Progression of gastric variceal hemorrhage (GVH) is poorer than esophageal variceal bleeding. However, data on its optimal treatment are limited. We designed a prospective study to compare the efficacy of endoscopic band ligation (GVL) and endoscopic N-butyl-2-cyanoacrylate injection (GVO). Liver patients with cirrhosis with or without concomitant hepatocellular carcinoma (HCC) and patients presenting with acute GVH were randomized into two treatment groups. Forty-eight patients received GVL, and another 49 patients received GVO. Both treatments were equally successful in controlling active bleeding (14/15 vs. 14/15, P ‫؍‬ 1.000). More of the patients who underwent GVL had GV rebleeding (GVL vs. GVO, 21/48 vs. 11/49; P ‫؍‬ .044). The 2-year and 3-year cumulative rate of GV rebleeding were 63.1% and 72.3% for GVL, and 26.8% for both periods with GVO; P ‫؍‬ .0143, log-rank test. The rebleeding risk of GVL was sustained throughout the entire follow-up period. Multivariate Cox regression indicated that concomitance with HCC (relative hazard: 2.453, 95% CI: 1.036-5.806, P ‫؍‬ .041) and the treatment method (GVL vs. GVO, relative hazard: 2.660, 95% CI: 1.167-6.061, P ‫؍‬ .020) were independent factors predictive of GV rebleeding. There was no difference in survival between the two groups. Severe complications attributable to these two treatments were rare. In conclusion, the efficacy of GVL to control active GVH appears not different to GVO, but GVO is associated with a lower GV rebleeding rate. (HEPATOLOGY 2006;43:690-697.) A lthough the outcome of variceal hemorrhage has improved over the past two decades, variceal hemorrhage is still the most serious complication of portal hypertension and chronic liver disease. 1 Although bleeding occurs less often from gastric varices (GV) than from esophageal varices (EV) (esophageal variceal hemorrhage [EVH] accounts for 70% to 80% of variceal hemorrhage), it has a poorer prognosis and is associated with more severe blood loss, a higher rebleeding rate, and a higher mortality rate. 1-3 However, limited data exist on the best treatment for GV hemorrhage (GVH). Endoscopic treatment is an alternative in the management of GVH and includes endoscopic injection of sclerosants or thrombin, 4,5 endoscopic band ligation, 6,7 and others. The success rate in controlling GVH by endoscopic injection of N-butyl-2-cyanoacrylate (GVO) appears higher than for other sclerosants according to previous non-randomized trials. 8,9 Though endoscopic variceal ligation is regarded as the optimal endoscopic treatment for EVH, 10 its safety and efficacy for the treatment of GVH is uncertain. 7,11 The rebleeding rate of GVO is variable and ranges from 10% to 42%. 12 At the time we started this trial, there were no randomized control trials, and even now, there is only one relatively small randomized clinical trial, 13 which was conducted to compare these two potential treatment modalities (endoscopic band ligation [GVL] vs. GVO) on the GVH; it showed results in favor of GVO for the treatment of GVH. We...

Bacterial infection may adversely affect the hemostasis of patients with gastroesophageal variceal bleeding (GEVB). Antibiotic prophylaxis can prevent bacterial infection in such patients, but its role in preventing rebleeding is unclear. Over a 25-month period, patients with acute GEVB but without evidence of bacterial infection were randomized to receive prophylactic antibiotics (ofloxacin 200 mg i.v. q12h for 2 days followed by oral ofloxacin 200 mg q12h for 5 days) or receive antibiotics only when infection became evident (on-demand group). Endoscopic therapy for the GEVB was performed immediately after infection work-up and randomization. Fifty-nine patients in the prophylactic group and 61 patients in the on-demand group were analyzed. Clinical and endoscopic characteristics of the gastroesophageal varices, time to endoscopic treatment, and period of follow-up were not different between the two groups. Antibiotic prophylaxis decreased infections (2/59 vs. 16/61; P < .002). The actuarial probability of rebleeding was higher in patients without prophylactic antibiotics (P ‫؍‬ .0029). The difference of rebleeding was mostly due to early rebleeding within 7 days (4/12 vs. 21/27, P ‫؍‬ .0221). The relative hazard of rebleeding within 7 days was 5.078 (95% CI: 1.854 -13.908, P < .0001). The multivariate Cox regression indicated bacterial infection (relative hazard: 3.85, 95% CI: 1.85-13.90) and association with hepatocellular carcinoma (relative hazard: 2.46, 95% CI: 1.30 -4.63) as independent factors predictive of rebleeding. Blood transfusion for rebleeding was also reduced in the prophylactic group (1.40 ؎ 0.89 vs. 2.81 ؎ 2.29 units, P < .05). There was no difference in survival between the two groups. In conclusion, antibiotic prophylaxis can prevent infection and rebleeding as well as decrease the amount of blood transfused for patients with acute GEVB following endoscopic treatment. (HEPATOLOGY 2004;39:746 -753.)

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To determine the efficacy of endoscopic variceal sclerotherapy (EVS) and ligation (EVL) in the management of esophageal variceal bleeding, 134 cirrhotic patients were randomized to receive either treatment. The clinical and endoscopic characteristics were similar in both groups. Active bleeding was controlled with ligation (20 of 20) as efficiently as with sclerotherapy (14 of 16). Elective sclerotherapy consumed less time than ligation (7.9 +/- 1.8 minutes vs. 11.5 +/- 2.7 minutes, P < .001), but there was no difference between emergent sclerotherapy (14.5 +/- 5.8 minutes) and ligation (14.9 +/- 4.1 minutes). Ligation reduced one grade of variceal size more quickly than sclerotherapy (1.1 +/- 0.4 vs. 2.0 +/- 1.7 session, P < .001). The rebleeding rate was lower with ligation (13 of 67 vs. 28 of 67, P < .01). Esophageal ulcer was the most common source of rebleeding. Recurrence of varices appears more probable with ligation (P = .079). The complication rate was higher with sclerotherapy (15 of 67 vs. 3 of 67, P < .01), with esophageal stricture being the most common cause. Survival rate was the same in both groups even after stratifying patients into good and poor hepatic reserve groups. Hepatic failure was the major cause of death, followed by exsanguination. In summary, EVL was superior to EVS regarding rebleeding and complications but not in other aspects such as time consumption in elective treatment and recurrence of varices. Substantial results for long-term follow-up are required before conclusion of the treatment of choice.

This study investigated whether nitric oxide (NO) plays a role in the intrahepatic portal circulation in normal rat livers perfused in situ. N omega-nitro-L-arginine (NNA), a specific NO biosynthesis inhibitor, significantly increased baseline portal pressure compared with controls (P < 0.05). Concentration-effect curves to norepinephrine (NE) were performed. Perfusate flow was maintained as constant, and perfusion pressure was continuously measured. NNA markedly enhanced the responsiveness to NE. This effect was abolished by the addition of L-arginine, a specific NO substrate. Presence of indomethacin did not alter the response to NE. The response to NE in the presence of indomethacin and NNA was significantly more than the response to NE in the presence of NNA alone. In vivo, intraportal infusion of NNA significantly enhanced the portal pressure compared with vehicle. This study demonstrates that NO contributes to the basal vascular tone and attenuates the response to NE in intrahepatic portal vascular bed of normal rats. These results support a functional role of NO in the regulation of the intrahepatic portal circulation in normal rats. This study also suggests a synergistic, albeit limited, role of prostacyclin in the intrahepatic circulation.