The Pathophysiology of Portal Vein Thrombosis in Cirrhosis: Getting Deeper into Virchow’s Triad

Anton, Aina; Campreciós, Genís; Pérez-Campuzano, Valeria; Orts, Lara; García-Pagán, Juan Carlos; Hernández‐Gea, Virginia

doi:10.3390/jcm11030800

Cited by 28 publications

(38 citation statements)

References 76 publications

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“…PVT has been a common complication that can increase the rate of bleeding, and deterioration of liver function. At present, there are a lot of studies on the risk factors of PVT formation [11][12][13][14] .…”

Section: Discussionmentioning

confidence: 99%

Analysis of related factors of portal vein thrombosis in liver cirrhosis

jin

liu

et al. 2022

Preprint

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Background and aims: To investigate the usefulness of IL-6、TNF-α、Protein C(PC) and Thromboelastography (TEG) to serve as a predictor of portal vein thrombosis (PVT) in patients with liver cirrhosis. At the same time, we explored the clinical significance of the above indicators in the disease progression. Methods: A total of 123 patients with liver cirrhosis were recruited from May 2021 to December 2021, according to the imaging findings. They were divided into the PVT group (n=52) and the non-PVT group (n=71). Furthermore, patients with PVT were divided into plasma transfusion groups (n=13) and non-plasma transfusion groups (n=39). The basic general information, past medical history, laboratory, and imaging examination data were collected and analyzed. Results: In univariate analysis, there was no significant difference in IL-6, PC, R, Angle, MA, and CI between the two groups (P > 0.05). TNF-α in the PVT group was significantly lower than that in the non-PVT group (P =0.001). K in the PVT group was significantly higher than that in the non-PVT group (P =0.031) There was no significant difference in IL-6, TNF-α, PC, or TEG between different Child-Pugh classification groups (P＞0.05). There was no significant difference in TEG between the plasma transfusion group and the non-plasma transfusion group. In Binary logistic regression analysis, TNF-α (OR=0.9881,95%CI=0.971,0.990,P＜0.001) ,K(OR=1.28,95%=1.053,1.569，P=0.014) ,APTT (OR=0.753,95%CI=0.656,0.865,P＜0.001) , diameter of portal vein (OR=1.310,95%CI=1.108，1.549，P=0.002）and the history of splenectomy or embolism (OR=7.565,95%CI=1.514，37.799，P=0.014）were related to the formation of PVT. Conclusions: TNF-α, K, APTT, the diameter of the portal vein and the history of splenectomy or embolism were the related factors of PVT formation, but IL-6 was not related to the formation of PVT.

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Section: Discussionmentioning

confidence: 99%

Analysis of related factors of portal vein thrombosis in liver cirrhosis

jin

liu

et al. 2022

Preprint

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“…As with any other thrombus, the pathogenesis of PVT is generally multifactorial and it is believed to be primarily determined by the interplay of the three physiological factors of Virchow’s triad: slow blood flow, hypercoagulability, and endothelial damage. Nevertheless, the exact contribution of each of these factors to PVT development was not fully elucidated [ 24 ].…”

Section: Pathophysiology and Risk Factorsmentioning

confidence: 99%

“…Indeed, in two large prospective studies, NSBB were not associated with an increased risk of PVT after adjustment for variables related to the severity of portal hypertension [ 28 , 29 ]. Therefore, the use of NSBB should not be limited based on this concern, even more so considering their larger benefits in patients with cirrhosis [ 24 ].…”

Section: Pathophysiology and Risk Factorsmentioning

confidence: 99%

“…This new equilibrium is fragile and can easily be tipped towards either a prohemorrhagic or a prothrombotic phenotype. Furthermore, it was suggested that this potential prothrombotic state is intimately involved in the progression of liver disease and could also be involved in PVT development [ 3 , 24 , 36 , 37 ].…”

