Expert Opinion

A major research gap: The use of anticoagulants in cirrhosis

Marco Senzolo1,2,3, Juan Carlos Garcia-Pagan3,4,5,*

Summary
Historically, anticoagulants were contraindicated in patients with cirrhosis owing to concerns about bleeding risks. However,
recent studies have shown that patients with cirrhosis are not naturally anticoagulated and are at increased risk of prothrombotic
events, such as portal venous thrombosis. In this article, we review preclinical and clinical data on the effects of anticoagulants in
cirrhosis, including their potential benefits in reducing liver fibrosis, portal hypertension, and improving survival. Despite promising
preclinical evidence, clinical translation has proven challenging. Nevertheless, we discuss the use of anticoagulation in specific
clinical scenarios, such as patients with atrial fibrillation and portal vein thrombosis, and highlight the need for further research,
including randomised-controlled trials, to determine the optimal role of anticoagulants in the management of patients
with cirrhosis.
© 2023 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver. This is an open access article under
the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Introduction
The relationship between anticoagulation and cirrhosis has
markedly changed during the last decades. For many years,
this relationship was one of strict and mutual avoidance
because the low platelet count and high international normal-
ised ratio usually found in patients with cirrhosis were inter-
preted as evidence of a spontaneous anticoagulated state and
a high risk of bleeding (portal hypertension and non-portal
hypertension-related). Moreover, potentially major bleeding in
frail patients at risk of minor trauma or falls has probably led to
hesistance to prescribe anticoagulants. Thus, anticoagulants
were considered highly dangerous and, in general, contra-
indicated in patients with cirrhosis. However, several studies
have shown that patients with cirrhosis are not naturally anti-
coagulated. In fact, they are more prone to develop pro-
thrombotic events (e.g. thrombosis of the portal venous
system), leading to an interest in these agents as potentially
therapeutic in cirrhosis. Although these findings have led to the
more liberal use of anticoagulants in patients with cirrhosis who
have developed thrombotic events, they have not yet culmi-
nated in the establishment of anticoagulants as a cornerstone
of treatment in these patients.
This article will briefly review the preclinical and clinical data
supporting anticoagulation in cirrhosis. We will also discuss the
past and current challenges in assessing the safety and effi-
cacy of anticoagulants in these patients and identify what is still
needed to define the proper role of anticoagulants in the
management of patients with cirrhosis.
Several studies have evaluated the effects of different types
and doses of anticoagulants (heparin, vitamin K antagonists
and direct oral anticoagulants [DOACs]) in different murine
models of cirrhosis (Table 1). These studies have shown the
beneficial effects of anticoagulation, including reducing liver
fibrosis, hepatic stellate cell activation, and portal hypertension,
and improving liver function and survival (1) Moreover, ac-
cording to studies conducted on mice fed high-fat diets,
dabigatran, a direct thrombin inhibitor, appears to have a pro-
tective effect against hepatic fibrin deposition, inflammation,
and hepatocellular damage.2 In addition, dabigatran has also
been associated with a reduction in high-fat diet-induced
weight gain.3
One might assume that such impressive effects would have
led to rapid clinical translation. However, frequently, the robust
efficacy of different strategies observed in animal models is not
confirmed in humans; therefore, establishing the efficacy of
anticoagulants in patients with cirrhosis is mandatory.
Randomised-controlled trials (RCTs) are the most robust way
to demonstrate the effectiveness and safety of new treatments,
and this approach has been used to establish indications for
anticoagulants in several other clinical situations, mainly in the
cardiovascular or osteoarticular domains.4,5 In these studies,
thousands of patients were included to evaluate the efficacy

Keywords: anticoagulation; cirrhosis; portal vein thrombosis.

