Background/Aims: Our objective is to assess donor complications in all right hepatic lobe living-donor liver transplantation (LDLT) at our center. Methods: Of a total of 352 liver transplantations performed, 60 were right-lobe LDLT. Most donors (88.3%) were related to the recipients. Results: Mean hospital stay was 5.4 8 0.6 days. No complications occurred due to preoperative evaluation. Most donors received one or two units of autologous blood transfusion. Only 5 (8.3%) needed nonautologous blood transfusion. Most complications were minor and treated conservatively. Bile leaks from the cut surface of the liver occurred in 5 donors (8.3%). Two patients had potentially fatal complications: perforated duodenal ulcer and portal vein thrombosis (PVT). The donor with perforated ulcer developed septicemia and multiple organ failure. He was discharged from the hospital with hemiparesis due to cerebral ischemia. The patient with PVT remained asymptomatic and the portal vein was recanalized by the 3rd postoperative month. One donor died in the immediate postoperative period of cardiac arrest due to cardiac arrhythmia. Conclusion: Right hepatectomy for LDLT may be associated with significant morbidity, including death and it should be performed only by surgeons with great experience.
Delivering retroviruses targeted to hepatocytes in vivo involves the injection of retroviruses directly into the blood stream of the portal vein. The aim of this work was to delineate the conditions for delivering retroviruses in vivo by perfusing in situ the bile duct of the regenerating rat liver, and to study the hepatocyte transgene expression. At 24 hr after partial hepatectomy, during the S phase of the cell cycle, regenerating livers were perfused for 2.8+/-0.5 hr through the bile duct with 36.2+/-6.8 ml (0.3+/-01 ml/min) of fresh culture supernatant containing amphotropic recombinant retroviruses encoding the beta-galactosidase gene. The virus total titer was 1.5 x 10(8) ffu (group I) or 6.5 x 10(8) ffu (groups II and III). The hepatic artery blood flow was either maintained (groups I and II) or interrupted (group III) during bile duct perfusion. Liver biopsies taken 7 days later showed that 31.4+/-24.2% (group I), 58.7+/-23.6% (group II), and 45.1+/-21.4% (group III) of hepatocytes expressed beta-galactosidase activity, predominantly in the periportal and mediolobular zones. This study demonstrates that hepatocytes of regenerating rat livers that have entered the S phase of the cell cycle as a result of partial hepatectomy can be transduced in vivo by retroviral vectors delivered in situ by bile duct perfusion. Furthermore, the number of transduced hepatocytes closely correlated with the viral total titer and was diminished by hepatic artery blood flow occlusion during perfusion.
In a prospective study, serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2) and prolactin (PRL) of 30 male patients with cirrhosis were determined two to four hours before and six months after liver transplantation. The results were compared according to the Model for End-stage Liver Disease (MELD). Results Results ResultsResults Results: male patients with liver cirrhosis have hypogonadism. FSH was normal, but inappropriately low due to androgen failure; E2 and PRL, on their turn, were high. After liver transplantation, FSH and LH levels increased (p < 0.05), whereas E2 and PRL normalized (p < 0.05). The MELD score did not influence changes in FSH, PRL and LH, however, the more severe the cirrhosis was, the more significant was the normalization of E2 (p = 0.01). Conclusion Conclusion Conclusion Conclusion Conclusion: Patients with cirrhosis and male hypogonadism have inappropriately normal levels of FSH and LH, associated with an increase in E2 and LRP. After liver transplantation, FSH and LH increased, while E2 and PRL returned to normal. Changes in E2 levels were most pronounced in patients with MELD > 18. The severity of cirrhosis had no influence on FSH, PRL and LH.
Controlling the S phase of the hepatocyte cell cycle would be of considerable help for stable retroviral foreign gene transfer. The aim of this article is to study hepatocyte regeneration during S phase in isolated, perfused rat liver followed by liver transplantation. Normal livers (G I: n ؍ 7) were perfused with blood from normal rats for 6.1 ؎ 0.3 hours. Regenerating livers (G II; n ؍ 7) obtained 18 hours after partial hepatectomy were perfused for 6.0 ؎ 0.3 hours with blood from rats partially hepatectomized 18 hours before. Regenerating livers (G III; n ؍ 7) obtained 22 hours after partial hepatectomy were perfused for 2.4 ؎ 0.1 hours with blood from normal rats. In the normothermal perfusion system, a bolus of 25 mg of 5-bromo-2Ј-deoxyuridine (BrdU) was added to the perfusate. Liver biopsies were taken at the end of each experiment. In group II, a biopsy was also taken 1 hour after BrdU introduction. At the end of each experiment, livers were orthotopically transplanted. The percentage of BrdU positive hepatocyte nuclei was 0.2% in G I; 14.8% and 38.4% after 1 hour and 6.1 hours, respectively, in G II; and 46.5% after 2.4 hours in G III. In G I, five rats died at day 1, 5, 6, 7, and 48 and two rats were still alive after 17 months. In G II, all the rats died before day five. In G III, two rats died at day one, one at day six, and four were still alive after 12 months. This study shows that, after 6 hours of normothermal perfusion, organ viability allows successful liver transplantation and that rat hepatocyte regeneration during cell cycle S phase in isolated normothermal conditions progresses in a similar way-quantity and timing-to liver regeneration found in vivo after partial hepatectomy. (HEPATOLOGY 1998;27:697-702.)Somatic gene delivery to the liver provides an approach to treat various inherited or acquired disorders. 1 Strategies for gene therapy include viral-mediated gene transfer. Several different viruses have been considered as potential vectors for gene transfer, including retroviruses. [2][3][4][5][6] Retroviral-mediated gene transfer only occurs in cells which are actively replicating at the time of infection. The integrated gene will persist for the lifetime of the infected cell and will be present in cells that arise by subsequent cell division. 7 This is a limitation in the normal liver caused by the quiescent state of hepatocytes. 7 In addition, the systemic administration of retroviral vectors in humans is limited by the risk of infecting germinal cells. Using an in vivo model of selective in situ perfusion of regenerating liver limited to 20 minutes, we have previously demonstrated that rat 8 and dog 9 hepatocytes can be infected by infusion of amphotropic retroviruses into the portal vein following partial hepatectomy. However, transduction rates were lower than 5% in rats and 1% in dogs with this method.In order to be of clinical use, a greater transduction rate is required. One possible way to improve the rate of gene transfer into hepatocytes would be to increase the duration...
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