ABSTRACT
BACKGROUND: Portal vein thrombosis (PVT) is a surgical challenge in liver transplantation (LTx). In contrast to LTx in decompensated liver disease, which are associated with a higher morbidity and mortality, PVT influence on outcome is still under debate. To evaluate this influence at different stages of liver decompensation, we compared the outcome of patients suffering from PVT to patients with patent portal vein within different score ranges. METHODS: We included 193 LTx (24 with PVT) in our study, transplanted between 2004 and 2007 at our institution. Patients were divided into four Model of End-Stage Liver Disease (MELD) score groups, and outcome was compared between PVT- and non-PVT patients. RESULTS: In non-decompensated liver disease (MELD <15), we found a significantly decreased survival in patients suffering from PVT (one-yr survival 57% vs. 89%). By contrast, MELD score >15 (decompensated liver disease) leads to an equal or even better survival in PVT-patients compared with patients without PVT (one-yr survival 91% vs.75%), with an only slightly increased morbidity. CONCLUSION: Outcome in patients with PVT seems to be dependent on pre-operative disease severity. In contrast to compensated liver disease, no influence of PVT on outcome could be found in decompensated liver disease, and should therefore not be considered as a contraindication in LTx.
Subject(s)
Liver Diseases/complications , Liver Diseases/surgery , Liver Transplantation , Portal Vein , Venous Thrombosis/complications , Adult , Aged , Cohort Studies , Female , Humans , Liver Diseases/mortality , Male , Middle Aged , Retrospective Studies , Risk Factors , Severity of Illness Index , Survival Analysis , Treatment Outcome , Venous Thrombosis/mortality , Venous Thrombosis/therapyABSTRACT
INTRODUCTION: Conditioning of liver grafts by bolus pretreatment with prostaglandins has been previously demonstrated to improve hepatic bile flow. However, the underlying mechanisms have not been investigated. To elucidate whether improved bile flow after prolonged ischemia is due to maintained bile acid secretion or due to increased paracellular permeability, we performed a study using increasing doses of the marker acid taurocholate in the isolated perfused rat liver system. METHODS: Livers were harvested from adult Lewis rats and stored for 24 hours in UW solution. Pretreatment of livers was performed 1 minute before preservation. One group received prostaglandin I2, the second group received prostaglandin E1, and the control group was treated with saline. After 24 hours of cold storage the grafts were investigated in the isolated perfused rat liver system by perfusion with an oxygenated Krebs-Ringer-Henseleit buffer. Increasing doses of the radiolabeled marker bile acid taurocholate were infused to investigate bile acid transport. RESULTS: Bile flow and bile acid output were increased by pretreatment of the livers with prostaglandin I2 and prostaglandin E1, as compared to the control group. More specifically, the maximum transport rate was tripled by prostaglandin I2 and by prostaglandin E1 preconditioning of liver grafts, in comparison to the control group (P < .01 vs prostaglanin I2 and E1). CONCLUSION: The results clearly demonstrate that increased bile flow after conditioning of liver grafts with prostaglandins is not due to increased paracellular permeability but is based on markedly improved bile acid output.
Subject(s)
Bile Acids and Salts/metabolism , Liver Transplantation/physiology , Liver/drug effects , Adenosine , Allopurinol , Animals , Bile/metabolism , Biological Transport , Glutathione , In Vitro Techniques , Insulin , Ischemic Preconditioning , Male , Organ Preservation Solutions , Raffinose , Rats , Rats, Inbred LewABSTRACT
HISTORY AND CLINICAL FINDINGS: A 54-year-old patient with painless jaundice and vomiting had been diagnosed with a Peutz-Jeghers syndrome 20 years before. INVESTIGATIONS: The blood analysis showed a cholestatic constellation as well as increased transaminases. Sonographic, radiological, endoscopic and histological findings indicated multiple hamartomatous polyps of the Peutz-Jeghers' type in the entire small and large bowel with occlusion of the papilla of Vater and the superior gastrointestinal tract by a big polyp. TREATMENT AND COURSE: After an initial percutaneous transhepatic cholangiographic drainage, Whipple's operation and a segmental resection of small and large bowel were performed. A highly differentiated adenocarcinoma of the duodenum was found in the resected specimen. CONCLUSION: This case demonstrates the potentially severe complications of a Peutz-Jeghers syndrome that had been neglected for years.