Steatosis of the donor liver is known to impact on patient and allograft outcome after orthotopic liver transplantation (OLT). The aim of this study is to evaluate the effect of increasing grades of cadaveric donor liver steatosis on recipient outcome. Between January, 1986 and December, 2000, 120 OLTs were performed with 72 mild, 25 moderate, and 23 severe steatotic donor livers. Donors of steatotic livers were more likely to be older (P ‫؍‬ .001) and have died of intracerebral haemorrhage than donors of nonsteatotic livers. Initial poor graft function (IPF) was more common in donor livers with either moderate or severe steatosis than in donor livers with mild steatosis (P ‫؍‬ .03). Primary graft nonfunction (PNF) occurred in only 1 donor liver with severe steatosis. PGE1 (PGE1) usage was higher in recipients of donor livers with moderate or severe steatosis versus donor livers with mild steatosis (P ‫؍‬ .001). Allograft loss was greater at 1 year both in the moderate and severe (P ‫؍‬ .03) steatotic liver groups. Patient survival at 3 months and overall allograft survival both were impacted negatively by increasing grades of donor liver steatosis (P ‫؍‬ .02, P ‫؍‬ .03). Threemonth allograft survival was reduced in the steatotic donor livers if the donor was 50؉ years old (P ‫؍‬ .033). Recipient status at OLT (P ‫؍‬ .001) and donor steatosis (P ‫؍‬ .046) impacted on 30 day allograft survival (multivariate analysis). In conclusion, increasing grades of donor liver steatosis were associated with worse IPF and increased PGE1 usage. There was a negative impact of steatosis on both recipient and early allograft survival. (Liver Transpl 2003;9:500-505.)

Recurrent hepatitis B virus (HBV)infection remains a major cause of morbidity and mortality after liver transplantation. Recently, antiviral therapy, such as lamivudine, has become available for prophylaxis against HBV reactivation posttransplantation and for the treatment of HBV recurrent disease. We report our initial experience with lamivudine therapy in patients with precore mutant-associated HBV infection undergoing liver transplantation (n ‫؍‬ 29). Outcomes were compared in three patient groups: group 1, precore mutant HBV infection not receiving lamivudine (n ‫؍‬ 10); group 2, recurrent precore mutant HBV infection posttransplantation subsequently treated with lamivudine (n ‫؍‬ 10); and group 3, HBV precore mutant patients undergoing liver transplantation and receiving lamivudine and low-dose hepatitis B immune globulin (HBIG) from the time of transplantation (n ‫؍‬ 9). In group 1, HBV recurred in 9 of 10 patients, with subsequent graft loss in all 9 patients. In group 2, all patients developed HBV recurrence at a mean of 7.3 months posttransplantation and started lamivudine therapy at a median of 16 months posttransplantation. Follow-up on lamivudine therapy was for a median of 11 months. Six of these 10 patients developed mutations in the HBV polymerase gene associated with lamivudine resistance. There were two liver failure-related deaths in this group. In group 3 patients, there was one death from graft-versus-host disease. The remaining 8 patients have been followed up for a mean of 15.6 months posttransplantation, and all remain hepatitis B surface antigen negative and HBV DNA negative. In conclusion, lamivudine therapy in association with low-dose HBIG is effective in preventing HBV reactivation posttransplantation. Rescue therapy with lamivudine in patients with HBV recurrence is only moderately effective, with a 60% lamivudine resistance rate in patients treated for longer than 6 months.

Prediction of prognosis in patients with locally advanced low rectal cancers treated with preoperative adjuvant therapies continues to be problematic. Thymidylate synthase immunohistochemistry appears to be the most promising factor of those assessed in predicting tumor down-staging after preoperative chemoradiotherapy for locally advanced low rectal cancers.

Long-term lamivudine monotherapy was effective in preventing development of HBV infection in HBsAg-negative liver transplant recipients from HBcAb-positive donors.

