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Affiliations
Christos Triantos
Department of Gastroenterology, University Hospital of Patras, Patras, Greece
Emmanuel Louvros
Department of Gastroenterology, University Hospital of Patras, Patras, Greece
Maria Kalafateli
Department of Gastroenterology, University Hospital of Patras, Patras, Greece
Anne Riddell
Katharine Dormandy Haemophilia Centre & Thrombosis Unit, Royal Free Hospital, London, UK
Ulrich Thalheimer
Institute of Liver and Digestive Health, UCL London, London, UK
Maria Michailidou
Department of Internal Medicine, University Hospital of Patras, Patras, Greece
Konstantinos Thomopoulos
Department of Gastroenterology, University Hospital of Patras, Patras, Greece
Chryssoula Lampropoulou-Karatza
Department of Internal Medicine, University Hospital of Patras, Patras, Greece
Charalambos Gogos
Department of Internal Medicine, University Hospital of Patras, Patras, Greece
Vasiliki Nikolopoulou
Department of Gastroenterology, University Hospital of Patras, Patras, Greece
Andrew K Burroughs
Department of Gastroenterology, University Hospital of Patras, Patras, Greece
How to Cite
Endogenous Heparinoids Detected by anti-Xa Activity are Present in Blood during Acute Variceal Bleeding in Cirrhosis. A Prospective Study
Abstract
Background & Aims: Endogenous heparinoids have been detected by thromboelastography and quantified by clotting based anti-Xa activity assays in patients with cirrhosis, but their presence in variceal bleeding has not been established yet.
Methods: Clotting based anti-Xa activity was measured in A) 30 cirrhotics with variceal bleeding, B) 15 noncirrhotics with peptic ulcer bleeding, C) 10 cirrhotics without infection or bleeding, and D) 10 cirrhotics with hepatocellular carcinoma (HCC).
Results: Anti-Xa activity was not detected in ulcer bleeders or in cirrhotics without infection or bleeding
but was present in seven (23%) variceal bleeders (median levels: 0.03 u/mL (0.01-0.07)) and was quantifiable for 3 days in six of seven patients. Four of seven variceal bleeders with anti-Xa activity present had HCC (p=0.023). Age, creatinine, platelet count and total infections the second day from admission were significantly correlated with the presence of measureable anti-Xa levels (p=0.014, 0.032, 0.004 and 0.019, respectively). In the HCC group, anti-Xa activity was present in three patients (30%) [median levels: 0.05 u/mL (0.01-0.06)].
Conclusions: In this study, variceal bleeders and 30% of the patients with HCC had endogenous heparinoids that were detected by a clotting based anti-Xa activity assay, whereas there was no anti Xa activity present in patients with cirrhosis without infection, or bleeding or HCC, nor in those with ulcer bleeding. Thus, the anti-Xa activity is likely to be a response to bacterial infection and/or presence of HCC in cirrhosis.
List of abbreviations: AFP, alpha-fetoprotein; aPTT, activated partial thromboplastin time; CP, Child-Pugh; FXa, activated factor X; GAGS, glycosaminoglycans; Hb, hemoglobin; HCC, hepatocellular carcinoma; HVPG, hepatic venous pressure gradient; INR, International normalized ratio; LMWHs, low molecular weight heparins; MELD, Model for End-stage Liver Disease; PPP, platelet-poor plasma; PRBC, packed red blood cells; PT, prothrombin time; SBP, sponataneous bacterial peritonitis; TEG, thromboelastography; WBC, white blood cells.