Platelet function rather than plasmatic coagulation explains hypercoagulable state in cholestatic liver disease

Pihusch, Rudolf; Rank, Andreas; Göhring, Peter; Pihusch, Markus; Hiller, Erhard; Beuers, Ulrich

doi:10.1016/s0168-8278(02)00239-8

Cited by 106 publications

(103 citation statements)

References 37 publications

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“…However, underlying PSC was far more common in the CCA group for both comparisons. PSC has been associated with hypercoagulability 28 and may be a risk factor for hepatic artery complications after transplantation. 22 Nevertheless, we did not observe higher rates of early vascular complications in either CCA recipients of living or deceased donor livers.…”

Section: Discussionmentioning

confidence: 99%

Vascular complications after orthotopic liver transplantation after neoadjuvant therapy for hilar cholangiocarcinoma

et al. 2007

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Liver transplantation after neoadjuvant chemoradiotherapy has emerged as an effective treatment for patients with localized, node-negative, unresectable hilar cholangiocarcinoma (CCA) or CCA arising in the setting of primary sclerosing cholangitis (PSC). However, concern has arisen regarding the potential for vascular complications due to high-dose neoadjuvant therapy before transplantation. We reviewed our experience with specific aims to determine the incidences of arterial, portal, and hepatic venous complications in patients transplanted for CCA compared with patients who undergo transplantation for other indications, and to describe patient outcome as a result of these vascular complications. We reviewed data for all patients who underwent liver transplantation for CCA between January 1993 and April 2006 and compared the incidences of vascular complications to whole organ and living donor recipient control groups. Sixty-eight patients underwent neoadjuvant therapy and subsequent liver transplantation. Arterial complications arose in 21%; portal venous complications arose in 22%; and overall, 40% developed vascular complications. Late hepatic artery complications occurred more often in living donor recipients transplanted for CCA compared with the living donor control group (P ϭ 0.047). Late portal vein complications occurred more often in both whole organ and living donor recipients transplanted for CCA compared with the control groups (P ϭ 0.01 and P ϭ 0.009). Hepatic venous complications were rare. Patient and graft survival were not different between CCA and control patients. Liver transplantation with neoadjuvant therapy is associated with far higher rates of late arterial and portal venous complications, but these complications do not adversely affect patient and graft survival. Liver Transpl 13: 1372Transpl 13: -1381Transpl 13: , 2007

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Section: Discussionmentioning

confidence: 99%

Vascular complications after orthotopic liver transplantation after neoadjuvant therapy for hilar cholangiocarcinoma

et al. 2007

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“…It remains unclear whether cirrhotic patients with PBC are at a higher risk for budesonideassociated thrombosis than cirrhotic patients with other liver diseases (e.g., autoimmune hepatitis). Patients with PBC and primary sclerosing cholangitis are in a hypercoagulable state, 24 and platelet function differs between patients with cholestatic (PBC, primary sclerosing cholangitis) and noncholestatic liver disease and is stable or even hyperactive in patients with PBC and primary sclerosing cholangitis. 24 The underlying factors that may have contributed to development of PVT in cirrhotic patients with PBC during treatment with budesonide are unknown.…”

Section: Discussionmentioning

confidence: 99%

Pharmacokinetics and pharmacodynamic action of budesonide in early- and late-stage primary biliary cirrhosis

Hempfling¹,

et al. 2003

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Budesonide has been discussed as a potential treatment option in primary biliary cirrhosis (PBC). Therefore, we studied the pharmacokinetics and pharmacodynamics of budesonide in patients with PBC stage I/II and stage IV. Twelve patients with early PBC stage I/II and 7 patients with PBC stage IV under continuous treatment with ursodeoxycholic acid (UDCA) were enrolled in an exploratory trial. Each patient received oral budesonide for 3 weeks at weekly increasing dosages of 3 mg once to thrice per day. Budesonide and cortisol plasma levels, urinary cortisol excretion, serum liver tests, and immunoglobulins were determined on days 1, 7, and 21 of the study. Patients with PBC stage IV showed significantly higher peak plasma concentrations

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“…Definite evidence for impaired fibrinolysis in alcohol misusers is still needed, as previous studies assessed single components of the fibrinolytic system. In patients with primary biliary cirrhosis or sclerosing cholangitis, a hypercoagulable state has been related to hypofibrinolysis, high levels of coagulation factors and hyper homocysteinemia [56][57][58]. In non-alcoholic steatohepatitis, a tendency to a pro-coagulant state, characterized by increased factor VIII and reduced protein C, is common [59].…”

Section: Factors Tipping the Hemostatic Balance In Cirrhosismentioning

confidence: 99%

Hemostatic balance in patients with liver cirrhosis: Report of a consensus conference

Andriulli

Tripodi

Angeli

et al. 2016

Digestive and Liver Disease

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a b s t r a c tPatients with cirrhosis present with hemostatic alterations secondary to reduced availability of procoagulant and anti-coagulant factors. The net effect of these changes is a rebalanced hemostatic system. The Italian Association of the Study of the Liver (AISF) and the Italian Society of Internal Medicine (SIMI) promoted a consensus conference on the hemostatic balance in patients with cirrhosis. The consensus process started with the review of the literature by a scientific board of experts and ended with a formal consensus meeting in Rome in December 2014. The statements were graded according to quality of evidence and strength of recommendations, and approved by an independent jury. The statements presented here highlight strengths and weaknesses of current laboratory tests to assess bleeding and thrombotic risk in cirrhotic patients, the pathophysiology of hemostatic perturbations in this condition, and outline the optimal management of bleeding and thrombosis in patients with liver cirrhosis.

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Platelet function rather than plasmatic coagulation explains hypercoagulable state in cholestatic liver disease

Cited by 106 publications

References 37 publications

Vascular complications after orthotopic liver transplantation after neoadjuvant therapy for hilar cholangiocarcinoma

Vascular complications after orthotopic liver transplantation after neoadjuvant therapy for hilar cholangiocarcinoma

Pharmacokinetics and pharmacodynamic action of budesonide in early- and late-stage primary biliary cirrhosis

Hemostatic balance in patients with liver cirrhosis: Report of a consensus conference

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