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Войти в исследования Journal of hepato-biliary-pancreatic sciences · 2020
High-mobility group protein B1: A predictive biomarker for hepatic encephalopathy after transjugular intrahepatic portosystemic shunt.
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Chen Quan, Zhang Yu, Yue Zhen-Dong, Zhao Hong-Wei, Wang Lei, Fan Zhen-Hua, Liu Fu-Quan
Аннотация
BACKGROUND: The aim of the present study was to investigate whether portal level of high-mobility group protein B1 (HMGB1) is associated with hepatic encephalopathy (HE) after transjugular intrahepatic portosystemic shunt (TIPS).
METHODS: We enrolled 127 consecutive patients who underwent TIPS and collected portal and peripheral blood samples in our department from December 2017 to May 2019. HMGB1 levels were determined using enzyme-linked immunosorbent assay kits. HMGB1 and other HE related parameters were estimated by competing risk analysis, receiver operating characteristic (ROC) analysis and Kaplan-Meier analysis.
RESULTS: Patients with HE after TIPS were older (P = .019) and had higher portal HMGB1 level (P = .038) than those without. Univariate competing risk analysis: age (sHR 1.025, P = .026), hepatorenal syndrome (sHR 3.149, P = .010), model for end-of-stage liver disease (MELD) score (sHR 1.055, P = .024), prior HE (sHR 4.029, P = .0005), portal HMGB1 before TIPS (sHR 1.177, P = .001) reached statistical significance. Multivariate analysis: age (sHR 1.025, P = .037), MELD score (sHR 1.062, P = .011), prior HE (sHR 2.492, P = .030) and portal HMGB1 level before TIPS (sHR 1.217, P = .0002) were significantly different. ROC analyses and Kaplan-Meier curve showed portal HMGB1 level changes before and after TIPS (ΔHMGB1) had good predictive value in the cut-off 0.012 ng/mL (AUC = 0.748, P < .001, Sensitivity = 0.743, Specificity = 0.655).
CONCLUSIONS: Portal HMGB1 may be a therapeutic target for post-TIPS HE.
METHODS: We enrolled 127 consecutive patients who underwent TIPS and collected portal and peripheral blood samples in our department from December 2017 to May 2019. HMGB1 levels were determined using enzyme-linked immunosorbent assay kits. HMGB1 and other HE related parameters were estimated by competing risk analysis, receiver operating characteristic (ROC) analysis and Kaplan-Meier analysis.
RESULTS: Patients with HE after TIPS were older (P = .019) and had higher portal HMGB1 level (P = .038) than those without. Univariate competing risk analysis: age (sHR 1.025, P = .026), hepatorenal syndrome (sHR 3.149, P = .010), model for end-of-stage liver disease (MELD) score (sHR 1.055, P = .024), prior HE (sHR 4.029, P = .0005), portal HMGB1 before TIPS (sHR 1.177, P = .001) reached statistical significance. Multivariate analysis: age (sHR 1.025, P = .037), MELD score (sHR 1.062, P = .011), prior HE (sHR 2.492, P = .030) and portal HMGB1 level before TIPS (sHR 1.217, P = .0002) were significantly different. ROC analyses and Kaplan-Meier curve showed portal HMGB1 level changes before and after TIPS (ΔHMGB1) had good predictive value in the cut-off 0.012 ng/mL (AUC = 0.748, P < .001, Sensitivity = 0.743, Specificity = 0.655).
CONCLUSIONS: Portal HMGB1 may be a therapeutic target for post-TIPS HE.