Section: Pathophysiology and Risk Factorsmentioning

confidence: 99%

“…Several studies have evaluated whether the hemostatic alterations associated with cirrhosis increase the risk of PVT and were extensively reviewed elsewhere [ 24 ]. Traditional coagulation tests (e.g., prothrombin time or partial thromboplastin time) do not adequately reflect this new hemostatic balance since they do not take into account the inhibition of thrombin by anticoagulant factors [ 3 , 36 ].…”

Section: Pathophysiology and Risk Factorsmentioning

confidence: 99%

See 2 more Smart Citations

Portal Vein Thrombosis in the Setting of Cirrhosis: A Comprehensive Review

Odriozola

Puente

Cuadrado‐Lavín

et al. 2022

JCM

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Portal vein thrombosis constitutes the most common thrombotic event in patients with cirrhosis, with increased rates in the setting of advanced liver disease. Despite being a well-known complication of cirrhosis, the contribution of portal vein thrombosis to hepatic decompensation and overall mortality is still a matter of debate. The incorporation of direct oral anticoagulants and new radiological techniques for portal vein recanalization have expanded our therapeutic arsenal. However, the lack of large prospective observational studies and randomized trials explain the heterogenous diagnostic and therapeutic recommendations of current guidelines. This article seeks to make a comprehensive review of the pathophysiology, clinical features, diagnosis, and treatment of portal vein thrombosis in patients with cirrhosis.

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Predicting de‐novo portal vein thrombosis after HCV eradication: A long‐term competing risk analysis in the ongoing PITER cohort

Kondili,

Zanetto,

Quaranta

et al. 2023

UEG Journal

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Background & AimsSustained virological response (SVR) by direct‐acting antivirals (DAAs) may reverse the hypercoagulable state of HCV cirrhosis and the portal vein thrombosis (PVT) risk. We evaluated the incidence and predictive factors of de novo, non‐tumoral PVT in patients with cirrhosis after HCV eradication.MethodsPatients with HCV‐related cirrhosis, consecutively enrolled in the multi‐center ongoing PITER cohort, who achieved the SVR using DAAs, were prospectively evaluated. Kaplan‐Meier and competing risk regression analyses were performed.ResultsDuring a median time of 38.3 months (IQR: 25.1–48.7 months) after the end of treatment (EOT), among 1609 SVR patients, 32 (2.0%) developed de novo PVT. A platelet count ≤120,000/μL, albumin levels ≤3.5 mg/dL, bilirubin >1.1 mg/dL, a previous liver decompensation, ALBI, Baveno, FIB‐4, and RESIST scores were significantly different (p < 0.001), among patients who developed PVT versus those who did not. Considering death and liver transplantation as competing risk events, esophageal varices (subHR: 10.40; CI 95% 4.33–24.99) and pre‐treatment ALBI grade ≥2 (subHR: 4.32; CI 95% 1.36–13.74) were independent predictors of PVT. After HCV eradication, a significant variation in PLT count, albumin, and bilirubin (p < 0.001) versus pre‐treatment values was observed in patients who did not develop PVT, whereas no significant differences were observed in those who developed PVT (p > 0.05). After the EOT, esophageal varices and ALBI grade ≥2, remained associated with de novo PVT (subHR: 9.32; CI 95% 3.16–27.53 and subHR: 5.50; CI 95% 1.67–18.13, respectively).ConclusionsIn patients with HCV‐related cirrhosis, a more advanced liver disease and significant portal hypertension are independently associated with the de novo PVT risk after SVR.

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The Pathophysiology of Portal Vein Thrombosis in Cirrhosis: Getting Deeper into Virchow’s Triad

Cited by 28 publications

References 76 publications

Analysis of related factors of portal vein thrombosis in liver cirrhosis

Analysis of related factors of portal vein thrombosis in liver cirrhosis

Portal Vein Thrombosis in the Setting of Cirrhosis: A Comprehensive Review

Predicting de‐novo portal vein thrombosis after HCV eradication: A long‐term competing risk analysis in the ongoing PITER cohort

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