Impaired fibrinolysis without hypercoagulability characterises patients with non-alcoholic fatty liver disease

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Introduction: Cardiovascular disease is the major cause of mortality in non-alcoholic fatty liver disease (NAFLD), a disease affecting one quarter of the world's population. Coagulation imbalance may be a contributing factor but is yet to be convincingly disclosed. Aim: To perform an extensive mapping of the hemostatic system; primary and secondary hemostasis and the fibrinolytic system in non-diabetic NAFLD patients. Materials and methods: Twenty-five non-diabetic, biopsy-proven NAFLD patients [12 simple steatosis; 13 non-alcoholic steatohepatitis (NASH)] investigated by a comprehensive panel of coagulation and fibrinolysis tests in a cross-sectional study. Fifty age- and sex-matched healthy persons served as controls for each of the dynamic analyses: platelet aggregation, thrombin generation, fibrin formation and lysis. Body composition, insulin resistance makers, and liver fat assessed by proton density magnetic resonance imaging were measured in the patients. Results: Fibrinolytic function was impaired in simple steatosis [median 50% clot lysis time 1123 (min–max, 618–1967) s] and NASH [1448 (521–2618) s] compared to healthy controls [403 (184–1179) s] (p < 0.0001). Plasminogen activator inhibitor-1 (PAI-1) increased stepwise above reference interval from simple steatosis [54 (29–80) ng/ml] to NASH patients [109 (65–153) ng/ml; p = 0.03]. Impaired fibrinolysis correlated with hepatic fat fraction and insulin resistance; PAI-1 correlated with obesity and insulin resistance (ρ ≥ 0.42; p ≤ 0.04). Platelet aggregation, coagulation factors, natural anticoagulants, and thrombin generation were comparable to healthy controls and established reference intervals. Conclusions: NAFLD patients had impaired fibrinolysis without significant prothrombotic changes in coagulation. The impact of this abnormality on the increased cardiovascular risk remains to be investigated.

OriginalsprogEngelsk
BogserieThrombosis Research
Vol/bind213
Sider (fra-til)9-15
Antal sider7
ISSN0049-3848
DOI
StatusUdgivet - maj 2022

Se relationer på Aarhus Universitet Citationsformater

ID: 260272499