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Article: Hyperbilirubinemia and cholelithiasis in Chinese patients with hemoglobin H disease

TitleHyperbilirubinemia and cholelithiasis in Chinese patients with hemoglobin H disease
Authors
KeywordsGallstones
Gilbert syndrome
Hemoglobin H disease
Jaundice
Issue Date2005
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00277/index.htm
Citation
Annals Of Hematology, 2005, v. 84 n. 10, p. 671-674 How to Cite?
Abstract
Hemoglobin H disease (HbH) is a hemoglobinopathy peculiar to parts of the world with high incidence αthalassemia mutations. Among 90 HbH cases, 50 cases suffered from clinically significant jaundice (bilirubin >30 mmol/l), including 14 with severe jaundice (bilirubin >60 mmol/l). Cholelithiasis was found in 38 cases. The incidence is roughly eight times higher than that in background control population but 50% lower than that in β-thalassemia. The risk of gallstones was related to higher bilirubin levels but not αglobin genotype, sex, ferritin, and hemoglobin levels. Homozygotes or double heterozygotes for Gilbert alleles (17.2%), but not heterozgyotes (42.2%), were found to have a significantly increased risk of gallstones and jaundice. However, common Chinese Gilbert syndrome alleles do not completely explain the variable risks. © Springer-Verlag 2005.
Persistent Identifierhttp://hdl.handle.net/10722/150888
ISSN
2013 Impact Factor: 2.396
ISI Accession Number ID
References

 

Author Affiliations
  1. Queen Mary Hospital Hong Kong
DC FieldValueLanguage
dc.contributor.authorAu, WYen_HK
dc.contributor.authorCheung, WCen_HK
dc.contributor.authorHu, WHen_HK
dc.contributor.authorChan, GCFen_HK
dc.contributor.authorHa, SYen_HK
dc.contributor.authorKhong, PLen_HK
dc.contributor.authorMa, SKen_HK
dc.contributor.authorLiang, Ren_HK
dc.date.accessioned2012-06-26T06:13:56Z-
dc.date.available2012-06-26T06:13:56Z-
dc.date.issued2005en_HK
dc.identifier.citationAnnals Of Hematology, 2005, v. 84 n. 10, p. 671-674en_HK
dc.identifier.issn0939-5555en_HK
dc.identifier.urihttp://hdl.handle.net/10722/150888-
dc.description.abstractHemoglobin H disease (HbH) is a hemoglobinopathy peculiar to parts of the world with high incidence αthalassemia mutations. Among 90 HbH cases, 50 cases suffered from clinically significant jaundice (bilirubin >30 mmol/l), including 14 with severe jaundice (bilirubin >60 mmol/l). Cholelithiasis was found in 38 cases. The incidence is roughly eight times higher than that in background control population but 50% lower than that in β-thalassemia. The risk of gallstones was related to higher bilirubin levels but not αglobin genotype, sex, ferritin, and hemoglobin levels. Homozygotes or double heterozygotes for Gilbert alleles (17.2%), but not heterozgyotes (42.2%), were found to have a significantly increased risk of gallstones and jaundice. However, common Chinese Gilbert syndrome alleles do not completely explain the variable risks. © Springer-Verlag 2005.en_HK
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00277/index.htmen_HK
dc.relation.ispartofAnnals of Hematologyen_HK
dc.subjectGallstonesen_HK
dc.subjectGilbert syndromeen_HK
dc.subjectHemoglobin H diseaseen_HK
dc.subjectJaundiceen_HK
dc.subject.meshAllelesen_US
dc.subject.meshAsian Continental Ancestry Groupen_US
dc.subject.meshChinaen_US
dc.subject.meshCholelithiasis - Blood - Etiology - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGallstones - Etiology - Geneticsen_US
dc.subject.meshGenotypeen_US
dc.subject.meshGilbert Disease - Blood - Etiology - Geneticsen_US
dc.subject.meshHemoglobin H - Analysis - Geneticsen_US
dc.subject.meshHemoglobinuria - Blood - Classification - Geneticsen_US
dc.subject.meshHeterozygoteen_US
dc.subject.meshHumansen_US
dc.subject.meshJaundice - Etiology - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshRisk Factorsen_US
dc.subject.meshSex Factorsen_US
dc.subject.meshAlpha-Thalassemiaen_US
dc.titleHyperbilirubinemia and cholelithiasis in Chinese patients with hemoglobin H diseaseen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hken_HK
dc.identifier.emailKhong, PL:plkhong@hkucc.hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authorityChan, GCF=rp00431en_HK
dc.identifier.authorityKhong, PL=rp00467en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s00277-005-1091-8en_HK
dc.identifier.pmid16044312en_HK
dc.identifier.scopuseid_2-s2.0-27644579930en_HK
dc.identifier.hkuros111085-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27644579930&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume84en_HK
dc.identifier.issue10en_HK
dc.identifier.spage671en_HK
dc.identifier.epage674en_HK
dc.identifier.isiWOS:000232340600008-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridAu, WY=7202383089en_HK
dc.identifier.scopusauthoridCheung, WC=36934683800en_HK
dc.identifier.scopusauthoridHu, WH=37019198400en_HK
dc.identifier.scopusauthoridChan, GCF=16160154400en_HK
dc.identifier.scopusauthoridHa, SY=7202501115en_HK
dc.identifier.scopusauthoridKhong, PL=7006693233en_HK
dc.identifier.scopusauthoridMa, SK=37020910400en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK

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