12,29]],"date-time":"2008-12-29T15:58:03Z","timestamp":1230566283000},"page":"e132-e137","source":"Crossref","is-referenced-by-count":22,"title":["Failure to Predict Hemolysis and Hyperbilirubinemia by IgG Subclass in Blood Group A or B Infants Born to Group O Mothers"],"prefix":"10.1542","volume":"123","author":[{"given":"Michael","family":"Kaplan","sequence":"first","affiliation":[{"name":"Department of Neonatology"},{"name":"Faculty of Medicine, Hebrew University, Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mira","family":"Na'amad","sequence":"additional","affiliation":[{"name":"Blood Bank, Shaare Zedek Medical Center, Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aner","family":"Kenan","sequence":"additional","affiliation":[{"name":"Faculty of Medicine, Hebrew University, Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard","family":"Rudensky","sequence":"additional","affiliation":[{"name":"Blood Bank, Shaare Zedek Medical Center, Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cathy","family":"Hammerman","sequence":"additional","affiliation":[{"name":"Department of Neonatology"},{"name":"Faculty of Medicine, Hebrew University, Jerusalem, Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hendrik J.","family":"Vreman","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine, Stanford, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald J.","family":"Wong","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine, Stanford, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David K.","family":"Stevenson","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Stanford University School of Medicine, Stanford, California"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"417","published-online":{"date-parts":[[2009,1,1]]},"reference":[{"key":"2021120905125001200_R1","doi-asserted-by":"crossref","unstructured":"Grundbacher FJ. 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