Aspirin may reduce liver fibrosis progression: Evidence from a multicenter retrospective study of recurrent hepatitis C after liver transplantation

Poujol-Robert, Armelle; Boëlle, Pierre‐Yves; Conti, Filoména; Durand, François; Duvoux, Christophe; Wendum, Dominique; Paradis, Valérie; Mackiewicz, Vincent; Chazouillères, Olivier; Corpechot, Christophe; Poupon, Raoul

doi:10.1016/j.clinre.2014.07.004

Cited by 41 publications

(42 citation statements)

References 32 publications

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“…6 Aspirin reduces liver fibrosis progression in patients with hepatitis C recurrence after liver transplantation. 7 Observations suggest that there is increased platelet activation in cirrhotic patients contrary to previous understanding. Ferro et al mentioned that cirrhotic patients have an ongoing prothrombotic state, and for that reason portal vein thrombosis and peripheral thromboses are frequently detected in cirrhosis.…”

contrasting

confidence: 55%

Letter: should HCV cirrhotics with high bilirubin or Gilbert's syndrome be excluded from paritaprevir, ombitasvir, or dasabuvir? Authors' reply

Banerjee

Reddy

2016

Aliment Pharmacol Ther

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A recent FDA drug safety communication warns about serious risks of liver damage, liver related death or liver transplantation when the 3D-regimen is used in patients with Child B or C cirrhosis. 6 Should patients with baseline bilirubin higher than 50 lmol/L due to Gilbert syndrome be excluded from treatment with the 3D-regimen?We strongly believe that baseline bilirubin greater than 50 lmol/L should not be considered as an exclusion criterion for treatment with paritaprevir/ritonavir/ ombitasvir/dasabuvir in compensated cirrhotic patients with Gilbert syndrome without signs of advanced liver disease. A pre-treatment genetic test to ascertain the presence of Gilbert related mutation is conceivable in patients with baseline mostly unconjugated bilirubin elevation. ACKNOWLEDGEMENTDeclaration of personal and funding interests: S. Madonia has served as an advisory board member for AbbVie.

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contrasting

confidence: 55%

Letter: should HCV cirrhotics with high bilirubin or Gilbert's syndrome be excluded from paritaprevir, ombitasvir, or dasabuvir? Authors' reply

Banerjee

Reddy

2016

Aliment Pharmacol Ther

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“…Experimental studies also indicate that components of the hemostatic system drive liver fibrosis (Anstee et al , 2011). Published clinical studies support this hypothesis (Villa et al , 2012; Poujol-Robert et al , 2014) and additional clinical trials are underway to examine the effect of anticoagulants in cirrhosis (e.g., NCT02271295, NCT02643212). Elevated VWF levels are one of the reported hemostatic alterations in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 92%

Von Willebrand factor deficiency reduces liver fibrosis in mice

Joshi

Kopec

Ray

et al. 2017

Toxicology and Applied Pharmacology

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Liver diseases are associated with complex changes in the hemostatic system and elevated levels of the platelet-adhesive protein Von Willebrand factor (VWF) are reported in patients with acute and chronic liver damage. Although elevated levels of VWF are associated with fibrosis in the general population, the role of VWF in acute and chronic liver injury has not been examined in depth in experimental settings. We tested the hypothesis that VWF deficiency inhibits experimental liver injury and fibrosis. Wild-type (WT) and VWF-deficient mice were challenged with carbon tetrachloride (CCl4) and the impact of VWF deficiency on acute liver injury and chronic liver fibrosis was determined. VWF deficiency did not significantly affect acute CCl4-induced hepatocellular necrosis in mice. Chronic CCl4 challenge, twice weekly for 6 weeks, significantly increased hepatic stellate cell activation and collagen deposition in livers of WT mice. Interestingly, hepatic induction of several profibrogenic and stellate cell activation genes was attenuated in VWF-deficient mice. Moreover, birefringent sirius red staining (indicating type I and III collagens) and type I collagen immunofluorescence indicated a reduction in hepatic collagen deposition in CCl4-exposed VWF-deficient mice compared to CCl4-exposed WT mice. The results indicate that VWF deficiency attenuates chronic CCl4-induced liver fibrosis without affecting acute hepatocellular necrosis. The results are the first to demonstrate that VWF deficiency reduces the progression of liver fibrosis, suggesting a mechanistic role of elevated plasma VWF levels in cirrhosis.

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“…Recent work suggests that aspirin reduces the risk of liver fibrosis in patients who have been transplanted for hepatitis C . Mechanistically, aspirin and clopidogrel inhibit dense granule release, blocking serotonin among other small molecules.…”

Section: Discussionmentioning

confidence: 99%

“…Recent work suggests that aspirin reduces the risk of liver fibrosis in patients who have been transplanted for hepatitis C. (93) Mechanistically, aspirin and clopidogrel inhibit dense granule release, blocking serotonin among other small molecules. These drugs also inhibit the expression of a-granule-stored proteins that are involved in heterotypic interactions between platelets/ leukocytes and the endothelium including P-selectin and CD40L.…”

Section: Discussionmentioning

confidence: 99%

Platelets: No longer bystanders in liver disease

et al. 2016

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Growing lines of evidence recognize that platelets play a central role in liver homeostasis and pathobiology. Platelets have important roles at every stage during the continuum of liver injury and healing. These cells contribute to the initiation of liver inflammation by promoting leukocyte recruitment through sinusoidal endothelium. They can activate effector cells, thus amplifying liver damage, and by modifying the hepatic cellular and cytokine milieu drive both hepatoprotective and hepatotoxic processes. Conclusion: In this review we summarize how platelets drive such pleiotropic actions and attempt to reconcile the paradox of platelets being both deleterious and beneficial to liver function; with increasingly novel methods of manipulating platelet function at our disposal, we highlight avenues for future therapeutic intervention in liver disease. (Hepatology 2016;64:1774‐1784)

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Aspirin may reduce liver fibrosis progression: Evidence from a multicenter retrospective study of recurrent hepatitis C after liver transplantation

Cited by 41 publications

References 32 publications

Letter: should HCV cirrhotics with high bilirubin or Gilbert's syndrome be excluded from paritaprevir, ombitasvir, or dasabuvir? Authors' reply

Letter: should HCV cirrhotics with high bilirubin or Gilbert's syndrome be excluded from paritaprevir, ombitasvir, or dasabuvir? Authors' reply

Von Willebrand factor deficiency reduces liver fibrosis in mice

Platelets: No longer bystanders in liver disease

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