Fibrinogen-Bound Sialic Acid Levels in the Dysfibrinogenaemia of Liver Disease

Francis, John G.; Armstrong, D. J.

doi:10.1159/000214666

Cited by 15 publications

(12 citation statements)

References 11 publications

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“…In stable and uncompensated cirrhosis, fibrinogen concentrations are in the reference range, but they are significantly decreased in the advanced stage of disease. Recent publications indicate that dysfibrinogenemia were associated with significantly higher sialic acid levels than controls or patients with normal fibrin polymerization [15] (fig. 1).…”

Section: Pathophysiology Of Hepatic Coagulopathy In Liver Diseasesmentioning

confidence: 99%

Delicate Balance of Bleeding and Thrombosis in End-Stage Liver Disease and Liver Transplantation

Saner

Gieseler²,

Akız³

et al. 2013

Digestion

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Liver transplantation in cirrhotic patients is accompanied by severe bleeding. Indeed, the first 100 recipients of liver allografts transplanted by Thomas E. Starzl died mainly by uncontrolled bleeding. Since then, much progress has been made as to the understanding of the pathophysiology and the treatment of hemostatic disorders in cirrhotic patients. The aim of this review is to provide a state-of-the-art overview on recent developments and treatment options for hemostatic disorder in cirrhotic patients. Patients with end-stage-liver disease (ESLD) do not suffer only from procoagulant deficiency; there is also a lack of natural anticoagulants (i.e. proteins C and S) and profibrinolytics. Conventional laboratory methods such as the determination of the international normalized ratio or the activated partial thromboplastin time cannot predict bleeding complications in these patients. Progressive diagnostic techniques reveal that cirrhotic patients have the same capacity to produce thrombin like healthy volunteers. Moreover, cirrhotic patients - and particularly those with primary biliary cirrhosis or primary sclerosing cholangitis - are at a higher risk for developing thrombosis as compared with healthy controls. Hemostatic alterations are common in cirrhotic patients; they involve both the pro- and the anticoagulant pathways. However, this is a very delicate balance, which may be shifted to either of these pathways by different treatments thereby causing bleeding or thrombosis, respectively.

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Section: Pathophysiology Of Hepatic Coagulopathy In Liver Diseasesmentioning

confidence: 99%

Delicate Balance of Bleeding and Thrombosis in End-Stage Liver Disease and Liver Transplantation

Saner

Gieseler²,

Akız³

et al. 2013

Digestion

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“…Inconsistent correlation between FIBTEM MCF and plasma fibrinogen concentration in patients undergoing liver transplantation can be explained by the presence of dysfibrinogenemia in this patient population which is associated with fibrin polymerization disorders [34,35,36,37,38,39,40]. Furthermore, it has been demonstrated in several publications and in a meta-analysis by Segal et al [41] that prolonged conventional coagulation tests are not associated with bleeding in cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Perioperative Thromboelastometry for Adult Living Donor Liver Transplant Recipients with a Tendency to Hypercoagulability: A Prospective Observational Cohort Study

Kamel

Hassanin

Ahmed

et al. 2018

Transfus Med Hemother

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Background: Hypercoagulability can lead to serious thromboembolic events. The aim of this study was to assess the perioperative coagulation status in liver transplant recipients with a tendency to hypercoagulability. Methods: In a prospective observational study (South African Cochrane Registry 201405000814129), 151 potential liver transplant recipients were screened for thrombophilic factors from October 2014 to June 2017, and 57 potential recipients fulfilled the inclusion criterion of presenting two or more of the following thrombophilic factors: low protein C, low protein S, low anti-thrombin, increased homocystein, increased antiphospholipid IgG/IgM antibodies, increased lupus anticoagulant, and positive Factor V Leiden mutation. Seven patients were excluded from the study because they fulfilled the exclusion criteria of cancelling the liver transplantation, oral anticoagulation, or intraoperative treatment with rFVIIa. Accordingly, 50 patients were included in the final analysis. Thromboelastometry (ROTEM) (EXTEM, INTEM and FIBTEM) and conventional coagulation tests (CCT) were performed preoperatively, during the anhepatic phase, post reperfusion, and on postoperative days (POD) 1, 3 and 7. ROTEM was used to guide blood product transfusion. Heparin was infused (60-180 U/kg/day) postoperatively for 3 days and then was replaced by low-molecular-weight heparin (20 mg/12 h). Results: FIBTEM MCF significantly increased postoperatively above reference range on POD 7 despite normal fibrinogen plasma concentrations (p < 0.05). Both EXTEM and INTEM demonstrated significant changes with the phases of transplantation (p < 0.05), but with no intra- or postoperative hypercoagulability observed. INTEM CT (reference range, 100-240 s) normalized on POD 3 and 7 (196.1 ± 69.0 and 182.7 ± 63.8 s, respectively), despite prolonged aPTT (59.7 ± 18.7 and 46.4 ± 15.7 s, respectively; reference range, 20-40 s). Hepatic artery thrombosis (HAT) and portal vein thrombosis (PVT) were reported in 12.0% and 2.0%, respectively, mainly after critical care discharge and with high FIBTEM MCF values in 57% on POD 3 and 86% on POD 7. Receiver operating characteristics curve analyses of FIBTEM MCF were significant predictors for thromboembolic events with optimum cut-off, area under the curve and standard error on POD 3 (>23 mm, 0.779 and 0.097; p = 0.004) and POD 7 (>28 mm, 0.706 and 0.089; p = 0.020). Red blood cells (mean ± SD, 8.68 ± 5.81 units) were transfused in 76%, fresh frozen plasma (8.26 ± 4.14 units) in 62%, and cryoprecipitate (12.0 ± 3.68 units) in 28% of recipients. None of the recipients received intraoperative platelet transfusion or any postoperative transfusion. Main transplant indication was hepatitis C infection in 82%. 76% of recipients included in this highly selected patient population showed increased lupus anticoagulant, 2% increased antiphospholipid IgG/IgM antibodies, 20% increased homocysteine, 74% decreased anti-thrombin, 78% decreased protein C, 34% decreased protein S, and 24% a positive Factor V Leiden mutation....

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“…About 60-70% of patients with liver disease have nonfunctional forms of fibrinogen due to an increased activity of sialyltransferase expressed by immature hepatocytes generated during hepatic injury. This leads to a low molecular weight fibrinogen with abnormal α chains and higher sialic acid content [26]. This counterbalances the high fibrinogen concentrations found in patients with chronic hepatitis, cholestatic jaundice, and hepatocellular carcinoma, which does not result in increased clotting ability.…”

Section: Fibrinogenmentioning

confidence: 99%