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Hemostatic alterations in metabolic dysfunction-associated steatotic liver disease (MASLD) and their link to venous
David E González-Mendoza1, Francisco Fernández-Nogueira1, Misael Uribe2
1Translational Research Unit, Medica Sur Clinic & Foundation, Puente de Piedra 150, Toriello Guerra Tlalpan, Z.C, 14050, Mexico City, Mexico.
Abstract:
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver condition worldwide. It is associated with obesity, insulin resistance, type 2 diabetes, hypertension, and dyslipidemia, contributing to increased cardiovascular risk. As MASLD progresses, it may evolve into more advanced liver damage, namely metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and, in advanced stages, hepatocellular carcinoma. The liver plays a central role in hemostasis by synthesizing procoagulant, anticoagulant, and fibrinolytic factors. In MASLD patients, alterations in these hemostatic pathways may contribute to a prothrombotic state. Insulin resistance and chronic inflammation further exacerbate these disturbances, increasing the risk of thromboembolism. In conclusion, MASLD may represent not only a hepatic disorder but also an emerging cardiovascular and thromboembolic risk factor. This review aims to provide an updated overview of MASLD and its relationship with venous thromboembolism (VTE), focusing on physiological mechanisms, molecular alterations, and current clinical evidence on both conditions.
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