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Portal Vein Thrombosis in Decompensated Cirrhosis

Rationale for Treatment

Senzolo, Marco, MD, PhD1; Riva, Nicoletta, MD2; Dentali, Francesco, MD, PhD2; Sartori, Maria Teresa, MED, PhD3; Ageno, Walter, MD2 for the IRSVT Study Investigators

Clinical and Translational Gastroenterology: April 2019 - Volume 10 - Issue 4 - p e00026
doi: 10.14309/ctg.0000000000000026

1Mutivisceral Transplant Unit, University Hospital of Padua, Padua

2Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy

3Clinical Medica I, Department of Medicine, University Hospital of Padua, Padua, Italy.

Correspondence: Marco Senzolo. E-mail:

Open Access This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

Received December 05, 2018

Accepted December 14, 2018

We thank Dott. Girleanu and coauthors for the comments and the interest in our article. We agree with the authors that patients with decompensated cirrhosis are a different population compared with patients with compensated liver disease (i.e., Child A class) when they develop portal vein thrombosis (PVT) (1). In fact, a recently published article that demonstrated that the occurrence of PVT does not influence the natural history of cirrhosis included only very stable patients with almost normal liver tests (2).

In this article, although the group of patients in Child C class was not very numerous, we were able to demonstrate for the first time that patients with cirrhosis with decompensated liver disease who do not resolve PVT are characterized by a higher risk of death at 2 years of follow-up; this was not the case in Child A patients.

This study was not interventional, and the therapeutic choice was left to the clinician's judgment. Actually, in the present cohort, the patients experienced the same number of bleeding episodes if PVT was not treated and during anticoagulation treatment, but significantly less after withdrawal of anticoagulation. We interpreted this finding in relation to the possible decrease in portal pressure in those who resolved PVT. The period of anticoagulation was shorter than that in the study by Villa et al. (3), and the dose was mostly therapeutic, which can justify the higher percentage of bleeding during treatment.

Moreover, the best therapeutic approach in patients with PVT and decompensated liver disease with severe portal hypertension may not be anticoagulation as first-line treatment in all the cases.

We agree that acute PVT is difficult to catch, especially in patients with cirrhosis, probably because collateralization of the splanchnic venous system is already present, and the acute occlusion of PVT may be less symptomatic in the short term. We agree with the authors that classification of the PVT should not be merely anatomical, but based on the chance of response to anticoagulation (4), underlying the stage of cirrhosis, presence or complications of portal hypertension, and eventual candidacy of the patient to liver transplant (5).

A new classification was recently proposed (6), which may be the base to create a treatment algorithm. Probably, a transjugular intrahepatic portosystemic shunt should be considered early in the course of PVT in some patients, in particular in liver transplant candidates. A proposal of treatment algorithm for complete PVT incorporating radiological intervention is represented in Figure 1.

Figure 1

Figure 1

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Guarantor of the article: Marco Senzolo, MD, PhD.

Specific author contributions: All authors contributed to the letter.

Financial support: None.

Potential competing interests: None.

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