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Effect of liver transplantation on the hepatopulmonary syndrome
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LIVER TRANSPLANTATION, SURGERY,ACUTE LIVER FAILURE
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[ C01/01 ]
[ C01/03
EFFECT OF LIVER TRANSPLANTATION ON THE HEPATOPULMONARY SYNDROME R. Allerx, V. Moreira2, D. Boixeda2, J.L. Moya2, C.M. Fern~ndez-Rodriguezl, J.L. Lied6l, R. Bfircena2 IFundaci6n Hospital Alcorc6n, Madrid, Spain. 2Hospital Ram6n y Cajal, Madrid, Spain. The reversal of hepatopulmonary syndrome (HPS) after liver transplantation (LT) remains controversial. The aims of this study were: (1) to analyze whether LT effectively reverses HPS, (2) the relationship, if any, between the HPS and the systemic hemodynamie disturbance, and (3) it possible association to pulmonary and systemic bemodynamie changes. Patients and methods: Systemic hemodynamic parameters [mean m e d a l pressure, (MAP), cardiac output (CO) and systemic vascular resistance (SVR)], the extent of intrapulmonary vasodilatation assessed by contrast transesophageal echocardiography, and gas exchange abnormalities were investigated in 23 patients with cirrhosis prior to and 6 mo (180.8 + 30.5 days) after LT. Results: LT was followed by a reduction in CO (6.7+1.7 vs 3.8+ 0.5 L/min; p<0.001), and a increase in MAP (79.8 + 22 vs. 93.6 + 8 mmHg; p<0.005) and SVR (1041 + 453 vs. 1981.7 + 294 dyn'sec'em'5; p<0.005). Twelve of 23 patients had intrapulmonary vasodilatation and increased alveolar-arterial oxygen difference, thereby fulfilling diagnostic criteria for HPS. Patients with HPS presented higher CO (p<0.05), lower SVR (p=0.01), lower TAM (p<0.05 than patients without HPS (p<0.05). LT caused normalization of intrapulmonary vasodilatation in all patients. Conclusions: LT normalizes hyperdynamic circulation and is a useful therapeutic option in patients with lIPS.
ISCHEMIC PRECONDITIONING ATTENUATESTHE DAMAGE BY LIPID PEROXIDATION IN THE RAT LIVER B. Zin~arol, B. Cavalieri~, G. Polil, J.C. Cutrlnl ~Department of Clinical and Biological Sciences,University of Turin, ASO San Luigi Gonzaga, Orbassano, Turin, Italy. 2A. Fa. R. Fatebenefratelli Hospital, San Maurizio Canavese, Turin, Italy. The purpose of this study was to clarify.the protective effects of the ischemic preconditioning (IP) in the liver of male Sprague Dowley rats. After anaesthesia rats were underwent to selective inflow occlusion to the median and lett lateral lobes. IP group was previously subjected to a cycle of ischemia-reperfusion (10/10 rain) followed by 90 rain of isebemia. Reperfusion was allowed by 4 hours. Blood samples were obtained from the posterior cava vein to measure ALT levels. Fragments from post-isehemic lobes were processed to evaluate TBARS levels, grading of necrosis and neutrophil infiltration. Reperfused TBARS levels in the non IP group increased 112% respect to the sham group level (1.44-0.2 nmol/mg protein) (p<0.01), whereas in the IP group an increase of 77% was detected (13<0.05). Postischemic livers from the non IP group showed a higher degree of necrosis with respect to the IP group (3.2-~-0.1 vs. 2.4:L-0.3, p<0.05). Neutrophils increased five and three fold in the non IP and IP groups (p<0.01 and 0.05, respectively). ALT level in the sham group was 27±1 U/I; rats without ]1~ showed an increase of 700%, whereas in the IP group the increase was of 185% (p<0.01). This results suggest that the hepatic protective effects of IP against the post-ischemic injury could be partly attributed to the reduction of lipid peroxidation and neutrophil infiltration.
[ C01/02 ]
[ corn,o, ]
VASCULAR COMPLICATIONS AFTER PEDIATRIC LIVER TRANSPLANTATION E. Sieders. P.M.J.G. Peeters, E.M. Ten Vergert, K.R de Jong, R.J. Porte, J.H. Zwavelin~.C.M.A. Bijleveld,M.J.H. Slooff Liver Transplant Group, University Hospital Groningen, The Netherlands. This study analysed the incidence, consequences, and risk factors for hepatic artery thrombosis (HAT), portal vein thrombosis (PVT), and venous outflow tract obstruction (VOTO) in a consecutive series of 157 pediatric liver transplantations. The incidence of vascular complications was 21%. The incidence of HAT was 10%, of PVT 4%, and of VOTO 6%. Patient survival after PVT and VOTO was lower and gra~ survival after HAT and PVT was lower compared with children and grafts without vascular complications. Risk factors for HAT were a low donor/recipient age ratio, a long operation time, and the use of the recipient's bifurcation of the proper hepatic artery for anastomosis. Risk factors for PVT were young age, low weight, segmental grafts, and the piggyback technique. Finally, risk factors for VOTO were fulminant hepatic failure, a high donor/recipient age and weight ratio, and segmental grafts. Vascular complications have a significant impact on patient and graft survival. Patient survival might improve by early retransplantation for PVT and by avoiding the identified risk factors.
