To assess the effectiveness of propranolol in the prevention of initial variceal hemorrhage, a double-blind, randomized trial was carried out in three centers. Patients with cirrhosis (78% alcoholic), hepatic venous pressure gradients greater than 12 mm Hg and endoscopically proven esophageal varices were randomly assigned to propranolol (51 patients) or placebo (51 patients). Of the 102 patients, 58% were Child's class A, 34% were Child's class B and 8% were Child's class C. Daily dosage was determined by the administration of progressively increasing doses of propranolol with the hepatic vein catheter in place to achieve a 25% decrease in hepatic venous pressure gradient, a decrease in hepatic venous pressure gradient to less than 12 mm Hg or a decrease in resting heart rate to less than 55 beats/min. During a mean follow-up period of 16.3 mo, 11 patients in the placebo group (22%) bled from esophageal varices compared with 2 in the propranolol group (4%) during a mean period of 17.1 mo (p less than 0.01). Three additional patients (6%) in the placebo group bled from portal hypertensive gastropathy compared with none in the propranolol group. Propranolol appeared effective in preventing bleeding from large varices. Eleven deaths (22%) occurred in the placebo group compared with eight deaths (16%) in the propranolol group (NS). The mean dose of propranolol was 132 mg/day, and the median dose was 80 mg/day. Using a compliance index (pill count, clinic attendance, alcohol and propranolol levels and alcohol history), 81% of the propranolol patients and 77% of the placebo patients were considered compliant. Complications severe enough to require cessation of therapy occurred in eight patients (16%) in the propranolol group and four in the placebo group (8%) (NS). We conclude that propranolol effectively prevents the first variceal hemorrhage in patients with alcoholic cirrhosis and large esophageal varices but does not improve survival.

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L -alpha-methyldopa (Aldomet)-induced liver disease is a relatively mild and uncommon complication of therapy with this drug. Most commonly it is characterized by a rise in serum alkaline phosphatase, glutamic oxaloacetic transaminase levels, and increased Bromsulphalein retention. Elevation of the serum bilirubin may occur. In its most benign form the condition is usually symptomless, but complaints, such as anorexia, abdominal pain, or pruritus, and signs, such as fever or hepatomegaly, may occur. Histologic changes similar to those of viral hepatitis have been observed. The condition is usually benign and remits on withdrawal of the drug. Progressively more mild exacerbations on readministration of the drug suggest that desensitization may be possible in patients who exhibit hepatic abnormalities. Its low and sporadic incidence is typical of a hypersensitivity reaction. It is suggested that routine liver function tests should be undertaken at intervals during therapy. The occasional occurrence of Aldomet-induced liver disease is no contraindication to the use of this antihypertensive agent.

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