Literature DB >> 22735303

Evaluation of coagulation abnormalities in acute liver failure.

Banwari Agarwal1, Gavin Wright, Alex Gatt, Anne Riddell, Vishwaraj Vemala, Susan Mallett, Pratima Chowdary, Andrew Davenport, Rajiv Jalan, Andrew Burroughs.   

Abstract

BACKGROUND & AIMS: In acute liver failure (ALF), prothrombin time (PT) and its derivative prothrombin time ratio (PTR) are elevated, and are considered predictors of increased bleeding risk. We aimed at determining whether increased PT/PTR reflects the haemostatic potential and bleeding risk in ALF patients.
METHODS: Twenty consecutive ALF patients were recruited. Samples were analysed on admission for standard laboratory clotting tests (e.g. PT), thromboelastography (TEG), individual pro and anticoagulant factors and thrombin generation (TG) kinetics with and without Protac, a snake venom protein C activator, and microparticle assay. TG was also measured in 20 age and sex matched healthy volunteers.
RESULTS: PT was significantly raised (50.7s ± 7.2, p=0.0001) but did not correlate with TEG parameters. TEG tracings were consistent with a hypocoagulable state in 20%, normal in 45%, and hypercoagulable in 35% of the patients. There was a concomitant and proportional reduction in plasma levels of both procoagulants and natural anticoagulant proteins, in conjunction with a significant elevation in plasma levels of factors-VIII (FVIII) and Von Willebrand factor, and microparticles, culminating in an overall efficient, albeit reduced, thrombin generation capacity in comparison with healthy individuals. A heparin-like effect (HLE) was also noted in most patients. No significant clinical bleeding complications occurred and no blood transfusions were required.
CONCLUSIONS: In ALF, despite grossly deranged PT in all patients, estimation of bleeding risk suggests that the coagulation disturbance in ALF patients is complex and heterogeneous for which an individualised approach is required.
Copyright © 2012 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

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Year:  2012        PMID: 22735303     DOI: 10.1016/j.jhep.2012.06.020

Source DB:  PubMed          Journal:  J Hepatol        ISSN: 0168-8278            Impact factor:   25.083


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