prandial venous ammonia concentrations in the OAOne hundred twenty-six patients with cirrhosis, hytreated group showed improvements in comparison perammonemia (ú50 mmol/L), and chronic (persistent) with placebo. In addition, venous fasting blood ammonia hepatic encephalopathy (HE), which developed spontaconcentration (P õ .01), mental state gradation (P õ neously without the existence of known precipitating .001), and PSEI (P õ .01), which includes the mental state factors, were enrolled in a randomized, double-blind, gradation, NCT-A time, and postprandial venous ammoplacebo-controlled clinical trial of intravenously adminnia in this trial, improved to a much higher degree in Hepatic encephalopathy (HE) is one of the major complicapresented are based on the total study sample (intent-to-tions of cirrhosis. Five years after the diagnosis of cirrhosis, treat analysis), which included 63 patients in the placebo the probability of developing at least one episode of this spegroup and 63 patients in the OA group. Of the 126 pa-cific form of decompensated cirrhosis is in the range of 26%. 1 tients, 114 met all the criteria for inclusion and com-Once clinical decompensation has occurred, however, the pleted the trial and treatment as outlined in the protocol prognosis (16% 1 to 22% 2 probability of survival at 5 years) (treated-per-protocol analysis). During baseline, the pla-compared with a survival probability of 55% 2 to 70% 1 in circebo and treatment groups were homogeneous with re-rhotic patients without HE is very poor. 1,2 Therefore, prevengard to mental states, NCT-A performance time, fasting tion and effective treatment of HE may have important progvenous blood ammonia levels, and Child-Pugh criteria. nostic implications in cirrhotic patients. Although a slight improvement occurred in the placeboHyperammonemia 3,4 by a variety of postulated mechagroup, NCT-A performance times (P õ .001) and post-nisms 3-8 is felt to be one of the primary pathogenetic factors in the development of HE. 8 The majority of therapeutic measures currently in use are therefore directed at reducing blood Abbreviations: HE, hepatic encephalopathy; SHE, subclinical hepatic encephalopathy; ammonia levels, 9-13 mainly by diminishing enteric ammonia OA, L-ornithine-L-aspartate; GS, glutamine synthetase; NCT-A, number connection test A; PSEI, portal systemic encephalopathy index.production. Otherwise, it is known that liver and muscle play From the 1 Martin-Luther-University Halle-Wittenberg, Department of Internal Median important part within the ammonia detoxification system, cine, Halle;

Sixty-three patients with degree III or IV esophageal varices and the so-called red color sign, but without previous bleeding were randomly assigned to either prophylactic sclerotherapy (PST) (n = 30) or to a control group (n = 33). In 58 cases the portal hypertension was caused by liver cirrhosis (40% alcoholics). The two groups were comparable with respect to demographic data and endoscopic appearance, causes and severity of liver damage. Sclerotherapy was performed as combined intra-and paravariceal injections of 2 or 3% polidocanol. All patients, both in the treatment and in the control groups, who bled from varices after randomization, received sclerotherapy until the varices were eradicated, and remained in their groups. After a mean follow-up of 44.5 months, the bleeding rate in the PST group was significantly lower (30% vs 75%, p less than 0.01). The difference became significant from the second year onward. Fourteen patients of the PST group and 19 of the controls died (4 and 14, respectively, p less than 0.05 as a result of the bleeding). Life table analysis (Kaplan-Meier) revealed no differences in survival between the two groups. At the present time PST cannot yet be recommended as a method for clinical routine use.

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