had higher rate of concomitant lifestyle diseases such as diabetesand hypertension, which suggested the relation between hepatocar-cinogenesis and lifestyle related diseases. Although NVH-HCC caseshad significantly high rate of hepatic steatosis, only 5 % of NVH-HCC cases were definitely diagnosed as NASH-related HCC by theclinical and pathological examination.

QS218. GRAFT VERSUS HOST DISEASE FOLLOWINGLIVER TRANSPLANTATION: A SINGLE CENTERSTUDY. Joshua D. Mezrich1, Matthew C. Koopmann1, LuisA. Fernandez1, L. Thomas Chin2, Anthony D’Alessandro1,Alexandru Musat1, Stuart Knechtle1, Munci Kalayoglu1;1University of Wisconsin School of Medicine and Public Health,Madison, WI; 2Florida Hospital Transplant Center, Orlando, FL

Introduction: Graft-versus-host disease (GVHD) following livertransplantation is a rarely diagnosed but highly morbid disease withfew treatment options. Few case series have been published on thetopic, all of which indicate extremely high mortality rates. Previousstudies have attempted to identify risk factors for disease onset, in orderto avoid its occurrence. Methods: We have reviewed our experience ata single center of over 1,400 liver transplants and identified sevendocumented cases of GVHD. All cases were documented by skin/bonemarrow biopsy and/or identification of donor-derived chimerism. Weexamined risk factors, including ages of donors and recipients, cause ofliver failure, immunosuppression, and HLA matching. Results: Allseven of the patients died after onset of disease. Disease symptoms anddiagnoses were somewhat conserved. No specific risk factor in thissmall group of patients appeared to predict development of GVHD.Conclusions: GVHD should be considered in patients following livertransplant that present with symptoms of diarrhea, pancytopenia, skinrash, and ultimately overwhelming sepsis. Diagnosis can be made withskin/bone marrow biopsy and analysis of donor-derived chimerism.Outcomes tend to be poor with no effective treatment. Further reportsof cases and characteristics may ultimately improve understanding ofrisk factors for the disease.

QS219. PHOSPHOINOSITIDE 3-KINASE--DEFICIENT MICEDEMONSTRATE IMPAIRED BACTERIAL CLEAR-ANCE FOLLOWING INDUCTION OF POLYMICRO-BIAL SEPSIS. Edward A. McSwiney, Jiang H. Wang,Henry P. Redmond; University College Cork, Cork, Ireland

Introduction: Phosphoinositide 3-kinase-� (PI3K-�), which belongs tothe family of class I PI3-kinases, is essential for directional leukocyterecruitment toward inflamed tissues. Using a gene knock-out model, weexamined for the first time the importance of PI3K-� on bacterialclearance following induction of polymicrobial sepsis in vivo. Methods:Age-, weight- and sex-matched PI3K �-deficient and wild-type C57BL/6mice underwent cecal ligation and puncture to induce polymicrobialsepsis. 5 mice from each group were euthanised at 12 h and 24 hfollowing surgery. Bacterial loads were determined in blood, liver andspleen following incubation on agar plates at 37°C for 24 hours. Statis-tical analysis was performed using SPSS (Version 14). Results: BothPI3K-� deficient and wild-type mice demonstrated increasing bacterialloads in all tissues with time. PI3K-� deficient mice showed signifi-cantly greater splenic bacterial loads (4.1�3.6 Vs 1.5�1.3 log10 CFU)(p�0.003), when compared with wild-type mice 12 hours followingsurgery. PI3K-� deficient mice also demonstrated increased blood(4.9�5.0 Vs 3.5�3.6 log10 CFU) and hepatic (4.5�4.5 Vs 1.2�0.9 log10

CFU) bacterial loads at 12 hours, although these differences failed toachieve statistical significance. At 24 hours following surgery, PI3K-�deficient mice showed statistically greater blood (5.2�4.2 Vs 4.3�4.1log10 CFU) (p�0.01) and hepatic (5.4�4.0 Vs 4.5�4.6 log10 CFU)(p�0.001) bacterial loads. Similarly, PI3K-� deficient mice also exhib-ited increased splenic (5.5�5.2 Vs 4.5�4.9 log10 CFU) (p�0.09) bacterialloads at 24 hours. Conclusion: Our results demonstrate that lack ofPI3K-� impairs adequate bacterial clearance following induction of

polymicrobial sepsis. Thus, targeting the PI3K-� pathway, as has beensuggested as a means of controlling macrophage infiltration in chronicinflammatory disease, may render the innate host defence system lesseffective to adequately respond to sepsis and SIRS.

QS220. COST EFFECTIVE ANALYSIS OF TIPS VERSUSSURGICAL PORTACAVAL SHUNT FOR VARICEALBLEEDING IN EARLY CIRRHOSIS. Damon Pierce1,Ram Nirula2; 1UT Southwestern Medical Center at Dallas, Dal-las, TX; 2University of Utah, School of Medicine, Salt Lake City,UT

Introduction: Upper gastrointestinal hemorrhage carries significantmorbidity and mortality in patients with portal hypertension and cir-rhosis. The optimal prevention strategy for rebleeding in these patientsremains controversial with respect to the safety and efficacy of TIPSversus a portocaval surgical shunt (PC). We sought to determine thelong-term cost-effectiveness of these two treatments. Methods: AMarkov state transition decision analysis was created to follow patientswith early cirrhosis who have an upper gastrointestinal bleed despitemedical therapy into either TIPS or PC. Patients were followed though-out the transition states until either death or survival. Probabilities ofGI rebleed, hepatic encephalopathy, surgical and TIPS-related compli-cations as well as death were obtained from an extensive literaturereview. The main outcome was dollars per life-year saved. Costs werederived from average Medicare reimbursements. Results: For a pa-tient with Child’s A cirrhosis who suffers an upper gastrointestinalbleed, the average cost per life year saved was $17,382 (�/� 9357) and$21,762 (�/� 5419) for TIPS and PC, respectively. The average lifeexpectancy was 6.1 years and 7.0 years for TIPS and PC respectively.This yielded an incremental cost-effectiveness rate (ICER) for portoca-val shunt of $4,514 per life year saved. Conclusion: Compared withsurgical shunts, TIPS resulted in reduced lifetime costs for the treat-ment of variceal bleeding but was associated with earlier mortality.Given the low incremental cost of PC it should be adopted as a cost-effective strategy in managing this patient population.

354 ASSOCIATION FOR ACADEMIC SURGERY AND SOCIETY OF UNIVERSITY SURGEONS—ABSTRACTS