IL-6 significantly correlates with p-STAT3 expression and presents high variceal bleeding with mortality in cirrhotic patients: A cross-sectional study

Abstract Background/Purpose Effective mediators activate downstream transducers regulating inflammation and angiogenesis. Correlation among mediators IL-6, IL-27, TNF-α, and VEGF with STAT proteins at diverse clinical-pathologic stages of cirrhotic patients remains limited. Methods Plasma mediators were assayed from 158 naive liver cirrhosis (LC-total group) and 144 non-LC individuals. The LC-total group included 69 hepatitis B virus-infected (LC-HBV) patients, 40 hepatitis C virus-infected (LC-HCV) patients, and 49 patients without HBV−/HCV− infection (LC-NBNC). Another 144 non-LC individuals comprised 54 healthy persons (HG) and 90 chronic hepatitis patients (CH-total) as the control group. To correlate with plasma mediators, 52 paired liver tissues (CH: 41 and LC: 11 cases) served for p-STAT1 and p-STAT3 immunostaining. Results Although IL-6, IL-27, TNF-α, and VEGF were expressed significantly in CH-total versus HG ( p  = 0.011, p p  = 0.007, p  = 0.004, respectively) and overall viral hepatitis patients versus HG ( p p p p p p  = 0.001; LC-HCV vs. HG, p  = 0.001, vs. CH-HCV, p  = 0.031; LC-NBNC vs. HG, p r  = −0.346, p r  = 0.271, p  = 0.001; INR: r  = 0.308, p p  = 0.001, p  = 0.007, respectively), variceal severity ( p  = 0.045), and bleeding ( p  = 0.047), as well as patients' mortality ( p  = 0.005). Furthermore, plasma IL-6 significantly correlated with tissues p-STAT3 expression ( r  = 0.737, p  = 0.010) (IL-27: r  = 0.078, p  = 0.820; TNF-α: r  = −0.145, p  = 0.670; VEGF: r  = 0.142, p  = 0.678) in cirrhotic patients than noncirrhotic patients. Conclusion Over-expression of IL-6 reflects hepatic dysfunction and varices bleeding with mortality, as well as correlates p-STAT3 expression in cirrhotic patients.