The aim of this study was to examine the importance of the serum hepatitis C viral load within the first year post-liver transplant in determining posttransplant survival. A retrospective analysis of 118 consecutive hepatitis C virus-positive liver transplant recipients who received an allograft from January 1997 to September 2005 was undertaken with a median duration of follow-up of 32.4 months. Univariate and multivariate analyses were used to examine the effects of recipient, donor, surgical, and viral factors on posttransplant outcomes. A total of 620 viral load estimations were undertaken in the first 12 months following transplantation. Patient and graft survival rates at 1, 3, and 5 years were 87.8%, 79.9%, and 70.1% and 87.0%, 79.2%, and 68.2%, respectively. According to multivariate analysis, a peak viral load Ն 10 7 IU/mL (P ϭ 0.004; hazard ratio, 8.68; 95% confidence interval, 2.04-37.02) and exposure to antirejection therapy (P ϭ 0.05; hazard ratio, 2.26; 95% confidence interval, 1.01-5.38) were both independent predictors of diminished patient and graft survival and hepatitis C-related allograft failure. The only other independent predictor of hepatitis C virus-related outcome after transplant was azathioprine use, which was associated with improved outcomes (P ϭ 0.04; hazard ratio, 0.25; 95% confidence interval, 0.07-0.91). A peak viral load in the first year after transplant of Ͼ10 8 , 10 7 to 10 8 , and Ͻ10 7 IU/mL was associated with a mean survival of 11.8, 70.6, and 89.1 months respectively (P Յ 0. Cirrhosis related to chronic infection with hepatitis C virus (HCV) has emerged as the most frequent indication for orthotopic liver transplantation. Presently, approximately 50% of transplants performed in the United States and Europe are for patients infected with HCV.1 The health burden due to HCV is expected to increase to such a degree that by the year 2020, the proportion of untreated HCV patients developing cirrhosis will have increased by 30%.1 Furthermore, it is projected that the number of HCV patients with cirrhosis will double and the number of HCV patients with cirrhosis developing hepatocellular carcinoma (HCC) will increase by 80%.

An anaphylactic reaction to cashew nut developed in a nonatopic 60-year-old man 25 days after receiving a liver allograft from a 15-year-old atopic boy who died of anaphylaxis after peanut ingestion. The liver recipient had no history of nut allergy. Posttransplantation skin prick test results were positive for peanut, cashew nut, and sesame seed, and the donor had allergen-specific IgE antibodies to the same 3 allergens. Contact tracing of the recipients of other solid organs from the same donor disclosed no other development of allergic symptoms after ingestion of peanut or cashew nut. Results of molecular HLA typing did not detect any donor-origin leukocytes in the recipient after transplantation, which excluded peripheral microchimerism. The patient inadvertently ingested peanut-contaminated food and suffered a second anaphylactic reaction 32 weeks after the transplantation. This case illustrates that transfer of IgE-mediated hypersensitivity can occur after liver transplantation and have potentially serious consequences. We therefore recommend that organ donors undergo screening for allergies, and that recipients be advised regarding allergen avoidance.

Microsatellite polymorphisms provide highly informative readily detectable markers for human linkage studies. This paper reports apparent non-Mendelian inheritance of a dinucleotide repeat polymorphism due to allele non-amplification. The previously hidden allele was revealed and Mendelian inheritance restored when a new CA strand primer was used for amplification. Sequencing of the hidden allele identified a single base substitution at the 3'-most position of the binding site for the original CA strand primer. Allele non-amplification is a potential source of confusion in linkage studies employing polymorphisms detected by the polymerase chain reaction. It should be considered whenever apparent non-Mendelian inheritance or non-paternity are encountered.

The growing imbalance between the number of cadaveric organ donors and recipients has led to an increasing use of high-risk donors as an option to expand the donor pool. The aim of this study was to evaluate our experience with the use of older liver (donor>50 yr of age) allografts. The medical records, postreperfusion biopsies and laboratory results were reviewed of the 393 patients who underwent orthotopic liver transplantation between 1986 and 1997. The outcome of the 61 patients who received older livers (OL) was compared to that of the other 332 recipients. Increasing use of OL was evident from 1992 onwards. Recipients of OL were older than recipients of younger livers (YL, p<0.001) and more commonly had underlying chronic viral hepatitis (CVH) or fulminant hepatic failure (p<0.05). Patient and allograft survival were only slightly less in recipients of OL versus YL (p=NS). Although postperfusion biopsies showed more damage in OL than YL allografts (p<0.05), this was not associated with increased primary graft failure. OL allografts can be transplanted with acceptable results into recipients without the concern of early allograft loss. SUMMARY OF ARTICLE: This report of one centre's experience with 61 recipients of older donor liver allografts identifies recipient factors that may also have a negative impact on allograft outcome. These factors include a diagnosis of either CVH or fulminant hepatic failure at the time of transplantation. Postreperfusion biopsies of older donor allografts tend to show more damage, but this is not associated with primary non-function.