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Hyperbilirubinemia, hemolysis, and increased bilirubin neurotoxicity
Abstract Increased hemolysis in the presence of severe neonatal hyperbilirubinemia appears to augment the risk of bilirubin neurotoxicity. The mechanism of this intensifying effect is uncertain. In direct antiglobulin titer (DAT) positive, isoimmune hemolytic disease, the bilirubin threshold at whic...
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Published in: | Seminars in perinatology 2014-11, Vol.38 (7), p.429-437 |
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container_title | Seminars in perinatology |
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creator | Kaplan, Michael, MBChB Bromiker, Ruben, MD Hammerman, Cathy, MD |
description | Abstract Increased hemolysis in the presence of severe neonatal hyperbilirubinemia appears to augment the risk of bilirubin neurotoxicity. The mechanism of this intensifying effect is uncertain. In direct antiglobulin titer (DAT) positive, isoimmune hemolytic disease, the bilirubin threshold at which neurotoxicity occurs appears to be lower than in DAT-negative hyperbilirubinemia. In other hemolytic conditions, the hemolysis may simply facilitate the development of extremely high serum bilirubin levels. Whether the hemolytic process per se exerts an independent effect or whether a very rapid rise in serum bilirubin might lead to greater penetration of the blood–brain barrier is unclear. In this review, we survey the synergistic role of hemolysis associated with severe hyperbilirubinemia in the potentiation of bilirubin-induced neurotoxicity and suggest methods of identifying at-risk babies with increased hemolysis to allow for their increased surveillance. |
doi_str_mv | 10.1053/j.semperi.2014.08.006 |
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The mechanism of this intensifying effect is uncertain. In direct antiglobulin titer (DAT) positive, isoimmune hemolytic disease, the bilirubin threshold at which neurotoxicity occurs appears to be lower than in DAT-negative hyperbilirubinemia. In other hemolytic conditions, the hemolysis may simply facilitate the development of extremely high serum bilirubin levels. Whether the hemolytic process per se exerts an independent effect or whether a very rapid rise in serum bilirubin might lead to greater penetration of the blood–brain barrier is unclear. 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The mechanism of this intensifying effect is uncertain. In direct antiglobulin titer (DAT) positive, isoimmune hemolytic disease, the bilirubin threshold at which neurotoxicity occurs appears to be lower than in DAT-negative hyperbilirubinemia. In other hemolytic conditions, the hemolysis may simply facilitate the development of extremely high serum bilirubin levels. Whether the hemolytic process per se exerts an independent effect or whether a very rapid rise in serum bilirubin might lead to greater penetration of the blood–brain barrier is unclear. In this review, we survey the synergistic role of hemolysis associated with severe hyperbilirubinemia in the potentiation of bilirubin-induced neurotoxicity and suggest methods of identifying at-risk babies with increased hemolysis to allow for their increased surveillance.