Systemic inflammation as a risk factor for portal vein thrombosis in cirrhosis: a prospective longitudinal study

Nery, Filipe; Carneiro, Paula; Correia, Sofia; Macedo, Carlos Sampaio; Gandara, Judit; Valadares, Diana; Ferreira, Sofia; Oliveira, João; Gomes, Manuel Teixeira; Miranda, Helena; Rautou, Pierre‐Emmanuel; Valla, Dominique

doi:10.1097/meg.0000000000001982

Cited by 17 publications

(15 citation statements)

References 31 publications

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“…Inflammation is believed to have crucial effects on thrombi formation as systemic inflammation has been proved to be associated with increased PVT risk ( 5 , 6 ). Transforming growth factor-beta (TGF-β), a multifunctional cytokine mainly derived from platelets ( 7 , 8 ), participates in many biological and pathologic functions, including the immune response, angiogenesis, venous thrombosis, and tissue fibrosis ( 9 ).…”

Section: Introductionmentioning

confidence: 99%

Platelet-derived TGF-β1 is related to portal vein thrombosis in cirrhosis by promoting hypercoagulability and endothelial dysfunction

Jiang

et al. 2022

Front. Cardiovasc. Med.

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BackgroundPortal vein thrombosis (PVT) is a serious complication of cirrhosis accompanied by unclear pathogenesis. Transforming growth factor-beta (TGF-β) has been implicated in atherosclerosis and venous thrombosis whereas study regarding its part in PVT is lacking. The aim of this study was to explore the role of cytokine TGF-β1 in PVT and the potential mechanism.Materials and methodsWe included patients with cirrhotic gastroesophageal varices and divided them into two groups according to the presence of PVT. Serum levels of TGF-β1 were detected using Cytometric Bead Array kit and compared between two groups. Coagulation status was assessed using thromboelastography (TEG). Primary liver sinusoidal endothelial cells were treated with TGF-β1 and evaluated for endothelial dysfunction by RT-PCR.ResultsOur results uncovered that TGF-β1 (6,866.55 vs. 3,840.60 pg/ml, P = 0.015) significantly increased in the PVT group. Splenectomy might promote PVT by increasing platelet-derived TGF-β1 levels. Other cytokines showed no difference between PVT and non-PVT groups. Besides, TGF-β1 was correlated with platelet, fibrinogen, TEG-CI, TEG-MA, and TEG-α (coef = 0.733, 0.494, 0.604, 0.608, and 0.511; P < 0.001, 0.027, 0.004, 0.004, and 0.021, respectively), which indicated a hypercoagulable state in PVT patients. RT-PCR of liver sinusoidal endothelial cells showed a markable increment of von Willebrand Factor (vWF), thrombomodulin(TM), intercellular adhesion moleclar-1(ICAM-1), and vascular endothelial growth factor(VEGF) after TGF-β1 treatment, suggesting the involvement of endothelial dysfunction.ConclusionElevated platelet-derived TGF-β1 exhibited association with hypercoagulability and promoting effect on endothelial dysfunction, closely related with PVT in cirrhotic patients.

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Section: Introductionmentioning

confidence: 99%

Platelet-derived TGF-β1 is related to portal vein thrombosis in cirrhosis by promoting hypercoagulability and endothelial dysfunction

Jiang

et al. 2022

Front. Cardiovasc. Med.

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“…Such relationship between endotoxemia, inflammation and PVT has already been proposed as an attractive explanation to the observed clinical and laboratory data [43]. Recently, increased levels of IL-6 and lymphopenia were shown related to PVT development independently of markers of portal hypertension, reinforcing the idea of the role of inflammation and endothelial activation in the pathogenesis of PVT [44].…”

Section: Hypercoagulabilitymentioning

confidence: 81%

Portal Vein Thrombosis in Patients with Cirrhosis

Nery

2021

Vascular Disorders of the Liver

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Epidemiology, Diagnosis and ClassificationPVT has been described to be more frequent in patients with more severe and advanced liver disease. Actually, a bulk of epidemiological data are derived from studies conducted in patients with advanced severe chronic liver disease, e.g. waitlisted for liver transplantation (LT). In the latter context, 1-year incidence of 7.4%[1] has been reported, but prevalence by the time of LT has been estimated between 15.9 and 26% [2, 3]. In a mixed population of patients with cirrhosis stage Child-Pugh A to C, Zocco et al. observed a 1-year incidence of 16.4% [4]. A similar 1-year incidence of 17.9% was found in another cohort of patients with decompensated liver disease [5]. Yet, PVT is also a concern in more stable patients, as it has been found to occur in up to 4.6%, 8.2% and 10.7% at respectively 1-, 3-and 5-years, in a population of mostly compensated liver disease patients [6].As PVT is more commonly a clinically silent event, it is mostly uncovered at Doppler ultrasound (DUS) performed for hepatocellular carcinoma (HCC) screening. Outside the context of LT, there is currently no recommendation to routinely screen for PVT in patients with cirrhosis [7]. PVT diagnosis is generally made by DUS. DUS sensitivity in detecting PVT increases with the degree of occlusion and extension [8]. It may be difficult to differentiate bland thrombi from malignant

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“…The relationship between PVT and in ammation has been controversial, with it being unknown whether in ammation is accidental in the development of venous thrombosis or instead of a consequence of venous thrombosis 19 . IL-6 and TNF-α are familiar cytokines and some studies suggested that in ammation played a key role in the pathogenesis of venous thromboembolism 3,20,21 . It was considered that they in uence coagulation from the following three aspects 22 : down-regulation of physiological anticoagulant pathways, inhibition of brin removal, and initiation of coagulation activation.…”

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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Systemic inflammation as a risk factor for portal vein thrombosis in cirrhosis: a prospective longitudinal study

Abstract: Supplemental Digital Content is available in the text.

Cited by 17 publications

References 31 publications

Platelet-derived TGF-β1 is related to portal vein thrombosis in cirrhosis by promoting hypercoagulability and endothelial dysfunction

Platelet-derived TGF-β1 is related to portal vein thrombosis in cirrhosis by promoting hypercoagulability and endothelial dysfunction

Portal Vein Thrombosis in Patients with Cirrhosis

Analysis of related factors of portal vein thrombosis in liver cirrhosis

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