Predicting portal thrombosis in cirrhosis: A prospective study of clinical, ultrasonographic and hemostatic factors

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

“…In the largest prospective study published so far (369 patients) and with a long followup (up to 48 months), performing an exhaustive evaluation of clinical, biochemical, inflammatory, acquired, and hereditary hemostatic profiles [31], as well as alterations in the hemostatic parameters, did not predict de novo PVT development. Regarding the biochemical traits, the study confirmed that many markers beyond the FVIII to protein C ratio, thrombomodulin resistance and the generation and vWF were altered, but none of them were independently associated with PVT development during the follow-up related to the stage of liver disease.…”

“…The ratio between FVIII (procoagulant) and protein C (anticoagulant) has long been suggested to reflect the coagulation status as it increases with disease progression. Nonetheless, contradictory results have been published when analyzing this ratio in cirrhotic patients with, vs without, PVT [30][31][32][33]. Recent data demonstrates that this ratio is a versatile predictor of the development of complications of cirrhosis but is unrelated to coagulation [34].…”

“…Recent data demonstrates that this ratio is a versatile predictor of the development of complications of cirrhosis but is unrelated to coagulation [34]. Similarly, the ratio of factor II to protein C has also been shown to decrease in cirrhotic patients with PVT [30,31,33] but its role as an independent risk factor for PVT development has not been demonstrated.…”

Predicting portal thrombosis in cirrhosis: Some issues

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We read with great interest the excellent manuscript based on a prospective study recently published by Turon F et al 1 In the 369 patients with cirrhosis without portal vein thrombosis (PVT), 29 patients developed non-tumoral PVT with reported incidences of 1.6%, 6.0% and 8.4% at 1, 3 and 5 years, respectively. In evaluating the incidence and risk factors for PVT development, the authors have concluded that platelet count, decreased portal blood flow velocity (PBFV) (<15 cm/sec) and history of variceal bleeding, rather than acquired or inherited hemostatic disorders and inflammatory status, were factors independently associated with a high PVT risk.

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Reply to: Correspondence on “Predicting portal thrombosis in cirrosis: A prospective study of clinical, ultrasonographic and hemostatic factors”

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To the Editor: We thank Li et al 1 and Dai et al 2 for their interest in our recent publication in the Journal of Hepatology. 3 Li et al reported the results of a thromboelastography assay in 58 patients with cirrhosis undergoing transjugular intrahepatic portosystemic shunt, 12 of whom had portal vein thrombosis (PVT). No differences in thromboelastography were found between the 12 patients with PVT and the 46 without.

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