</description><subject>Bilirubin</subject><subject>Bilirubin - biosynthesis</subject><subject>Bilirubin - blood</subject><subject>Bilirubin - genetics</subject><subject>Bilirubin neurotoxicity</subject><subject>Blood-Brain Barrier</subject><subject>Coombs Test</subject><subject>DAT-positive hemolytic disease</subject><subject>End tidal carbon monoxide</subject><subject>Hemolysis</subject><subject>Hemolysis - immunology</subject><subject>Hemolysis - physiology</subject><subject>Humans</subject><subject>Hyperbilirubinemia, Neonatal - blood</subject><subject>Hyperbilirubinemia, Neonatal - complications</subject><subject>Infant, Newborn</subject><subject>Kernicterus</subject><subject>Kernicterus - blood</subject><subject>Kernicterus - etiology</subject><subject>Neonatal and Perinatal Medicine</subject><subject>Risk Factors</subject><issn>0146-0005</issn><issn>1558-075X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqFkU1P3DAQhq2qqGxpf0JRjj2QMHbsxHuhQrQFJKQe2kq9WY49EbPkY2snFfn39WoXDly4jA_zzDvyM4x94lBwUOX5pojYbzFQIYDLAnQBUL1hK66UzqFWf96yVWpUOQCoY_Y-xg1AKdcc3rFjoYSWsoYV-3qzpJCGOgpzQwP2ZM-ye-zHbokUzzI7-IwGF9BG9Nkzlw04h3EaH8nRtHxgR63tIn48vCfs9_dvv65u8rsf17dXl3e5kwKmXNZSKqF4y3XL15VorFO21nUjUXDQ68oK71pXQ-m1dFp7rHEteelrrWTZ8PKEfd7nbsP4d8Y4mZ6iw66zA45zNLxSQkKlKkio2qMujDEGbM02UG_DYjiYnUCzMQeBZifQgDZJYJo7PayYmx7989STsQR82QOYPvqPMJjoCAeHngK6yfiRXl1x8SLBdTSQs90DLhg34xyGZNFwE4UB83N3xd0RuUxV67L8D_8wmQs</recordid><startdate>20141101</startdate><enddate>20141101</enddate><creator>Kaplan, Michael, MBChB</creator><creator>Bromiker, Ruben, MD</creator><creator>Hammerman, Cathy, MD</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20141101</creationdate><title>Hyperbilirubinemia, hemolysis, and increased bilirubin neurotoxicity</title><author>Kaplan, Michael, MBChB ; Bromiker, Ruben, MD ; Hammerman, Cathy, MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-47445251f18f1962bac5a787b4e210896a2dcfc703d84c88de7e9413d78543b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Bilirubin</topic><topic>Bilirubin - biosynthesis</topic><topic>Bilirubin - blood</topic><topic>Bilirubin - genetics</topic><topic>Bilirubin neurotoxicity</topic><topic>Blood-Brain Barrier</topic><topic>Coombs Test</topic><topic>DAT-positive hemolytic disease</topic><topic>End tidal carbon monoxide</topic><topic>Hemolysis</topic><topic>Hemolysis - immunology</topic><topic>Hemolysis - physiology</topic><topic>Humans</topic><topic>Hyperbilirubinemia, Neonatal - blood</topic><topic>Hyperbilirubinemia, Neonatal - complications</topic><topic>Infant, Newborn</topic><topic>Kernicterus</topic><topic>Kernicterus - blood</topic><topic>Kernicterus - etiology</topic><topic>Neonatal and Perinatal Medicine</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kaplan, Michael, MBChB</creatorcontrib><creatorcontrib>Bromiker, Ruben, MD</creatorcontrib><creatorcontrib>Hammerman, Cathy, MD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Seminars in perinatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kaplan, Michael, MBChB</au><au>Bromiker, Ruben, MD</au><au>Hammerman, Cathy, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperbilirubinemia, hemolysis, and increased bilirubin neurotoxicity</atitle><jtitle>Seminars in perinatology</jtitle><addtitle>Semin Perinatol</addtitle><date>2014-11-01</date><risdate>2014</risdate><volume>38</volume><issue>7</issue><spage>429</spage><epage>437</epage><pages>429-437</pages><issn>0146-0005</issn><eissn>1558-075X</eissn><abstract>Abstract Increased hemolysis in the presence of severe neonatal hyperbilirubinemia appears to augment the risk of bilirubin neurotoxicity. 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subjects | Bilirubin Bilirubin - biosynthesis Bilirubin - blood Bilirubin - genetics Bilirubin neurotoxicity Blood-Brain Barrier Coombs Test DAT-positive hemolytic disease End tidal carbon monoxide Hemolysis Hemolysis - immunology Hemolysis - physiology Humans Hyperbilirubinemia, Neonatal - blood Hyperbilirubinemia, Neonatal - complications Infant, Newborn Kernicterus Kernicterus - blood Kernicterus - etiology Neonatal and Perinatal Medicine Risk Factors |
title | Hyperbilirubinemia, hemolysis, and increased bilirubin neurotoxicity |
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