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Analysis of rheumatoid factor according to various hepatitis B virus infectious statuses

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dc.contributor.authorChoi, S. T.-
dc.contributor.authorLee, H. W.-
dc.contributor.authorSong, J. -S.-
dc.contributor.authorLee, S. -K.-
dc.contributor.authorPark, Y. -B.-
dc.date.available2019-03-08T22:03:14Z-
dc.date.issued2014-03-
dc.identifier.issn0392-856X-
dc.identifier.issn1593-098X-
dc.identifier.urihttps://scholarworks.bwise.kr/cau/handle/2019.sw.cau/12461-
dc.description.abstractObjective Rheumatoid factor (RF) can be seen in hepatitis B virus (HBV) infection. We investigated RF positive rates according to various HBV infectious statuses and vaccination, and the relationship between RF titers and serum HBV DNA levels. Methods We examined 13,670 individuals who visited the Severance Hospital in Seoul, Korea, for a routine health check-up, and obtained serum samples from all individuals. Results RF was positive in 3.5% of all subjects, and HBsAg was positive in 4.3%. HBsAg was positive in 21.7% of all RF positive subjects. RF was positive in 17.5% of the HBsAg positive group, while it was positive in 2.9% of the HBsAg negative group (p<0.001). The RF positive rate was increased in positive HBsAg, female sex, and older age. The RF positive rate was lower in those who had anti-HBs after HBV vaccination than in HBsAg positive subjects (2.7% vs. 17.5%, p<0.001). Among the RF positive patients, the RF titer in HBsAg positive patients were higher than that in HBsAg negative patients (159.7+/-217.11U/mL vs. 83.0+/-179.2 IU/mL, p=0.001). The load of HBV DNA may be closely correlated with RF titer in patients with chronic hepatitis B (r=0.508, p=0.005). Conclusion Persistent HBV infection is an important cause for the positive RF in HBV endemic areas. Hepatitis B viral load is associated with RF titer. HBV vaccination may reduce the risk of RF formation.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherCLINICAL & EXPER RHEUMATOLOGY-
dc.titleAnalysis of rheumatoid factor according to various hepatitis B virus infectious statuses-
dc.typeArticle-
dc.identifier.bibliographicCitationCLINICAL AND EXPERIMENTAL RHEUMATOLOGY, v.32, no.2, pp 168 - 173-
dc.description.isOpenAccessN-
dc.identifier.wosid000335936200004-
dc.identifier.scopusid2-s2.0-84904744734-
dc.citation.endPage173-
dc.citation.number2-
dc.citation.startPage168-
dc.citation.titleCLINICAL AND EXPERIMENTAL RHEUMATOLOGY-
dc.citation.volume32-
dc.type.docTypeArticle-
dc.publisher.location이탈리아-
dc.subject.keywordAuthorrheumatoid factor-
dc.subject.keywordAuthorhepatitis B virus-
dc.subject.keywordAuthorHBsAg-
dc.subject.keywordAuthorHBV DNA-
dc.subject.keywordAuthorHBV vaccination-
dc.subject.keywordPlusANTIGEN-ANTIBODY COMPLEXES-
dc.subject.keywordPlusCLASSIFICATION CRITERIA-
dc.subject.keywordPlusAMERICAN-COLLEGE-
dc.subject.keywordPlusSURFACE-ANTIGEN-
dc.subject.keywordPlusARTHRITIS-
dc.subject.keywordPlusHBSAG-
dc.relation.journalResearchAreaRheumatology-
dc.relation.journalWebOfScienceCategoryRheumatology-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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