LIVER TRANSPLANTATION: PREDICTORS OF ACUTE REJECTION S. de Rave1, B.E. Hansen2, for the Rotterdam Liver Transplantation Group 1Department of Hepatogastroenterology, University Hospital Rotterdam, The Netherlands. 2Department of Biostatistics, University Hospital Rotterdam, The Netherlands. A number of factors have been reported to influence the risk of acute rejection after liver transplantation. In most cases these factors were identified using unlvariate tests. Only one large study that used a multivariate analysis has been publishedI. We analysed the data on 179 liver transplantations performed in our centre between 1986 and 1997 using a multivariate Cox model. Factors predisposing to acute rejection were chronic hepatitis C (P=0.001), absence of oedema (P=0.021), an elevated ASAT (40-200 U/l: P=0.034 and >200: P=0.051) and the presence of the HLA DR6 antigen (1>=0.028) in the recipient. Patients who had IgG antibodies against the cytomegalovirus (P=0.045) or hepatitis B infections (P=0.011) had a lower risk of acute rejection.None of the other factors that emerged from previous studies by others proved to have a significant influence in our patient group. The occurrence of acute rejection was associated with a 2.2-fold increased risk of gratt failure in the first year after liver transplantation (95% confidence interval 1.2-3.9, P=0.01, time dependent Cox model). We conclude that it may well be possible to identify patient groups with risks of acute rejection after liver transplantation ranging from <25% to >75%. Models like the one described here should be incorporated in comparisons between different immunosuppressiveregimens and could form the basis for individually tailored primary rejection prophylaxis after liver transplantation. More specifically, high risk patients might benefit from intensified initial immunosuppression. ~) Wiesner RH et al. Acute hepatic allograft rejection: incidence, risk factors, and impact on outcome. Hepatology 1998;28:638-645.
140
LIVER TRANSPLANTATION, SURGERY,ACUTE LIVER FAILURE
]
[ C01/01 ]
[ C01/03
EFFECT OF LIVER TRANSPLANTATION ON THE HEPATOPULMONARY SYNDROME R. Allerx, V. Moreira2, D. Boixeda2, J.L. Moya2, C.M. Fern~ndez-Rodriguezl, J.L. Lied6l, R. Bfircena2 IFundaci6n Hospital Alcorc6n, Madrid, Spain. 2Hospital Ram6n y Cajal, Madrid, Spain. The reversal of hepatopulmonary syndrome (HPS) after liver transplantation (LT) remains controversial. The aims of this study were: (1) to analyze whether LT effectively reverses HPS, (2) the relationship, if any, between the HPS and the systemic hemodynamie disturbance, and (3) it possible association to pulmonary and systemic bemodynamie changes. Patients and methods: Systemic hemodynamic parameters [mean m e d a l pressure, (MAP), cardiac output (CO) and systemic vascular resistance (SVR)], the extent of intrapulmonary vasodilatation assessed by contrast transesophageal echocardiography, and gas exchange abnormalities were investigated in 23 patients with cirrhosis prior to and 6 mo (180.8 + 30.5 days) after LT. Results: LT was followed by a reduction in CO (6.7+1.7 vs 3.8+ 0.5 L/min; p<0.001), and a increase in MAP (79.8 + 22 vs. 93.6 + 8 mmHg; p<0.005) and SVR (1041 + 453 vs. 1981.7 + 294 dyn'sec'em'5; p<0.005). Twelve of 23 patients had intrapulmonary vasodilatation and increased alveolar-arterial oxygen difference, thereby fulfilling diagnostic criteria for HPS. Patients with HPS presented higher CO (p<0.05), lower SVR (p=0.01), lower TAM (p<0.05 than patients without HPS (p<0.05). LT caused normalization of intrapulmonary vasodilatation in all patients. Conclusions: LT normalizes hyperdynamic circulation and is a useful therapeutic option in patients with lIPS.
