F angiotensin-converting enzyme (ACE) gene; G1691A of the Leiden factor gene; G20210A of the factor II gene; 4G/5G of plasminogen activator inhibitor-1 (PAI-1); Alu repeat I/D of the plasminogen tissular activator (tPA) gene; and finally the first intron of TNF- (TNF- +250). In addition, seven neutral markers were genotyped to follow genomic control strategies that would detect spurious associations due to population substructure [1]. The neutral markers chosen are biallelic Alu repeats distributed PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/1944902 in different chromosomes. We used SPSS-12.2 software for statistical purposes. Results Greater bleeding in the 24-hour postoperative period was associated with: ACE (DD: 891 [SD 531] ml; ID: 512 [SD 458] ml, II: 1125 [SD 735] ml; P = 0.046), TNF- +250 (AA: 747 [SD 459] ml; AG: 568 [SD 482] ml; GG: 1350 [SD 775] ml; P = 0.029), and PAI-1 (4G/4G: 792 [SD 477] ml; 4G/5G: 554 [SD 376] ml; 5G/5G: 1036 [SD 694] ml; P = 0.037). Homozygous 5G showed lower levels of PAI-1 (36.98 [7.68] vs 120.3 [14.3], P = 0.02), lower levels of leptins preoperatively (11.15 [2.15] vs 25.56 [3.93], P = 0.016), at admission (3.54 [0.84] vs 18.67 [3.72], P = 0.02), and at 4 hours (3.43 [1.12] vs 15.48 [3.27], P < 0.001) and 24 hours postoperatively (11.12 [4.36] vs 29.57 [4.82], P = 0.013) and greater coagulation factors consumed. Those patients achieved a greater advantage of antifibrinolytic prophylaxis with tranexamic acid. Conclusion We found three polymorphisms associated with excessive postoperative bleeding. This may enable us to identify patients at risk before CPB intervention and to optimize prophylactic therapy. Reference 1. Reich, Goldstein: Genet Epidemiol 2004, 20:4.Table 1 (abstract P224) Forrest 1 (23 patients) Hct ( ) WBC (mmc) PLT (mmc) Creatinine (mg/dl) BUN (mg/dl) BUN/creatinine Na (mEq/l) DBP SBP Heart rate (bpm) Number of blood transfusions 26.9 ?7.2 11,217 ?4884 243,147 ?79,587 1.6 ?1.0* 53.1 ?16.6* 39.9 ?14.1* 139.8 ?5.7 72.6 ?14.8 125.4 ?31.1 93.9 ?20.8 3.8 ?2.9* Forrest 2 (61 patients) 28.7 ?7.3 11,944 ?4573 252,923 ?84,948 1.1 ?0.4 45 ?15.3 39.4 ?14.2* 138.7 ?3.5 70.1 ?13.0 117.7 ?21.1* 95.1 ?19.1 3.2 ?2.7 7.1 ?4.8 PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/6104837 Forrest 3 (44 patients) 28.2 ?7.0 10,381 ?4749 225,590 ?86,796* 1.2 ?0.5 40 ?10.9 34.6 ?11.2 139.7 ?4.1 75.8 ?12.9 133.0 ?25.5 90.0 ?13.7 2.1 ?1.9 8.6 ?8.P226 Tranexamic acid decreased postoperative bleeding and systemic inflammatory response syndrome associated with cardiopulmonary bypass: a prospective, randomized, double-blind controlled studyJ Jimenez Rivera, J Iribarren Sarrias, I Nassar, J Rodriguez, J Raya, P Garrido, R Perez Hernandez, A Milena, L Lorente, R Martinez, M Mora Hospital Universitario de Canarias, La Laguna, SC Tenerife, Spain Critical Care 2006, 10(Suppl 1):P226 (doi: 10.1186/cc4573) Background Postoperative bleeding reflects haemostatic alterations associated with cardiopulmonary bypass (CPB), which may lead toHospital stay (days) 12.0 ?6.7*S*P < 0.05. DBP, diastolic blood pressure; SBP, systolic blood pressure.Available online http://ccforum.com/supplements/10/Ssystemic inflammatory response syndrome (SIRS). We evaluated the efficacy of tranexamic acid (TA) for SIRS and postoperative bleeding. Patients and methods We performed a prospective, randomized, double-blind controlled study of 50 consecutive patients who underwent elective CPB. Twenty-four patients received TA, and 26 received saline solution before and after CPB. We performed an intention-to-treat analysis, comparing SIRS incidence, postoperative 2.