{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T17:47:26Z","timestamp":1774633646349,"version":"3.50.1"},"reference-count":30,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,11,20]],"date-time":"2013-11-20T00:00:00Z","timestamp":1384905600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Egyptian Ministry of Higher Education"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2014,5]]},"abstract":"Abstract<\/jats:title>\n \n Background & Aims<\/jats:title>\n \n Patients with liver disease often show profound abnormalities in their haemostatic system. Studies using thrombin generation demonstrate rebalanced coagulation in patients with chronic liver disease. Our aim was to evaluate the haemostatic profile in patients with acute liver injury\/failure (\n ALI<\/jats:styled-content>\n \/\n ALF<\/jats:styled-content>\n ) compared with healthy controls.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Thrombin generation was measured in the presence and absence of thrombomodulin (\n TM<\/jats:styled-content>\n ) to activate protein C (\n PC<\/jats:styled-content>\n ) with endogenous thrombin potential (\n ETP<\/jats:styled-content>\n ; the area under the thrombin generation curve) a key parameter. Routine coagulation assays were also performed.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Thirty two patients with\n ALI<\/jats:styled-content>\n \/\n ALF<\/jats:styled-content>\n and 40 controls were recruited. Patients had grossly abnormal coagulation profiles with decreased pro\u2010 and anticoagulant factors compared with controls (\n P<\/jats:italic>\n \u00a0<\u00a00.001 for all comparisons), except for median Factor\n VIII<\/jats:styled-content>\n which was increased 247\u00a0U\/dl [interquartile range: 214\u2013347] in patients compared with 120\u00a0U\/dl [97\u2013139;\n P<\/jats:italic>\n \u00a0<\u00a00.001] in controls. Mean\n ETP<\/jats:styled-content>\n was significantly lower in patients 886\u00a0nM.min (\u00b1 436) compared with controls 1596\u00a0nM.min (\u00b1 259;\n P<\/jats:italic>\n \u00a0<\u00a00.001). However, when the assay was repeated with\n TM<\/jats:styled-content>\n to activate\n PC<\/jats:styled-content>\n , there was no significant difference in mean\n ETP<\/jats:styled-content>\n \u00a0+\u00a0\n TM<\/jats:styled-content>\n between patients and controls (632\u00a0\u00b1\u00a0418 vs 709\u00a0\u00b1\u00a0301\u00a0nM.min respectively;\n P<\/jats:italic>\n \u00a0=\u00a00.666). Furthermore, the\n ETP<\/jats:styled-content>\n ratio (\n ETP<\/jats:styled-content>\n \u00a0+\u00a0\n TM<\/jats:styled-content>\n \/\n ETP<\/jats:styled-content>\n ) was significantly higher in patients 0.89 (0.60\u20130.97) compared with controls 0.48 (0.3\u20130.6;\n P<\/jats:italic>\n \u00a0=\u00a00.002) and negatively correlated with\n PC<\/jats:styled-content>\n (\n R<\/jats:italic>\n \u00a0=\u00a0\u22120.487,\n P<\/jats:italic>\n \u00a0=\u00a00.003) and Factor V (\n R<\/jats:italic>\n \u00a0=\u00a0\u22120.431,\n P<\/jats:italic>\n \u00a0=\u00a00.01).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n ALI<\/jats:styled-content>\n \/\n ALF<\/jats:styled-content>\n patients have normal\n ETP<\/jats:styled-content>\n in the presence of\n TM<\/jats:styled-content>\n . This supports rebalanced coagulation mediated by acquired\n PC<\/jats:styled-content>\n resistance because of the reduction in\n PC<\/jats:styled-content>\n , Factor V and concomitant increase in Factor\n VIII<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/liv.12369","type":"journal-article","created":{"date-parts":[[2013,10,27]],"date-time":"2013-10-27T07:50:07Z","timestamp":1382860207000},"page":"672-678","source":"Crossref","is-referenced-by-count":91,"title":["Evidence of rebalanced coagulation in acute liver injury and acute liver failure as measured by thrombin generation"],"prefix":"10.1111","volume":"34","author":[{"given":"Mohamed","family":"Habib","sequence":"first","affiliation":[{"name":"Department of Haematological Medicine King's Thrombosis Centre London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lara N.","family":"Roberts","sequence":"additional","affiliation":[{"name":"Department of Haematological Medicine King's Thrombosis Centre London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raj K.","family":"Patel","sequence":"additional","affiliation":[{"name":"Department of Haematological Medicine King's Thrombosis Centre London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julia","family":"Wendon","sequence":"additional","affiliation":[{"name":"Institute of Liver Studies King's College Hospital NHS Foundation Trust London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William","family":"Bernal","sequence":"additional","affiliation":[{"name":"Institute of Liver Studies King's College Hospital NHS Foundation Trust London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roopen","family":"Arya","sequence":"additional","affiliation":[{"name":"Department of Haematological Medicine King's Thrombosis Centre London 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