Research progress of blood hypercoagulable state in liver cirrhosis

Abstract

Abstract: The patients with liver cirrhosis are often complicated with coagulation dysfunction, and blood hypercoagulable state is one of the manifestations. Blood hypercoagulable state is not only involved in thrombosis, the latest evidence confirms that it is also involved in liver injury, liver regeneration and liver fibrosis. This review attempts to discuss the mechanism of blood hypercoagulable state in liver cirrhosis, the role of intestinal microecological environment in it and the latest influence mechanism of blood hypercoagulable state in liver cirrhosis.To provide a new concept for the diagnosis and treatment of patients with liver cirrhosis.

Key words: blood hypercoagulable state, liver fibrosis, liver regeneration, liver injury, intestinal microecological environment

CLC Number:

R512.6

QI Wan-rong, MAO Xiao-rong, LI Jun-feng. Research progress of blood hypercoagulable state in liver cirrhosis[J]. Basic & Clinical Medicine, 2021, 41(3): 423-427.

References

[1] Carnevale R, Raparelli V, Nocella C, et al. Gut-derived endotoxin stimulates factor Ⅷ secretion from endothelial cells. implications for hypercoagulability in cirrhosis[J]. J Hepatol, 2017, 67: 950-956.
[2] Jackel S, Kiouptsi K, Lillich M, et al. Gut microbiota regulate hepatic von Willebrand factor synthesis and arterial thrombus formation via toll-like receptor-2[J]. Blood, 2017, 130: 542-553.
[3] James S, Ana-Violeta F, Jack T, et al. Stimulated release of intraluminal vesicles from weibel-palade bodies[J]. Blood, 2019, 133: 2707-2717.
[4] Valeria R, Stefania B, Roberto C, et al. Low-grade endotoxemia and platelet activation in cirrhosis[J]. Hepatology, 2017, 65: 571-581.
[5] Scot AF, Matthew TH, Qi ZS, et al. A conditional knockout mouse model reveals endothelial cells as the principal and possibly exclusive source of plasma factor Ⅷ[J]. Blood, 2014, 123: 3706-3713.
[6] Kopec AK, Spada AP, Contreras PC, et al. Caspase inhibition reduces hepatic tissue factor-driven coagulation in vitro and in vivo[J]. Toxicol Sci, 2018,162:396-405.
[7] Heestermans M, Salloum-Asfar S, Streef T, et al. Mouse venous thrombosis upon silencing of anticoagulants depends on tissue factor and platelets, not FXII or neutrophils[J]. Blood, 2019, 133: 2090-2099.
[8] Hisada Y, Mackman N. Cancer-associated pathways and biomarkers of venous thrombosis[J]. Blood, 2017, 130: 1499-1506.
[9] Dafna G, Holly C-F, Kevin SB, et al. Von Willebrand factor delays liver repair after acetaminophen-induced acute liver injury in mice[J]. J Hepatol, 2020,72:146-155.
[10] Shan Z, Liu X, Chen Y, et al. Chitinase 3-like-1 promotes intrahepatic activation of coagulation through induction of tissue factor in mice[J]. Hepatology, 2018, 67: 2384-2396.
[11] Liang Y, Pan Q, Wang R, et al. Microvesicles derived from TGF-β1 stimulated hepatic stellate cells aggravate hepatocellular injury[J]. Stem Cells Dev, 2019, 28: 1128-1139
[12] James PL, Jonathan GS, Matthew JF. The multifaceted role of fibrinogen in tissue injury and inflammation[J]. Blood, 2019, 133: 511-520.
[13] Plompen EP, Darwish MS, Hansen BE, et al. Prothrombotic genetic risk factors are associated with an increased risk of liver fibrosis in the general population: the rotterdam study[J]. J Hepatol, 2015, 63: 1459-1465.
[14] Knight V, Lourensz D, Tchongue J, et al. Cytoplasmic domain of tissue factor promotes liver fibrosis in mice[J]. World J Gastroenterol, 2017, 23: 5692-5699.
[15] Joshi N, Kopec AK, Ray JL, et al. Fibrin deposition following bile duct injury limits fibrosis through an alphambeta2-dependent mechanism[J]. Blood, 2016, 127: 2751-2762.
[16] Patrick S, David P, Stefanie H, et al. Perioperative von Willebrand factor dynamics are associated with liver regeneration and predict outcome after liver resection[J]. Hepatology, 2018, 67: 1516-1530.
[17] Groeneveld D, Pereyra D, Veldhuis Z, et al. Intrahepatic fibrin(ogen) deposition drives liver regeneration after partial hepatectomy in mice and humans[J]. Blood, 2019, 133: 1245-1256.
[18] Kopec AK, Joshi N, Cline-Fedewa H, et al. Fibrin(ogen) drives repair after acetaminophen-induced liver injury via leukocyte alphambeta2 integrin-dependent upregulation of mmp12[J]. J Hepatol, 2017, 66: 787-797.
[19] Gao SQ, Robert SM, Amanda RB, et al. Excessive plas-min compromises hepatic sinusoidal vascular integrity after acetaminophen overdose[J]. Hepatology, 2018, 68: 1991-2003.
[20] Rajpal S, Ahluwalia J, Kumar N, et al. Elevated von willebrand factor antigen levels are an independent risk factor for venous thromboembolism: first report from north india[J]. Indian J Hematol Blood Transfus, 2019, 35:489-495.
[21] Filipe N, Sylvie C, Bertrand C, et al. Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study[J]. Hepatology, 2015, 61: 660-667.
[22] Hernandez-Gea V, Gottardi AD, Leebeek FWG, et al. Current knowledge in pathophysiology and management of budd-chiari syndrome and non-cirrhotic non-tumoral splan-chnic vein thrombosis[J]. J Hepatol, 2019, 71: 175-199.