To investigate the natural history of compensated cirrhosis, 293 consecutive patients without previous major complications (ascites, jaundice, encephalopathy or gastrointestinal hemorrhage) were studied in terms of morbidity (probability of developing decompensated cirrhosis during follow-up) and survival. Patients were diagnosed by liver histology between 1968 and 1980. Median follow-up was 63 months. Decompensation of cirrhosis was considered when a patient first developed one of the major complications of the disease. Ten years after diagnosis, the probability of developing decompensated cirrhosis and the survival probability rate were 58 and 47%, respectively. A multivariate survival analysis (Cox's regression model) using clinical, biochemical and histological data obtained at diagnosis disclosed seven factors that predicted prognosis: serum bilirubin; serum gamma-globulin concentration; hepatic stigmata; prothrombin time; sex; age, and alkaline phosphatase. According to the contribution of each one of these factors to the final model, a prognostic index was constructed that allows calculation of the estimated survival probability. The predicting value of this index was validated by a split sample testing technique.

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To investigate if oral, nonabsorbable antibiotics prevent bacterial infections in cirrhotics with gastrointestinal hemorrhage, 140 consecutive patients were randomly allocated into two groups: 68 patients (Group I) were given oral, non absorbable antibiotics (gentamicin + vancomycin + nystatin or neomycin + colistin + nystatin) from the inclusion into the trial up to 48 hr after cessation of the hemorrhage, or until emergency surgery or death in those cases who continued bleeding; and 72 patients (Group II) did not receive oral, nonabsorbable antibiotics. Both groups were similar in relation to clinical and laboratory data and characteristics of the hemorrhage. The incidence of infection was significantly lower in Group I than in Group II (11 patients in Group I and 25 in Group II developed proved infections; p less than 0.025). This difference was due to the fact that spontaneous bacteremia and peritonitis and urinary tract infection caused by enteric bacteria occurred almost exclusively in Group II. Two patients of Group I and 10 of Group II developed spontaneous bacteremia and/or peritonitis caused by enteric bacteria (p less than 0.025). These results indicate that prophylactic administration of oral, nonabsorbable antibiotics markedly reduces the incidence of infections caused by enteric bacteria in cirrhotic patients with gastrointestinal hemorrhage.

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The present trial compared the effectiveness and complications of intravenous somatostatin and vasopressin in treatment of variceal bleeding. Sixty-one cirrhotic patients with endoscopically proven active variceal bleeding were included. Both drugs were given as continuous intravenous infusions for 48 hr. Thirty patients received somatostatin (250 micrograms per hr after a bolus of 50 micrograms) and 31 vasopressin (0.4 units per min). Initial control of bleeding was achieved in 26 (87%) patients receiving somatostatin and in 23 (74%) of those treated with vasopressin. However, 10 patients [not significant statistically] in the somatostatin group and 5 in the vasopressin group rebled during treatment, after a mean of 15 and 20 hr, respectively. Therefore, complete control of bleeding during the 48 hr of therapy was achieved in 16 (53%) patients treated with somatostatin and in 18 (58%) of those receiving vasopressin. Mortality during hospitalization was similar in both groups (somatostatin 47%, vasopressin 45%). Differences were observed in complications associated with each therapy. Vasopressin produced major complications in 8 patients (left ventricular failure in 4 and severe abdominal pain requiring drug withdrawal in 4), and minor complications in 14; somatostatin infusion produced minor complications in 3 patients (p less than 0.01). In addition, the serum sodium concentration was significantly reduced by vasopressin (from 134.3 +/- 1.6 to 128.3 +/- 1.4 mEq per liter, p less than 0.001) but not by somatostatin (134.6 +/- 1.1 vs. 133.2 +/- 1.1 mEq per liter). This study shows that somatostatin is as effective as vasopressin in controlling variceal hemorrhage, but has a much lower rate of complications.