ISCHEMIC PRECONDITIONING ATTENUATESTHE DAMAGE BY LIPID PEROXIDATION IN THE RAT LIVER B. Zin~arol, B. Cavalieri~, G. Polil, J.C. Cutrlnl ~Department of Clinical and Biological Sciences,University of Turin, ASO San Luigi Gonzaga, Orbassano, Turin, Italy. 2A. Fa. R. Fatebenefratelli Hospital, San Maurizio Canavese, Turin, Italy. The purpose of this study was to clarify.the protective effects of the ischemic preconditioning (IP) in the liver of male Sprague Dowley rats. After anaesthesia rats were underwent to selective inflow occlusion to the median and lett lateral lobes. IP group was previously subjected to a cycle of ischemia-reperfusion (10/10 rain) followed by 90 rain of isebemia. Reperfusion was allowed by 4 hours. Blood samples were obtained from the posterior cava vein to measure ALT levels. Fragments from post-isehemic lobes were processed to evaluate TBARS levels, grading of necrosis and neutrophil infiltration. Reperfused TBARS levels in the non IP group increased 112% respect to the sham group level (1.44-0.2 nmol/mg protein) (p<0.01), whereas in the IP group an increase of 77% was detected (13<0.05). Postischemic livers from the non IP group showed a higher degree of necrosis with respect to the IP group (3.2-~-0.1 vs. 2.4:L-0.3, p<0.05). Neutrophils increased five and three fold in the non IP and IP groups (p<0.01 and 0.05, respectively). ALT level in the sham group was 27±1 U/I; rats without ]1~ showed an increase of 700%, whereas in the IP group the increase was of 185% (p<0.01). This results suggest that the hepatic protective effects of IP against the post-ischemic injury could be partly attributed to the reduction of lipid peroxidation and neutrophil infiltration.
[ C01/02 ]
[ corn,o, ]
VASCULAR COMPLICATIONS AFTER PEDIATRIC LIVER TRANSPLANTATION E. Sieders. P.M.J.G. Peeters, E.M. Ten Vergert, K.R de Jong, R.J. Porte, J.H. Zwavelin~.C.M.A. Bijleveld,M.J.H. Slooff Liver Transplant Group, University Hospital Groningen, The Netherlands. This study analysed the incidence, consequences, and risk factors for hepatic artery thrombosis (HAT), portal vein thrombosis (PVT), and venous outflow tract obstruction (VOTO) in a consecutive series of 157 pediatric liver transplantations. The incidence of vascular complications was 21%. The incidence of HAT was 10%, of PVT 4%, and of VOTO 6%. Patient survival after PVT and VOTO was lower and gra~ survival after HAT and PVT was lower compared with children and grafts without vascular complications. Risk factors for HAT were a low donor/recipient age ratio, a long operation time, and the use of the recipient's bifurcation of the proper hepatic artery for anastomosis. Risk factors for PVT were young age, low weight, segmental grafts, and the piggyback technique. Finally, risk factors for VOTO were fulminant hepatic failure, a high donor/recipient age and weight ratio, and segmental grafts. Vascular complications have a significant impact on patient and graft survival. Patient survival might improve by early retransplantation for PVT and by avoiding the identified risk factors.
LIVER TRANSPLANTATION: PREDICTORS OF ACUTE REJECTION S. de Rave1, B.E. Hansen2, for the Rotterdam Liver Transplantation Group 1Department of Hepatogastroenterology, University Hospital Rotterdam, The Netherlands. 2Department of Biostatistics, University Hospital Rotterdam, The Netherlands. A number of factors have been reported to influence the risk of acute rejection after liver transplantation. In most cases these factors were identified using unlvariate tests. Only one large study that used a multivariate analysis has been publishedI. We analysed the data on 179 liver transplantations performed in our centre between 1986 and 1997 using a multivariate Cox model. Factors predisposing to acute rejection were chronic hepatitis C (P=0.001), absence of oedema (P=0.021), an elevated ASAT (40-200 U/l: P=0.034 and >200: P=0.051) and the presence of the HLA DR6 antigen (1>=0.028) in the recipient. Patients who had IgG antibodies against the cytomegalovirus (P=0.045) or hepatitis B infections (P=0.011) had a lower risk of acute rejection.None of the other factors that emerged from previous studies by others proved to have a significant influence in our patient group. The occurrence of acute rejection was associated with a 2.2-fold increased risk of gratt failure in the first year after liver transplantation (95% confidence interval 1.2-3.9, P=0.01, time dependent Cox model). We conclude that it may well be possible to identify patient groups with risks of acute rejection after liver transplantation ranging from <25% to >75%. Models like the one described here should be incorporated in comparisons between different immunosuppressiveregimens and could form the basis for individually tailored primary rejection prophylaxis after liver transplantation. More specifically, high risk patients might benefit from intensified initial immunosuppression. ~) Wiesner RH et al. Acute hepatic allograft rejection: incidence, risk factors, and impact on outcome. Hepatology 1998;28:638-645.
140