Received 3 March 2023; received in revised form 28 May 2023; accepted 2 June 2023; available online 10 June 2023
* Corresponding authors. Address: Gastroenterology & Multivisceral Transplant Unit, Azienda Ospedale - Università Padova, Department of Surgery,
Oncology and Gastroenterology, University of Padova, Padova, Italy; Tel.: +39-049-8218726. (M. Senzolo), or Barcelona Hepatic Hemodynamic
Laboratory, Liver Unit, Hospital Clínic, Institut de Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona.
CIBEREHD (Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas). Health Care Provider of the European Reference
Network on Rare Liver Disorders (ERN-Liver). (J.C. Garcia-Pagan).
E-mail addresses: marcosenzolo@hotmail.com (M. Senzolo), jcgarcia@clinic.cat (J.C. Garcia-Pagan).
https://doi.org/10.1016/j.jhep.2023.06.001

Journal of Hepatology, December 2023. vol. 79 j 1566–1570

 Table 1. Studies evaluating the effects of different types and doses of anticoagulants in different murine models of cirrhosis.
Author & year Design
Kassel et al., 2012 n.a.
Li et al., 2006 n.a.
Lee et al., 2011 n.a.
Journal of Hepatology, December 2023. vol. 79 j 1566–1570
Vilaseca et al., Randomised-controlled
2017 study
Cerini et al., 2016 Randomised-controlled
study
Fortea et al., 2018 n.a.
Assy et al., 2007 n.a.
Li et al., 2017 Randomised-controlled
study
Yan et al., 2017 Randomised-controlled
study
Abdel-Salam et al., Randomised-controlled
2005 study
Abe et al., 2007 n.a.
Lee et al., 2019 n.a.
Mahmoud et al., Randomised-controlled
2019 study
Mahmoud et al., Randomised-controlled
2019 study
ATIII, antithrombin III; BDL, bile duct ligated; CDAA, choline-deficient, L-amino acid-defined; CCl4, carbon tetrachloride; HF/HC, high-fat high-calorie, L-amino acid-defined; DMN, dimethylnitrosamine; LAAH, low
anticoagulant activity heparin; LMWH, low molecular weight heparin; LHP, low molecular weight heparinepluronic nanogel; NAFLD, non-alcoholic fatty liver disease; TAA, thioacetamide; UFH, unfractionated heparin.
1567
Animal type Number Model of liver damage Treatment groups Outcome Duration
C57BL/6 n.a. Western diet (40% kCal Vehicle pumps and argatroban Antifibrotic effect 23 wk
from milk fat), NAFLD pumps
Sprague-Dawley rats 52 CCl4/porcine serum, he- Normal control, CCl4, porcine Liver function tests and area of 10 wk
patic fibrosis serum, CCl4 + LAAH, and porcine collagens
serum + LAAH
Sprague-Dawley rats 24 1% DMN, hepatic fibrosis Control, DMN, DMN + LMWH, and Antifibrotic effect 4 wk
DMN + LHP
Wistar rats, Sprague- n.a. CCl4/TAA, cirrhosis Rivaroxaban and vehicle Antifibrotic effects, HSC activation, 18 wk
Dawley rats and portal pressure
Wistar rats and Sprague- n.a. CCl4/TAA, cirrhosis Enoxaparin and vehicle Antifibrotic effect and inflammation 15 wk
Dawley rats response
Sprague-Dawley rats n.a. CCl4, cirrhosis Saline, CCl4 + saline, and Survival, liver function tests, anti- 12 wk
CCl4 + enoxaparin fibrotic effect, and inflammation
response
Sprague-Dawley rats 28 TAA, hepatic cirrhosis Controls, aspirin, and enoxaparin Survival, liver function tests, and 5 wk
antifibrotic effect fibrosis
Sprague-Dawley rats 45 TAA, hepatic fibrosis TAA, TAA + low-dose aspirin, Liver function tests and antifibrotic 4 wk
TAA + high-dose aspirin, and effect
TAA + enoxaparin
C57BL/6 n.a. CCl4, cirrhosis Different groups of enzymatically Liver function tests, antifibrotic ef- 8 wk
depolymerized heparins and saline fect, and inflammation response
Sprague-Dawley rats 48 BDL, cholestatic liver injury Sham, BDL, BDL + UFH, Liver function tests 3 wk
BDL + nadroparin, BDL + tinza-
parin, and BDL + enoxaparin
Wistar rats n.a. CCl4, hepatic fibrosis CCl4 and CCl4 + dalteparin Antifibrotic effect 7 wk
Sprague-Dawley rats 24 TAA, hepatic fibrosis Saline and dabigatran etexilate Liver function tests, antifibrotic ef- 12 wk
fect, fibrin deposition, intrahepatic
angiogenesis, and portal
hypertension
Albino rats 24 CCl4, hepatic fibrosis Control group, CCl4, and Liver function tests, antifibrotic ef- 6 wk
CCl4 + rivaroxaban fect, and inflammation response
Albino rats 56 CCl4, hepatic fibrosis Normal control, fibrosis control, Liver function tests, antifibrotic ef- 6 wk
dabigatran-treated, and fect, and inflammation response
clopidogrel-treated group
Expert Opinion
and safety of anticoagulants. Positive results from these
studies have led to the approval of several anticoagulants for
everyday clinical situations, including atrial fibrillation4 and
thromboprophylaxis after a fracture,5 among others. However,
patients with chronic liver disorders were usually excluded from
these studies due to their higher risk of experiencing severe
side effects, including haemorrhagic and hepatic toxicity.
Experiencing such side effects could have precluded the
approval of anticoagulants for the aforementioned clin-
ical indications.
The risks associated with developing drugs for niche
markets, where the patient population is small, and the risk of
side effects may be higher (i.e. use of anticoagulants in pa-
tients with cirrhosis), has likely discouraged pharmaceutical
companies from investing in such potential indications.
Indeed, despite the solid preclinical evidence, the authors of
this manuscript are not aware of any industry-sponsored trial
assessing the safety or efficacy of anticoagulants in patients
with cirrhosis. An additional challenge of performing clinical
studies to evaluate the potential utility of anticoagulants in
patients with cirrhosis arises from the competition for patient
recruitment with other industry-sponsored studies, which
