The incidence of esophageal adenocarcinoma has risen rapidly over the past 25 years in the United States as well as in several Western European countries. This increase had been most dramatic among white males. The majority of these cancers arise from a background of premalignant Barrett esophagus. However, less than 10% of the patients with esophageal adenocarcinoma were known to have Barrett esophagus previously. It is uncertain which risk factors contribute to the increasing incidence of esophageal adenocarcinoma, although gastroesophageal reflux disease, cigarette smoking, and obesity have been implicated. Whereas infection with Helicobacter pylori and use of non-steroidal anti-inflammatory drugs are associated with reduced risk, low intakes of fruit, vegetables, and cereal fibers seem to increase the risk of esophageal adenocarcinoma. Presently there is no evidence that strongly supports any specific strategy to screen a subgroup of the population at risk for Barrett esophagus and adenocarcinoma of the esophagus.
It is widely agreed that hepatitis B virus immunoglobulinSeveral reports have clearly shown that liver transplantation in patients with hepatitis B virus (HBV) infection-as defined by positivity for hepatitis B surface antigen (HBsAg)-is associated with a high rate of recurrence of HBV infection after transplantation, resulting in severe graft disease in most cases and in a significant decrease in both graft and patient survival.  It is widely accepted that the risk of HBV recurrence after liver transplantation is directly proportional to the level of viral replication before transplantation, with those recipients seropositive for HBeAg and HBV DNA by hybridization technique having the highest rate of recurrence after transplantation, irrespective of the type of liver disease. 2,4 Many prophylactic strategies have been proposed to prevent HBV infection of the graft, but only long-term passive immunoprophylaxis with HBV-specific immunoglobulin (HBIG) has obtained a significant reduction in the risk of HBV graft infection and in both graft and patient mortality after liver transplantation.  The presence of serum HBV DNA before transplantation is, however, a major predictor of lack of response to this prophylactic regimen.In light of these evidences, the European Concerted Action on Viral Hepatitis (EUROHEP) recommended in 1994 to refrain from transplanting chronic HBV carriers found to be positive for either hepatitis B e antigen (HBeAg) or HBV DNA by direct hybridization. Moreover, the rest of the recipients with HBV-related disease should receive HBIG immunoprophylaxis to maintain anti-HBs levels above 100 IU/L for at least 12 months after transplantation. 6 Currently, the beneficial effect of long-term HBIG administration has become widely accepted; still no consensus has been reached regarding the optimal duration of HBIG treatment. The rate of HBV graft infection recurrence 12 months after liver transplantation seems to be much decreased but it can still undoubtedly occur. 4,6, Moreover the finding of HBV DNA in peripheral mononuclear blood beyond 12 months of effective HBIG prophylaxis argues in favor of a potentially indefinite risk of graft infection. 11-13 As a consequence, most liver transplant centers are currently administering HBIG on a life-long basis. Because HBIG use is highly expensive, an alternative strategy aiming at the discontinuation of HBIG prophylaxis during the second year of treatment would be an important cost-effective measure. We present here an assessment of the efficacy of a new prophylactic strategy consisting of the discontinuation of HBIG administration followed by active immunization with HBV vaccination in patients transplanted for HBVrelated liver diseases.
PATIENTS AND METHODSPatients. Between July 1990 and April 1996, 36 HBsAg-positive recipients were submitted to liver transplantation at the Hospital Abbreviations: HBV, hepatitis B virus; HBsAg, hepatitis B virus surface antigen; HBIG, hepatitis B virus immunoglobulin; HBeAg, hepatitis B vi...
Orthotopic liver transplantation (OLT) can be associated with excessive blood loss. As a result, there may be increased risk of adverse outcomes. Activated recombinant factor VII (rFVIIa) has demonstrated the ability to improve hemostasis in a variety of disorders; however, there has been a limited amount of research into its use in OLT. The purpose of this dose-finding study was to examine the efficacy and safety of rFVIIa in the reduction of bleeding in patients undergoing OLT. In this doubleblind trial, patients with end-stage liver disease scheduled for OLT were randomized to 1 of 4 parallel study groups. They received a single intravenous bolus of rFVIIa (20, 40, or 80 g/kg) or placebo prior to surgery. The primary assessment endpoint was the total number of red blood cell (RBC) units transfused perioperatively. Safety was evaluated by adverse events reported. Eighty-three comparable patients were randomized to receive study product, with 82 ultimately undergoing OLT. There were no significant differences in required RBC units between the placebo and rFVIIa study groups. The number of adverse events was comparable between study groups. In conclusion, rFVIIa has a good safety profile in patients undergoing OLT. However, the doses studied did not have any effect on the number of RBC transfusions required. (Liver Transpl 2005;11:895-900.)
To identify factors predictive of early postoperative graft function, we analyzed 54 variables--including easily available clinical and laboratory data prospectively obtained from organ donors, transplant recipients and surgical procedures in 168 consecutive liver transplantations. Early postoperative graft function was classified into three groups according to a scoring system ranging from 3 to 9 based on peak serum ALT values, mean bile output and lowest prothrombin activity measured during the 72 hr after transplant: group 1 (score 3 to 4, good graft function; n = 73), group 2 (score 5 to 6, moderate dysfunction; n = 50) and group 3 (score, 7 to 9, severe dysfunction; n = 45). In univariate analyses, 8 of the 54 variables analyzed were statistically significant (p < 0.05) predictors of severe graft dysfunction: high serum sodium concentration and brain death caused by cranial trauma in organ donors, advanced age and low prothrombin activity in transplant recipients, prolonged total ischemia time and large transfusions of red blood cells, fresh frozen plasma and platelets during surgery. After introduction of these eight variables in a multivariate analysis, only four were found to independently predict early postoperative graft function: donor serum sodium concentration, total ischemia time, platelet transfusion during surgery and recipient prothrombin activity. In 52 liver transplantations, in which the predictive value of liver tissue adenine nucleotide concentration and several biochemical sensitive markers of donor nutritional status was also analyzed, only the ATP level in liver tissue obtained at the time of organ reperfusion was identified as an independent predictor of initial graft function.(ABSTRACT TRUNCATED AT 250 WORDS)
HCV infection recurrence leads to severe liver damage and subsequently to clinical decompensation in a significant proportion of OLT recipients. Some clinical and biochemical characteristics can predict the severity of HCV-induced graft damage.
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