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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. [1][2][3][4] 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. [4][5][6][7] 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,[8][9][10] 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...

We tested the hypothesis that the presence of bacterial DNA (bactDNA) in ascitic fluid and serum is associated with decreased survival in patients with cirrhosis. In a prospective, multicenter study, we analyzed the clinical evolution of 156 patients with cirrhosis and ascites (first or recurrence) with lower than 250 polymorphonuclear cells (PMN)/ L, negative ascites bacteriological culture, and absence of other bacterial infections being admitted for evaluation of largevolume paracentesis, according to the presence of bactDNA at admission. Survival, causes of death, and successive hospital admissions were determined during a 12-month follow-up period. BactDNA was detected in 48 patients. The most prevalent identified bactDNA corresponded to Escherichia coli (n ‫؍‬ 32/48 patients, 66.6%). Patients were followed for 12 months after inclusion and in this period 34 patients died: 16 of 108 (15%) From the

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The present double-blind study was aimed at investigating the hemodynamic and humoral effects of somatostatin or placebo in patients with cirrhosis. Patients were randomly assigned to receive either an injection of 250 micrograms of somatostatin followed by a constant infusion of somatostatin at 250 micrograms/h (n = 13), an injection of 250 micrograms of somatostatin followed by a 500 micrograms/h continuous infusion (n = 10), or an injection of placebo followed by a placebo infusion (n = 9). Placebo had no effect. Somatostatin bolus markedly decreased the hepatic venous pressure gradient: by 52% at 1 minute; P < .001; 19% at 3 minutes, P < .01; and by 13% at 5 minutes, P < .04. Azygos blood flow decreased similarly by 45% at 1 minute, P < .001; 16% at 3 minutes, P < .02; and 9.5% at 5 minutes, P = .05. Mean arterial pressure increased by 25% (P < .001). Continuous somatostatin infusions (250 or 500 micrograms/h) had no systemic effects, but significantly reduced hepatic venous pressure gradient (250 micrograms/h: -6.1%, P < .05 and 500 micrograms/h: -15%, P < .01) and hepatic blood flow (250 micrograms/h: -10%, 500 micrograms/h: -18%, P < .05). Azygos blood flow was not changed after 250 micrograms/h infusion but was reduced after 500 micrograms/h (-23%, P < .02). Somatostatin but not placebo, suppressed glucagon to normal levels. This study shows that a bolus injection of somatostatin caused an immediate and marked decrease of hepatic venous pressure gradient and azygos blood flow. Continuous infusion of somatostatin had a mild but sustained effect on splanchnic hemodynamics; this effect was more pronounced with the higher dose.

Patients with alcoholic cirrhosis show a high frequency of complications. The low mortality rate in our cohort of patients probably reflects the improvement in the management of patients with cirrhosis; it is mainly influenced by baseline MELD, age, HE development, and continued abstinence. Patients who develop HE should be considered for hepatic transplantation.