may be based on a weaker preclinical rationale. Therefore,
recruiting a sufficient number of patients to a study, which is
essential for ensuring that the results are statistically signifi-
cant and clinically meaningful, would be unlikely. Conse-
quently, some studies were prematurely stopped owing to
much lower recruitment than expected and thus insufficient
sample sizes (NCT02271295 and NCT02643212).
Despite all these considerations, we must recognise that
clinicians and researchers interested in investigating the role of
anticoagulants in patients with cirrhosis have been able to
provide some very interesting data in different clinical sce-
narios: i) anticoagulation used in patients with cirrhosis for a
specific indication not related to the liver disease (i.e. atrial
fibrillation); ii) anticoagulation in patients with cirrhosis who
have developed a thrombotic event, mainly portal vein throm-
bosis (PVT); and iii) anticoagulation to impact the natural history
of patients with cirrhosis.
Anticoagulation for indications not related to
liver disease
A higher incidence of atrial fibrillation has been observed in
patients with cirrhosis, regardless of the underlying cause6 and
from 2012 to 2019, there has been a 10% increase in the
prescription of anticoagulants, primarily DOACs, for atrial
fibrillation in patients with cirrhosis.7 A recent study analysed a
US national database of patients, mainly with Child-Pugh A
cirrhosis, who developed atrial fibrillation.8 The results showed
that DOACs were associated with a lower risk of all-cause
mortality than no anticoagulant treatment. A meta-analysis of
seven studies involving 19,798 patients with both atrial fibril-
lation and cirrhosis revealed that anticoagulative treatment did
not significantly increase the risk of bleeding compared to no
anticoagulation. Furthermore, the use of DOACs was associ-
ated with a lower risk of bleeding compared to warfarin.6
However, it is worth noting that most of the available data are
based on retrospective analyses and that most studies
included only a minimal number of patients with decom-
pensated cirrhosis.
1568 Journal of Hepatology, December 2023. vol. 79 j 1566–1570
Anticoagulation indicated for PVT
Data on the impact of PVT on decompensation and mortality in
patients with cirrhosis come from cohort studies, which are
mostly retrospective.8 Extended thrombosis is believed to in-
crease the risk of variceal bleeding, rebleeding, decompen-
sation, and post-transplant death in patients undergoing liver
transplantation.10–14 However, current data support that the
impact of PVT on survival is limited to those patients with
complete but not partial PVT, which is the most common form
of PVT at presentation. Only a fraction of those with partial PVT
will progress and develop a complete obstruction of the vein
(12%),12 while about 45% will improve without treatment.15
Without solid clinical evidence, these data support the use of
anticoagulants in patients with cirrhosis and PVT (usually
occluding at least 50% of the lumen). After a relatively short
period, retrospective observational studies including several
patients with cirrhosis and PVT treated with anticoagulants9
and meta-analyses of these studies have been pub-
lished.15,16 Briefly, anticoagulative treatment was associated
with a higher rate of recanalisation, a lower risk of recurrent
splanchnic vein thrombosis, and improved survival compared
to no anticoagulation. As a result of this evidence, current
clinical guidelines17,18 recommend the use of anticoagulation
in patients with cirrhosis and PVT who are either current or
potential liver transplant candidates, particularly in cases
where the thrombus occupies more than 50% of the lumen or
extends to the spleno-mesenteric confluence. It is implausible
that we will have any RCT comparing anticoagulation vs. no
treatment in this clinical setting. However, in the most opti-
mistic studies, the reported success of recanalisation or pre-
venting thrombosis progression does not exceed 60-70% of
patients during treatment. Given these limitations, there is a
need for further investigation into the use of more invasive
therapeutic strategies, such as transjugular intrahepatic por-
tosystemic shunt, compared to anticoagulation in patients with
cirrhosis and extensive PVT who are candidates for
liver transplantation.
One potential area for future RCTs would be to compare
anticoagulation vs. no treatment in patients with thrombosis
occupying less than 50% of the main portal vein lumen or
intrahepatic branches. It would help determine the optimal
treatment approach for this patient population; however, given
the described natural history of untreated PVT, the number
needed to treat to prevent progression from completing oc-
clusion, which would impact survival, would likely be very high.
Consequently, the industry’s reluctance to develop such
studies make it unlikely that they will ever be realised.
There are relevant gaps in knowledge concerning the benefit
of anticoagulants: is the benefit only observed in patients
achieving portal vein recanalisation, or are there effects of an-
ticoagulants beyond those obtained with portal vein recanali-
sation? Current data are controversial.19–22
Impact of anticoagulation on the natural history
of patients with cirrhosis
The clear benefit of anticoagulation in reducing portal hyper-
tension and liver fibrosis derives from preclinical models of
cirrhosis, together with data obtained in some retrospective
studies suggesting an effect of heparin and acenocoumarol in

