ArticleHepatology international2026
Circulating fibronectin levels are linked to liver function, matrix remodeling, and hemostatic complications in advanced chronic liver disease.
Article in Hepatology international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03267615 (VICIS - Vienna Cirrhosis Study), which is not on this map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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VICIS - Vienna Cirrhosis Study
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18 authors.
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Abstract
BACKGROUND AND
aimsFibronectin is a multifunctional matrix glycoprotein involved in tissue remodeling and hemostasis; however, its clinical relevance in cirrhosis remains unclear. This study characterized circulating fibronectin across stages of advanced chronic liver disease (ACLD) and assessed its correlation to pathophysiological biomarkers and predictive value for liver-related complications.
methodsPatients with ACLD undergoing hepatic venous pressure gradient (HVPG) measurement were prospectively enrolled with circulating fibronectin measured simultaneously. Associations were assessed using correlation analyses and systems modeling. Competing-risk regression was used to evaluate clinical outcomes.
resultsAmong 298 patients (median HVPG 17 [12-21] mmHg; MELD 3.0 12 [9-17]), fibronectin levels were lower in decompensated than compensated ACLD (30.3 vs. 38.8 mg/dL; p < 0.001). Fibronectin correlated with hepatic synthesis (cholinesterase: Spearman's r = 0.64) and MELD 3.0 (r = - 0.47; both p < 0.001) while showing an independent positive association with ELF (β = 0.19; p < 0.001). In systems modeling, hepatic synthesis explained most of fibronectin variance (cholinesterase: 37%), followed by fibrinolysis (antiplasmin: 14%) and matrix remodeling (ELF: 12%). In exploratory analyses, higher fibronectin levels were independently associated with variceal bleeding (aSHR 1.04, p = 0.017), and lower fibronectin levels with portal vein thrombosis (aSHR 0.95, p = 0.031), when adjusted for HVPG, MELD 3.0, or IL-6. Fibronectin was not associated with other hepatic decompensation events, hepatocellular carcinoma, or liver-related mortality.
conclusionCirculating fibronectin reflects hepatic synthetic capacity and matrix remodeling. Its divergent exploratory associations with variceal bleeding and portal vein thrombosis suggest that fibronectin may capture aspects of hemostatic vulnerability. CLINICAL TRIAL NUMBER: NCT03267615.
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