2019
DOI: 10.1080/17474124.2019.1651644
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Visceral fat is associated with cirrhotic portal vein thrombosis

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Cited by 8 publications
(5 citation statements)
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“…The potential mechanism of PVT in obesity is the presence of inflamed dysfunctional adipose tissue, which can promote hemostasis, inflammation, and the mechanical participation of central obesity. A recent study showed that visceral fat is a hazard factor for PVT in patients with cirrhosis after liver transplantation [ 41 ]. The results of our study showed that the BMI was a hazard factor for PVT in patients with cirrhosis after resection.…”
Section: Discussionmentioning
confidence: 99%
“…The potential mechanism of PVT in obesity is the presence of inflamed dysfunctional adipose tissue, which can promote hemostasis, inflammation, and the mechanical participation of central obesity. A recent study showed that visceral fat is a hazard factor for PVT in patients with cirrhosis after liver transplantation [ 41 ]. The results of our study showed that the BMI was a hazard factor for PVT in patients with cirrhosis after resection.…”
Section: Discussionmentioning
confidence: 99%
“…11 surgical scalpel to induce wounds of approximately 2-mm diameter. Bleeding time was monitored by gen-liver disease are susceptible to both local thrombosis (54,55), i.e., in the portal vein, and to systemic thrombosis (56)(57)(58)(59). In terms of possible relevance to normal physiology, acute fluctuations in hepatic PAI-1 expression, e.g., in response to a meal or during infection (60)(61)(62), might require a compensatory increase in tPA to prevent impaired fibrinolysis.…”
Section: Discussionmentioning
confidence: 99%
“…In addition to affecting systemic fibrinolysis in obesity, regulation of fibrinolysis by hepatocytes may have other important implications in both disease and normal physiology. For example, obesity markedly increases the risk for chronic liver disease by promoting the development of NASH ( 53 ), and patients with liver disease are susceptible to both local thrombosis ( 54 , 55 ), i.e., in the portal vein, and to systemic thrombosis ( 56 59 ). In terms of possible relevance to normal physiology, acute fluctuations in hepatic PAI-1 expression, e.g., in response to a meal or during infection ( 60 62 ), might require a compensatory increase in tPA to prevent impaired fibrinolysis.…”
Section: Discussionmentioning
confidence: 99%
“…( 107,125 ) Obesity, metabolic syndrome, and NASH cirrhosis are also recognized as independent risk factors for PVT. ( 126‐128 ) There are contrasting data on the prevalence of factor V Leiden and G20210A prothrombin gene mutation in this population, and testing for these disorders in the cirrhosis population is rarely useful and does not change management. ( 113,129 ) A detailed thrombophilia workup in the patient with cirrhosis is not generally recommended unless specific concerns are raised during the history, routine laboratory and imaging workup (Table 7).…”
Section: Pvt Prevalence and Risk Factors: Patients With Cirrhosismentioning
confidence: 99%