Are Chronic Hepatitis C Viral Infections More Benign in Patients With Hemophilia?

Assy, Nimer; Pettigrew, Norman M.; Lee, Sam S; Chaudhary, R. K.; Johnston, James Scott; Gy, Minuk

doi:10.1111/j.1572-0241.2007.01223.x

Cited by 22 publications

(19 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Finally, in a recent study, Assy et al 30 have shown that chronic HCV infection in 12 patients with haemophilia causes less severe liver disease than in patients without haemophilia, and that the extent of histological abnormalities correlates with the severity of the underlying coagulopathy.…”

Section: Prothrombotic Factors and Hcv-associated Hepatic Fibrosis: Hmentioning

confidence: 95%

Coagulation and fibrosis in chronic liver disease

Calvaruso

Maimone

Gatt

et al. 2008

Gut

View full text Add to dashboard Cite

In the hepatic tissue repair mechanism, hepatic stellate cells (HSCs) are recruited at the site of injury and their changes reflect paracrine stimulation by all neighbouring cell types, including sinusoidal endothelial cells, Kupffer cells, hepatocytes, platelets and leucocytes. Thrombin converts circulating fibrinogen to fibrin, promotes platelet aggregation, is a potent activator of endothelial cells, acts as a chemoattractant for inflammatory cells and is a mitogen and chemoattractant for fibroblasts and vascular smooth muscle cells. Most of the cellular effects elicited by thrombin are mediated via a family of widely expressed G-protein-coupled receptors termed protease activated receptors (PARs). All known members of the PAR family stimulate cell proliferation/activation in a rat HSC line. Thrombin receptors are constitutively expressed in the liver, and their expression increases in parallel with the severity and/or the duration of liver disease. In human studies, thrombotic risk factors were found to be independently associated with the extent of fibrosis; severity of hepatitis C virus (HCV)-associated liver disease appears to be less in patients with haemophilia when compared with those with HCV alone. Several studies, based mostly on rat models, demonstrate that anticoagulants or antiplatelet agents prevent hepatic necrosis and fibrosis by acting on HSCs. These drugs could be therapeutic agents in patients with chronic liver disease and specific studies should be initiated.

show abstract

Section: Prothrombotic Factors and Hcv-associated Hepatic Fibrosis: Hmentioning

confidence: 95%

Coagulation and fibrosis in chronic liver disease

Calvaruso

Maimone

Gatt

et al. 2008

Gut

View full text Add to dashboard Cite

show abstract

“…56,58,59 In addition, patients with factor V Leiden appear to have a faster progression of hepatitis, 60 whereas hepatitis C-related liver disease in patients with hemophilia has been suggested to be milder compared with hepatitis C progression in patients without hemophilia. 61 The concept of rebalanced hemostasis-laboratory evidence From the preceding 2 sections, it is evident that patients with liver disease may experience both bleeding complications as well as thrombotic episodes. The occurrence of bleeding complications has been explained by the reduced platelet count, the decreased plasma levels of coagulation factors, and the decreased plasma levels of inhibitors of fibrinolysis.…”

Section: Clinical Evidence Of Hypercoagulationmentioning

confidence: 99%

Rebalanced hemostasis in patients with liver disease: evidence and clinical consequences

Lisman

Porte

2010

Blood

568

541

View full text Add to dashboard Cite

Patients with liver disease frequently acquire a complex disorder of hemostasis secondary to their disease. Routine laboratory tests such as the prothrombin time and the platelet count are frequently abnormal and point to a hypocoagulable state. With more sophisticated laboratory tests it has been shown that patients with liver disease may be in hemostatic balance as a result of concomitant changes in both pro-and antihemostatic pathways. Clinically, this rebalanced hemostatic system is reflected by the large proportion of patients with liver disease who can undergo major surgery without any requirement for blood product transfusion. However, the hemostatic balance in the patient with liver disease is relatively unstable as evidenced by the occurrence of both bleeding and thrombotic complications in a significant proportion of patients. Although it is still common practice to prophylactically correct hemostatic abnormalities in patients with liver disease before invasive procedures by administration of blood products guided by the prothrombin time and platelet count, we believe that this policy is not evidence-based. In this article, we will provide arguments against the traditional concept that patients with liver failure have a hemostasis-related bleeding tendency. Consequences of these new insights for hemostatic management will be discussed. (Blood. 2010;116(6):878-885)

show abstract

“…Observational studies in humans have suggested a faster disease progression of patients with fibrosis who were also carriers of factor V Leiden, although not all studies agree . In addition, patients with hemophilia and hepatitis‐related fibrosis appeared to have a slower disease progression compared to patients with hepatitis without hemophilia . The combined results of experimental animal studies and observational human studies have led to the proposal that anticoagulant drugs may be used as adjunct therapy in patients with early cirrhosis to prevent disease progression, decompensation, and delay or prevent liver transplantation or death .…”

Section: Intrahepatic Thrombosis As a Contributor To Disease Progressionmentioning

confidence: 99%

“…109,110 In addition, patients with hemophilia and hepatitis-related fibrosis appeared to have a slower disease progression compared to patients with hepatitis without hemophilia. 111 The combined results of experimental animal studies and observational human studies have led to the proposal that anticoagulant drugs may be used as adjunct therapy in patients with early cirrhosis to prevent disease progression, decompensation, and delay or prevent liver transplantation or death. 112 Indeed, a recent randomized clinical study showed that prolonged daily administration of low-molecular-weight heparin substantially delayed decompensation and death, without significant side effects.…”

Section: Intrahepatic Thrombosis As a Contributor To Disease Progrementioning

confidence: 99%

Pathogenesis, prevention, and management of bleeding and thrombosis in patients with liver diseases

Lisman

Porte

2017

Research and Practice in Thrombosis and Haemostasis

111

129

View full text Add to dashboard Cite

Essentials Patients with liver diseases may acquire substantial changes in all components of hemostasis.Hemostasis is in unstable balance due to simultaneous changes in pro‐ and antihemostatic systems.Intrahepatic activation of hemostasis may contribute to disease progression.Optimal strategies for prevention and treatment of bleeding and thrombosis are currently unknown. Patients with liver diseases may develop alterations in all components of the hemostatic system. Thrombocytopenia, low levels of coagulation factors and inhibitors, low levels of fibrinolytic proteins, and increased levels of endothelial‐derived proteins such as von Willebrand factor are all part of the coagulopathy of liver disease. Due to concomitant changes in pro‐ and antihemostatic drivers, the net effects of these complex hemostatic changes have long been unclear. According to current concepts, the hemostatic system of patients with liver disease is in an unstable balance, which explains the occurrence of both bleeding and thrombotic complications. This review will discuss etiology and management of bleeding and thrombosis in liver disease and will outline unsolved clinical questions. In addition, we will discuss the role of intrahepatic activation of coagulation for progression of liver disease, a novel paradigm with potential consequences for the general management of patients with liver disease.

show abstract

Are Chronic Hepatitis C Viral Infections More Benign in Patients With Hemophilia?

Abstract: HCV infections in hemophiliacs may be less severe than in HCV infected patients without hemophilia.

Cited by 22 publications

References 24 publications

Coagulation and fibrosis in chronic liver disease

Coagulation and fibrosis in chronic liver disease

Rebalanced hemostasis in patients with liver disease: evidence and clinical consequences

Pathogenesis, prevention, and management of bleeding and thrombosis in patients with liver diseases

Contact Info

Product

Resources

About