2012
DOI: 10.5114/pjp.2012.32767
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Serum vaspin may be a good indicator of fibrosis in chronic hepatitis C and is not altered by antiviral therapy

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Cited by 17 publications
(22 citation statements)
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“…In the present study, there was no difference in vaspin serum levels between patients with different stages of cirrhosis according to Child-Pugh and MELD scores. This is in accordance with previous results showing that there is no further increase in vaspin serum levels when advanced fibrosis appears[21,22]. …”
Section: Discussionsupporting
confidence: 94%
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“…In the present study, there was no difference in vaspin serum levels between patients with different stages of cirrhosis according to Child-Pugh and MELD scores. This is in accordance with previous results showing that there is no further increase in vaspin serum levels when advanced fibrosis appears[21,22]. …”
Section: Discussionsupporting
confidence: 94%
“…The current study for the first time compared serum vaspin levels in cirrhotic patients with and without PVT and did not find any difference between these groups. Our previous study in CHC patients suggested serum vaspin to be a potential predictor of advanced liver fibrosis, with evident increases in subjects with advanced fibrosis[21]. However, in patients with insignificant fibrosis, serum vaspin level were significantly lower than in controls.…”
Section: Discussionmentioning
confidence: 98%
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“…Moreover, IR is a strong predictor of poor response to antiviral therapy, alongside advanced hepatic steatosis and fibrosis [6,14]. Numerous reports have demonstrated altered levels of some adipokines such as leptin, adiponectin, resistin, visfatin, vaspin, chemerin and fibroblast growth factor (FGF) 21 in CHC patients [4,15,16,17,18,19,20].…”
Section: Introductionmentioning
confidence: 99%
“…Nonetheless, in patients without fibrosis and with insignificant fibrosis vaspin serum levels were significantly lower. An evident increase invaspinlevelswasobservedinpatientswithatleast periportalfibrosis(stage2),withnofurtherincrease inpatientswithadvancedfibrosis.Thenextintriguing aspect was the fact that serum vaspin levels in patientswithadvancedfibrosiswassimilartothosein thecontrolgroup [33].Althoughitsimproperclearancebyimpairedliveror/andacompensatoryincrease havingaprotectiveeffectdirectedagainstfurtherliver injury and fibrosis progression could be possible explanations, a potential negative action of vaspin when NAFLD progresses to more advanced stages withfibrosismaynotbeexcluded.Thispresumption is based on the fact that vaspin inhibits expression of profibrogenic factors such as leptin, TNF-α, and resistin [21].Nevertheless,whenfibrosiswasestablished vaspin serum levels were not associated with itsseverityassessedaccordingChild-PughandModel ofEnd-StageLiverDisease(MELD)scores [34].Itis wellknownthatIRisanimportantriskfactoroffibrosisprogressioninchronicliverdiseases,including NAFLD [4,12,35,36,37].Inourstudy,HOMA-IR was significantly associated with fibrosis stage supportingearlierfindings.Inthecurrentstudy,hepatic vaspinmRNAexpressionwashigherinpatientswith fibrosis,butthedifferencedidnotreachstatisticalsignificance.Unfortunately,significantfibrosis(stage2) was observed only in 16% of patients. Moreover, therewerenopatientswithbridgingfibrosisorcirrhosis.Thissmallnumberofpatientswithsignificant and the lack of those with advanced fibrosis in our groupmayinfluencetheobtainedresults.…”
Section: Discussionmentioning
confidence: 99%