A hypercoagulable state does not play a major role in the development of portal vein thrombosis in patients with cirrhosis

Turón, Fanny; Driever, Ellen; Baiges, Anna; Reyes, Eira Cerda; García-Criado, Maria Ángeles; Gilabert, Rosa; Brú, Concepció; Berzigotti, Annalisa; Núñez, Isabel Testón; Orts, Lara; Reverter, Juan Carlos; Blasi, Annabel; Seijó, Susana; Reverter, Enric; Bosch, Jaime; Borràs, Roger; Hernández‐Gea, Virginia; Lisman, Ton; Pagán, Juan Carlos García

doi:10.1016/s0168-8278(20)31883-3

Cited by 2 publications

(7 citation statements)

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“…HCV clearance has been shown to improve routine coagulation parameters and reduce the procoagulant imbalance, possibly leading to a more stable haemostatic equilibrium. 26,27 However, according to preliminary data from our group, 28 Several studies have identified portal blood flow velocity as the main risk factor for PVT development. The majority of patients achieving SVR show a decrease in HVPG, 3,[5][6][7][8][9][10] which may be explained by a decline in intrahepatic hepatic vascular resistance and an amelioration of hyperdynamic circulation/splanchnic vasodilatation and both mechanisms would result in opposing changes in portal venous blood flow.…”

Section: Discussionmentioning

confidence: 99%

Risk of non‐tumoural portal vein thrombosis in patients with HCV‐induced cirrhosis after sustained virological response

Mandorfer

Turón

Lens

et al. 2021

Liver International

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Background & Aims: Sustained virological response (SVR) to direct-acting antivirals ameliorates portal hypertension, improves hepatic function and may reverse the procoagulant state observed in patients with cirrhosis. However, an unexpected incidence of portal vein thrombosis (PVT) immediately after antiviral therapy has recently been reported. Therefore, we analysed the long-term impact of SVR on the development of non-tumoural PVT.Methods: Our study comprised of two well-characterized prospective cohorts (hepatitis C virus '(HCV)-Cured': n = 354/'HCV-Active': n = 179) of patients with HCV cirrhosis who underwent standardized ultrasound surveillance. In the main analysis, the event of interest was de novo non-tumoural PVT and events known to modify its natural history (orthotopic liver transplantation, transjugular intrahepatic portosystemic shunt, death, tumoural PVT and anticoagulation) were considered as competing risk. Adjusted models were built using propensity scores for baseline covariates.Moreover, predictive factors were investigated by conventional multivariate analysis.Results: Ten (2.8%) patients in the 'HCV-Cured' cohort developed a non-tumoural PVT during a median follow-up of 37.1 months, while 8 (4.5%) patients in the 'HCV-Active' cohort were diagnosed with non-tumoural PVT during a median follow-up | 2955 MANDORFER Et Al.

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Section: Discussionmentioning

confidence: 99%

Risk of non‐tumoural portal vein thrombosis in patients with HCV‐induced cirrhosis after sustained virological response

Mandorfer

Turón

Lens

et al. 2021

Liver International

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“…However, as the differences between patients with and without HCC were relatively modest and perhaps somewhat influenced by a nonidentical disease severity between the two groups, this hypothesis needs confirmation by further studies. Additionally, further prospective studies with development of PVT as clinical endpoint are still required to assess whether prothrombotic alterations of hemostasis, as detected in our study, are implicated in the pathogenesis of PVT in patients with cirrhosis, ( 5,6 ) including those with HCC.…”

Section: Discussionmentioning

confidence: 98%

“…( 21 ) In patients without liver disease, increased activation of coagulation is one of the main factors responsible for the increased thrombotic tendency in patients with cancers. ( 20 , 36 ) While awaiting large prospective trials to establish whether alterations of hemostasis are truly implicated in the pathogenesis of PVT in patients with cirrhosis, ( 5 , 6 ) and to further confirm the association between HCC and increased thrombotic tendency in these patients, we performed a case‐control study to investigate alterations of coagulation in this patient population. Because hemostasis in cirrhosis is complex, ( 1 , 3 ) and altered fibrinolysis may also be responsible for the thrombotic tendency in digestive cancers, ( 19 , 37 ) we included determination not only of coagulation but also of fibrinolysis.…”

Section: Discussionmentioning

confidence: 99%

“…(5) In a recent study including 310 patients with mostly compensated cirrhosis followed prospectively for a median of 48 months, Turon et al found that portal vein flow <15 cm/s, but not plasmatic hypercoagulability, was predictive of PVT. (6) On the other hand, the pathogenesis of PVT in cirrhosis is multifactorial and likely results from alterations in one or more components of the Virchow's triad (i.e., decreased portal vein inflow, hypercoagulability, and local damage of the portal vein wall). (5) Therefore, it is plausible that a more profound hypercoagulable state, at least in some patients, could contribute to the development of this thrombotic complication.…”

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More Pronounced Hypercoagulable State and Hypofibrinolysis in Patients With Cirrhosis With Versus Without HCC

et al. 2021

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In patients with cirrhosis, particularly those with hepatocellular carcinoma (HCC), hypercoagulability may be associated with purported increased risks of portal vein thrombosis and cirrhosis progression. In this study, we extensively investigated hemostatic alterations potentially responsible for the thrombotic tendency in HCC, and evaluated whether such alterations were predictive of hepatic decompensation. Patients with cirrhosis at all stages were prospectively recruited and underwent an extensive hemostatic assessment, including all procoagulant factors and inhibitors, thrombin generation with and without thrombomodulin (TG), profibrinolytic and antifibrinolytic factors, and plasmin-antiplasmin complex. In study part 1 (case control), we compared alterations of coagulation and fibrinolysis in patients with cirrhosis with versus without HCC. In study part 2 (prospective), the subgroup of patients with decompensated cirrhosis was followed for development of further decompensation, and predictors of outcome were assessed by multivariate analysis. One-hundred patients were recruited (50 each with and without HCC). Severity of cirrhosis was comparable between groups. Median HCC volume was 9 cm 3 (range: 5-16). Compared with controls, patients with HCC demonstrated a significantly more prothrombotic hemostatic profile due to increased TG and reduced activation of fibrinolysis, independent of cirrhosis stage. During a median follow-up of 175 days, 20 patients with decompensated cirrhosis developed further episodes of decompensation that were predicted by low FVII and high plasminogen activator inhibitor-1 levels, independent of Model for End-Stage Liver Disease score. Conclusion: Patients with cirrhosis with HCC have profound hyper-coagulable changes that can account for their increased thrombotic tendency. In contrast, hypercoagulability in patients with decompensated cirrhosis is more likely a consequence of chronic liver disease rather than a driver for cirrhosis progression. (Hepatology Communications 2021;0:1-14). P atients with cirrhosis have complex alterations of hemostasis that include low platelet count and increased levels of von Willebrand factor, reduced hepatic synthesis of both procoagulant factors and inhibitors, and altered fibrinolysis. (1) Current theory posits that these alterations result in a rebalanced but precarious hemostatic system that may easily tilt toward either hypocoagulability (increased bleeding tendency) or hypercoagulability (increased clotting tendency).

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A hypercoagulable state does not play a major role in the development of portal vein thrombosis in patients with cirrhosis

Cited by 2 publications

References 0 publications

Risk of non‐tumoural portal vein thrombosis in patients with HCV‐induced cirrhosis after sustained virological response

Risk of non‐tumoural portal vein thrombosis in patients with HCV‐induced cirrhosis after sustained virological response

More Pronounced Hypercoagulable State and Hypofibrinolysis in Patients With Cirrhosis With Versus Without HCC

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