Hepatitis G virus infection in patients with hepatocellular carcinoma in Recife, Brazil

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dc.contributor.authorLeão-Filho, Gustavo Carneiro
dc.contributor.authorLopes, Edmundo P. A.
dc.contributor.authorFerraz, Alvaro Antonio B.
dc.contributor.authorMoura, Izolda
dc.contributor.authorPernambuco, J. Ricardo
dc.contributor.authorReis, Cynthia [UNIFESP]
dc.contributor.authorSilva, Antônio Eduardo B. [UNIFESP]
dc.contributor.authorFerraz, Maria Lucia G. [UNIFESP]
dc.contributor.institutionUniversidade Federal de Pernambuco (UFPE)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:48:53Z
dc.date.available2016-01-24T13:48:53Z
dc.date.issued2007-08-01
dc.description.abstractThe evidence of a higher incidence of hepatitis G virus (HGV) infection among patients with hepatocellular carcinoma (HCC) and the relatively high prevalence of patients with primary liver carcinoma without apparent risk factors in our country motivated the present study, the objective of which was to determine the frequency of HGV-ribonucleic acid (RNA) in a series of patients with HCC. the diagnosis of HCC was established based on a-fetoprotein levels (>400 ng/ml), a compatible image and/or biopsy of the hepatic nodules. Markers of hepatitis B virus (HBV) (HBsAg and anti-HBc), hepatitis C virus (HCV) (anti-HCV) and HGV (HGVRNA) were investigated using MEIA and RT-PCR (reverse transcriptase polymerase chain reaction). There were 32 patients evaluated, including 20 males (63%), with a mean age of 58 years. Twenty-eight (88%) patients were cirrhotic (Child-Pugh: A = 8 patients, B = 14, and C = 6) and 50% reported alcohol consumption. Serological hepatitis markers were detected in 26 (81%) patients, including HBV in 19 (59%), HCV in 12 (38%) and HGV in 9 (28%). Only one (3%) patient was positive for HGV alone. the prevalence of HGV in blood donors from the same region is 10%. the findings suggest that, despite the frequent detection of HGV markers in patients with HCC, isolated infection with this agent does not seem to be a relevant factor in the etiology of this carcinoma.en
dc.description.affiliationUniv Fed Pernambuco, Recife, PE, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent632-636
dc.identifierhttp://dx.doi.org/10.1093/jjco/hym063
dc.identifier.citationJapanese Journal of Clinical Oncology. Oxford: Oxford Univ Press, v. 37, n. 8, p. 632-636, 2007.
dc.identifier.doi10.1093/jjco/hym063
dc.identifier.issn0368-2811
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29882
dc.identifier.wosWOS:000250144200012
dc.language.isoeng
dc.publisherOxford Univ Press
dc.relation.ispartofJapanese Journal of Clinical Oncology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.licensehttp://www.oxfordjournals.org/access_purchase/self-archiving_policyb.html
dc.subjecthepatitis G virusen
dc.subjecthepatocellular carcinomaen
dc.subjectcirrhosisen
dc.subjecthepatitis B virusen
dc.subjecthepatitis C virusen
dc.titleHepatitis G virus infection in patients with hepatocellular carcinoma in Recife, Brazilen
dc.typeinfo:eu-repo/semantics/article
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