No abstract

This study was performed to examine the relationships between portal pressure measurements and the presence of esophagogastric varices, the size of varices and the occurrence of hemorrhage from varices in 93 patients with alcoholic cirrhosis, using standardized measurements of portal pressure by hepatic vein catheterization. The mean hepatic vein pressure gradient (HVPG) was significantly higher in 49 patients who had bled from varices than in 44 cirrhotic patients who had not (20.4 +/- 5.1 vs. 16.0 +/- 5.2; p less than 0.001). None of the 49 patients who had bled from varices had an HVPG less than 12 mm Hg. Among the 87 patients who had been examined by endoscopy for varices, all 72 with varices had an HVPG greater than 12 mm Hg. Six of 15 cirrhotic patients without varices had HVPG less than 12 mm Hg. The mean HVPG in the 15 patients without varices (15.1 +/- 6.8 mm Hg) was lower than the 72 patients with varices (19.3 +/- 4.8 mm Hg; p less than 0.01). Of the 72 patients with varices, 40 had large varices, 28 had small varices, and in four patients variceal size could not be assessed adequately. The mean HVPG was similar in the patients with large or small varices (19.8 +/- 4.8 vs. 18.3 +/- 5.0 mm Hg; p greater than 0.10). There was a positive relationship between the presence of large varices and the occurrence of bleeding from varices.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

In June 1996, the American Association for the Study of Liver Diseases sponsored a single topic workshop combining a two-day symposium on liver microcirculation in health and diseases 1 followed by a two day consensus workshop on portal hypertension and variceal bleeding. The goal of the combined conference was to identify areas of critical importance in the understanding and treatment of portal hypertension and to foster future collaborative research projects.The portal hypertension-variceal bleeding conference consisted of eight panel discussions, each highlighting a specific topic related to evaluation and treatment of portal hypertension. The chair of each panel was charged to summarize the current state of knowledge in the field and to suggest areas for future investigation. In addition, there were three invited lecturers on specific areas of interest. This report will summarize the conclusions of each of the panels. In comparing the summary statements from the different panels, there may be differences in emphasis, definitions of endpoints, or choices for therapy. These differences are a reflection of the state of the field where areas of disagreement exist.

No abstract

In a double-blind, randomized study the efficacy of lactulose was compared with neomycin-sorbitol in 45 episodes of acute nitrogenous portal-systemic encephalopathy (PSE) induced by dietary protein, azotemia, or gastrointestinal hemorrhage. All patients had underlying cirrhosis, and at the time of randomization had encephalopathy of at least grade 2 severity and arterial ammonia concentrations greater than 150 microgram/100 ml. Two thirds of the patients in each group returned to normal mental status and more than 80% in each group showed at least one grade improvement in mental state. In addition, there was equivalent improvement in asterixis, in the performance of the Number Connection Test, in the electroencephalographic pattern, and in arterial ammonia concentration. The principal difference between the two groups was a greater reduction in stool pH after lactulose therapy than after neomycin-sorbitol therapy. One patient randomized to neomycin-sorbitol had to be withdrawn from the study because of persistent vomiting related to the administration of the medication. Otherwise there were no complications attributable to therapy in either group. These data suggest that neomycin-sorbitol and lactulose are equally effective in the treatment of acute nitrogenous portal-systemic encephalopathy.

Peptic ulcer is a rare complication of corticosteroid therapy that should not be considered a contraindication when steroid therapy is indicated.

The present study was designed to investigate the effect of propranolol on portal pressure of patients with alcoholic cirrhosis and portal hypertension and to correlate these effects with clinical and laboratory parameters. The mean baseline hepatic venous pressure gradient in the 50 patients studied was of 18.2 +/- 4.1 mm Hg. It decreased significantly 2 hr after the oral administration of 40 mg of propranolol to 15.7 +/- 4.2 mm Hg (a mean reduction of 13.4 +/- 17%). This reduction in hepatic venous pressure gradient resulted mainly from a decrease in mean wedged hepatic venous pressure. There was no correlation between the decrease in hepatic venous pressure gradient and the decrease in heart rate. When results were analyzed individually, only 15 (30%) showed a large decrease in hepatic venous pressure gradient (greater than 20%), 15 (30%) showed a moderate decrease (10 to 19%), and in 20 patients (40%) there was no reduction or an increase in hepatic venous pressure gradient. Comparison of "responders" (those that reduced hepatic venous pressure gradient greater than 10%) and "nonresponders" (hepatic venous pressure gradient reduction less than 10%) showed no significant differences in baseline laboratory and hemodynamic parameters, in the severity of the liver disease, in the heart rate and blood pressure response to propranolol, nor in the propranolol plasma levels achieved 2 hr after propranolol administration. Propranolol plasma levels correlated with the reduction in heart rate but not with the reduction in hepatic venous pressure gradient. Of 14 nonresponders to 40 mg of propranolol who received additional doses, six showed a reduction in hepatic venous pressure gradient.(ABSTRACT TRUNCATED AT 250 WORDS)