Uire APCR, probably because the platelet derived Factor V originates f…
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작성자 Tamika 작성일 24-03-28 19:21 조회 14 댓글 0본문
Uire APCR, probably because the platelet derived Factor V originates from the plasma pool [23-25]. However, these results do not correlate with previous work which states that APCR associated with a Factor V Leiden donor is fully transferable to the graft recipient [22]. Some of the variables associated with post-transplant thrombotic event could relate to difficulties in surgical technique, such as in a child recipient, and also their primary cause of liver transplantation, biliary atresia. In a recent study [26], post-transplant complication rates, including the re-operation rate, were higher in the younger group. In our study, fibrinogen level was the one variable independently associated with post-transplant thrombotic event in the global cohort of liver recipients. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/744568 Previously this factor has been associated both with thrombosis and inflammation. A meta-analysis showed that risk of coronary heart disease may increase 1.8 fold for 1 g/L of increased fibrinogen, independent of traditional risk factors [27]. But, in the retrospective cohort of recipients, the toxicity was the only variable independently associated. This factor could be involved in graft thrombosis due to its role in endothelial injury and inflammation. Plasma levels of fibrinogen (high) and protein C recipient (low) were associated post-transplant thrombotic event in the prospective group. Low plasma levels of protein C recipient was associated, in this work, with liver disease relapse (Additional File 2, Table S2), and this fact could be a consequence of disbalance of coagulation factors in terminal cirrhosis [28]. A previous paper had shown that PC was decreased at dayAyala et al. BMC Gastroenterology PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/3081428 2011, 11:130 http://www.biomedcentral.com/1471-230X/11/Page 7 ofFigure 1 Liver transplant recipient overall survival (OS). A. Post-transplant thrombosis was associated with a poor outcome (P < 0.03). B. High FVIII:C levels were associated with a poor outcome: the median OS was 69.6 and 132.1 months in groups with high and low FVIII:C, respectively (P < 0.003). Median 4,4,5,5-Tetramethyl-2-(2-methylprop-1-en-1-yl)-1,3,2-dioxaborolane follow-up was 21.7 months (range 1-184.6 months).(p = 0.04) and day 30 (p = 0.009) in DDLT and DDRT/ LRT groups with complications, respectively [29]. Nevertheless, high plasma fibrinogen levels are not a consequence of liver function alteration, and could be an important pro-thrombotic factor in development graft thrombosis that has not been previously described. Our results were in agreement with previous studies [12] showing that the presence of post-transplant thrombotic event, HAT in the majority of cases, in thisliver recipient cohort influenced recipient overall survival. High factor VIII was associated with a poor outcome, as previously reported. Levels of factor VIII, a potent pro-coagulant involved in thrombin generation, increased progressively with Child-Pugh Score (from Child-Pugh class A to C)[30]. A correlation between the severity of liver disease and von Willebrand factor (VWF) plasma antigen levels has been previously documented [31,32]. In agreement with other authors [33],Figure 2 High FVIII:C levels and Recipient Overall Survival. High FVIII:C levels were associated with a poor outcome separately in both young and elderly 3-Bromo-5-chloro-2-fluoroaniline groups (Log Rank 8.56; p = 0.0034).Ayala et al. BMC Gastroenterology 2011, 11:130 http://www.biomedcentral.com/1471-230X/11/Page 8 ofTable 5 Multiple Cox Regression Analysis for OS in a cohort of liver transplantation.Variable AGE (CONTINUOUS VARIABLE) PARTIAL GRAFT (Y.
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