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      Hemostatic Alterations in Liver Disease: A Review on Pathophysiology, Clinical Consequences, and Treatment

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          Abstract

          In most patients with acute or chronic liver failure, extensive changes in all pathways contributing to hemostasis are found. These hemostatic alterations concern both pro- and antihemostatic pathways, and therefore the net result of the hemostatic dysbalance is unclear. Although it is generally believed that patients with liver disease have a hemostasis-related bleeding tendency, this concept is challenged in recent literature. Although the bleeding problems in patients with liver disease are obvious, the clinically most relevant bleeding episodes, i.e., bleeding from ruptured varices or ulcers, are due to vascular abnormalities and portal hypertension, and not to an abnormal hemostatic system. Moreover, patients with liver disease sometimes experience thrombosis of the portal vein or hepatic artery, which is in part attributed to hypercoagulation. In addition, a substantial part of the patients with liver disease undergoing liver transplantation can nowadays undergo this major surgical procedure, which involves significant hemostatic challenges, without transfusion of blood products. Therefore, the recent debate on the presence of a major hemostatic defect in patients with liver disease seems justified. This paper will review the hemostatic changes that occur in acute and chronic liver failure, and will review hemostasis testing and reversal of coagulopathy in these patients.

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          Most cited references36

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          Elevated levels of von Willebrand Factor in cirrhosis support platelet adhesion despite reduced functional capacity.

          Cirrhosis of the liver is frequently accompanied by complex alterations in the hemostatic system, resulting in a bleeding tendency. Although many hemostatic changes in liver disease promote bleeding, compensatory mechanisms also are found, including high levels of the platelet adhesive protein von Willebrand Factor (VWF). However, conflicting reports on the functional properties of VWF in cirrhosis have appeared in literature. We have measured a panel of VWF parameters in plasma from patients with cirrhosis of varying severity and causes. Furthermore, we assessed the contribution of VWF to platelet adhesion, by measuring the ability of plasma from patients with cirrhosis to support adhesion of normal or patient platelets under flow conditions. VWF antigen levels were strongly increased in patients with cirrhosis. In contrast, the relative collagen binding activity, as well as the relative ristocetin cofactor activity, was significantly lower in patients as compared with controls, indicating loss of function. Accordingly, patients had a reduced fraction of high-molecular-weight VWF multimers. Both strongly elevated and reduced activity and antigen levels of the VWF cleaving protease ADAMTS13 were found in individual patients. Adhesion of either normal or patient platelets to a collagen surface was substantially increased when these platelets were resuspended in plasma of patients with cirrhosis, as compared with control plasma. In conclusion, highly elevated levels of VWF in patients with cirrhosis contribute to the induction of primary hemostasis despite reduced functional properties of the molecule. This phenomenon might compensate for defects in platelet number and function in patients with cirrhosis.
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            Guidelines for the use of fresh-frozen plasma, cryoprecipitate and cryosupernatant.

            The indications for transfusing fresh-frozen plasma (FFP), cryoprecipitate and cryosupernatant plasma are very limited. When transfused they can have unpredictable adverse effects. The risks of transmitting infection are similar to those of other blood components unless a pathogen-reduced plasma (PRP) is used. Of particular concern are allergic reactions and anaphylaxis, transfusion-related acute lung injury, and haemolysis from transfused antibodies to blood group antigens, especially A and B. FFP is not indicated in disseminated intravascular coagulation without bleeding, is only recommended as a plasma exchange medium for thrombotic thrombocytopenic purpura (for which cryosupernatant is a possible alternative), should never be used to reverse warfarin anticoagulation in the absence of severe bleeding, and has only a very limited place in prophylaxis prior to liver biopsy. When used for surgical or traumatic bleeding, FFP and cryoprecipitate doses should be guided by coagulation studies, which may include near-patient testing. FFP is not indicated to reverse vitamin K deficiency for neonates or patients in intensive care units. PRP may be used as an alternative to FFP. In the UK, PRP from countries with a low bovine spongiform encephalopathy incidence is recommended by the Departments of Health for children born after 1 January 1996. Arrangements for limited supplies of single donor PRP of non-UK origin are expected to be completed in 2004. Batched pooled commercially prepared PRP from donors in the USA (Octaplas) is licensed and available in the UK. FFP must be thawed using a technique that avoids risk of bacterial contamination. Plastic packs containing any of these plasma products are brittle in the frozen state and must be handled with care.
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              Coagulation disorders and hemostasis in liver disease: pathophysiology and critical assessment of current management.

              Normal coagulation has classically been conceptualized as a Y-shaped pathway, with distinct "intrinsic" and "extrinsic" components initiated by factor XII or factor VIIa/tissue factor, respectively, and converging in a "common" pathway at the level of the FXa/FVa (prothrombinase) complex. Until recently, the lack of an established alternative concept of hemostasis has meant that most physicians view the "cascade" as a model of physiology. This view has been reinforced by the fact that screening coagulation tests (APTT, prothrombin time--INR) are often used as though they are generally predictive of clinical bleeding. The shortcomings of this older model of normal coagulation are nowhere more apparent than in its clinical application to the complex coagulation disorders of acute and chronic liver disease. In this condition, the clotting cascade is heavily influenced by numerous currents and counter-currents resulting in a mixture of pro- and anticoagulant forces that are themselves further subject to change with altered physiological stress such as super-imposed infection or renal failure. This report represents a summary of a recent multidisciplinary symposium held in Charlottesville, VA. We present an overview of the coagulation system in liver disease with emphasis on the limitations of the current clinical paradigm and the need for a critical re-evaluation of the current tenets governing clinical practice. With the realization that there is often limited or conflicting data, we have attempted to represent diverse opinion and experience from the perspectives of both hepatology and hematology beginning with a brief update on the physiology of normal coagulation.
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                Author and article information

                Journal
                DSU
                Dig Surg
                10.1159/issn.0253-4886
                Digestive Surgery
                S. Karger AG
                978-3-8055-8301-5
                978-3-318-01476-1
                0253-4886
                1421-9883
                2007
                July 2007
                27 July 2007
                : 24
                : 4
                : 250-258
                Affiliations
                aDepartment of Clinical Chemistry and Haematology, University Medical Centre Utrecht, Utrecht, bSurgical Research Laboratory, Department of Surgery, University Medical Centre Groningen, Groningen, and cDepartment of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands
                Article
                103655 Dig Surg 2007;24:250–258
                10.1159/000103655
                17657149
                5660f5d4-7a14-4154-8ac7-46c8df327d4a
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 2, Tables: 1, References: 62, Pages: 9
                Categories
                Paper

                Oncology & Radiotherapy,Gastroenterology & Hepatology,Surgery,Nutrition & Dietetics,Internal medicine
                Hemostatic abnormalities,Primary hemostasis,Secondary hemostasis,Fibrinolytic system,Hemostatic dysbalance,Hemostasis testing

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