decreasing portal hypertensive complications and improving
survival in patients with cirrhosis. This leads to the notion that
portal hypertension-related decompensations and survival are
the most relevant endpoints when evaluating the efficacy of
anticoagulants. By assessing the impact of anticoagulants on
these outcomes, researchers could better understand the true
clinical benefits of this therapy in this patient population and
guide clinicians in selecting the most appropriate treatment
approach. In this regard, a small RCT investigating the role of
prophylactic doses of low molecular weight heparin vs. no
treatment showed a significant decrease in the risk of
decompensation and death during 2-year follow-up in the
treatment arm.21 A recent meta-analysis, including cohort
studies of patients with cirrhosis and PVT, shows a decline in
overall mortality compared to no treatment, regardless of the
resolution of PVT, suggesting a beneficial effect of anticoagu-
lants beyond their effect on PVT.21 However, as previously
mentioned, this contrasts with two published studies19,20 in
which the benefit was only observed, or more pronounced,
when recanalisation was achieved. The previously mentioned
study conducted by Serper et al. suggests a benefit of anti-
coagulants beyond their capacity to recanalise PVT, showing
that both warfarin and DOACs were associated with a lower
incidence of hepatic decompensations and subsequent mor-
tality in patients with cirrhosis and atrial fibrillation.8
Affiliations
1
Gastroenterology and Multivisceral Transplant Unit, Azienda Ospedale - Università Padova, Padova, Italy; 2Department of Surgery, Oncology and Gastroenterology,
University of Padova, Padova, Italy; 3Health Care Provider of the European Reference Network on Rare Liver Disorders (ERN-Liver), Germany; 4Barcelona Hepatic
Hemodynamic Laboratory, Liver Unit, Hospital Clínic, Institut de Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona;
5
CIBEREHD (Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas), Spain
Abbreviations
PVT, portal vein thrombosis; RCT, randomised-controlled trial.
Financial support
The authors received no financial support to produce this manuscript.
Conflict of interest
The authors declare no conflicts of interest that pertain to this work.
Please refer to the accompanying ICMJE disclosure forms for further details.
Authors’ contributions
MS and JCGP conception, writing of the paper and revision of the literature.
Data availability statement
Data sharing is not applicable to this review article as no new data were created
or analysed in this study.
Supplementary data
Supplementary data to this article can be found online at https://doi.org/10.1016/
j.jhep.2023.06.001.
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Further evidence supporting this beneficial effect of anti-
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