A prospective controlled comparison of portal-systemic (PSS) and distal splenorenal shunts (DSRS) in cirrhotic patients who had survived hemorrhage from esophagogastric varices was undertaken 5 yr ago at five hospitals by the Boston-New Haven Collaborative Liver Group. The clinical and endoscopic criteria for massive hemorrhage were satisfied in 155 patients. Thirty-four patients were excluded, primarily because of uncontrolled hemorrhage. Thirty-four were rejected because the were poor operative risks and 21 because they did not satisfy criteria. Thirteen patients refused to participate; the remaining 53 were randomized; 29 to receive PSS and 24, DSRS. The two groups were similar in clinical, laboratory, and manometric characteristics. The DSRS group was older and tended to have had more previous hemorrhages. Followup ranged from 1 to 56 months (mean 21). After PSS, which was performed by 10 different surgeons, 6 patients died during the hospital admission (21%) compared to 2 after DSRS (12%). There were 6 late deaths in the PSS group and 4 in the DSRS group. Portal-systemic encephalopathy occurred in 5 of the 23 survivors of PSS (23%), and in 6 of the 19 who survived DSRS (32%. Two patients in the PSS group bled (9%), 1 after thrombosis and 1 after stenosis of the shunt. Three patients in the DSRS group bled (16%) and all had thrombosis of the shunt. PSS was associated with an unexplained but inordinately high operative mortality. Although the DSRS was accomplished with an acceptably low operative mortality, it was associated with frequent portal-systemic encephalopathy, shunt occlusion, and recurrent hemorrhage. Similar incidences of portal-systemic encephalopathy, shunt occlusion, and recurrent hemorrhage were observed in the PSS group. More patients and longer followup are necessary to determine which of these portal decompressive procedures is superior.

Clinical Trials as Topic↗

PubMedDate not supplied

The misuse of cimetidine in patients with cirrhosis.

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Cimetidine↗

PubMedDate not supplied

Comparison of dietary protein with an oral, branched chain-enriched amino acid supplement in chronic portal-systemic encephalopathy: a randomized controlled trial.

A randomized study was conducted in 37 hospitalized patients at six cooperating hospitals in which protein-intolerant cirrhotic patients were fed increasing amounts of either dietary protein or a branched-chain enriched amino acid solution (BCAA) until they attained an intake of 80 gm protein per day or equivalent or until they developed stage 2 encephalopathy. All patients initially received 20 gm of dietary protein for 1 week, after which 20 gm of protein or BCAA were added weekly. Nitrogen balance improved from negative to positive in all patients in whom it was measured and increased equally in both groups. Seven of the 20 patients in the protein group and 1 of 17 in the BCAA group developed encephalopathy of stage 2 or greater (p less than 0.05). Changes in each component of the portal-systemic encephalopathy syndrome were compared, and differences were statistically significant for mental status grade (p less than 0.01), asterixis (p less than 0.05), Portal-systemic encephalopathy index (p less than 0.01), but insignificant for Number Connection Test, EEG or ammonia. Plasma amino acid profiles showed an increase in BCAA in the study group. Thus, oral BCAA supplements appear to induce positive nitrogen balance to approximately the same degree as an equivalent amount of dietary protein without inducing encephalopathy as frequently.

Adult↗

PubMedDate not supplied

Short-term effects of propranolol on portal venous pressure.

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)

Adult↗