SUMMARY BackgroundCapsule endoscopy can identify small bowel mucosal inflammatory change. However, there has been no validated index for capsule endoscopy findings. This manuscript documents the development of such an index.

In a high-prevalence population, PillCam ESO may represent an accurate noninvasive alternative to EGD for the detection of esophageal varices and portal hypertensive gastropathy. A large-scale trial is underway to validate and expand these findings.

Because of its ability to decrease portal pressure, azygos blood flow, and postprandial splanchnic hyperemia, octreotide administration could be effective in reducing early rebleeding in patients undergoing endoscopic variceal sclerotherapy (EVS). We report the results of a trial comparing EVS + octreotide versus EVS alone. Consecutive patients with cirrhosis and endoscopically proven variceal hemorrhage were considered eligible for the trial if hemodynamically stable for at least 24 hours after bleeding stopped. Patients with advanced liver cancer or having received EVS treatment in the past were not enrolled. After enrollment patients were submitted to EVS (day 1); all patients were randomized to receive octreotide, 100 micrograms three times a day subcutaneously, or an identical placebo, up to day 29; EVS was repeated at days 8, 15, and 29. Fifty-eight patients were randomized to receive either EVS + octreotide (n = 26) or EVS alone (n = 32). The two groups were evenly balanced for sex, age, Child-Pugh class, history of previous bleeding, endoscopic appearance of varices, or treatment received in emergency. Eight of 26 (31%) patients in the EVS + octreotide group rebled, compared with 11 of 32 (34%) in the EVS group. Four of the eight (50%) patients in the former group and 8 of 11 (73%) in the latter, respectively, bled within day 15. There were 10 (38.5%) deaths in the EVS + octreotide group (seven bleeding-related), compared with seven (21.9%) (five bleeding-related) in the EVS group; these differences did not reach statistical significance. Administration of octreotide, 100 micrograms three times a day, subcutaneously, to patients undergoing EVS for prevention of recurrent variceal bleeding does not decrease the incidence of early rebleeding.

Isosorbide-5-mononitrate (Is-5-Mn), alone or combined with beta-blockers, has been proposed for prophylaxis of variceal bleeding in cirrhosis. However, renal insufficiency, might be an important undesirable effect of this therapy, especially in patients with ascites. We assessed the changes in renal function induced in 26 cirrhotic patients by acute or chronic administration of Is-5-Mn. The acute administration of 20 mg of Is-5-Mn to 21 patients reduced mean blood pressure (83.4 +/- 2.4 vs. 92.8 +/- 3.4 mm Hg, P < .001), urine volume (5.5 +/- 0.8 vs. 8.7 +/- 1.1 mL/min, P < .05), urine sodium excretion (114 +/- 19 vs. 244 +/- 41 muEq/min, p < .001), urine potassium excretion (41 +/- 3.4 vs. 67 +/- 8.5 muEq/min, P < .001), and atrial natriuretic factor (74 +/- 10 vs. 98 +/- 12 pg/mL, P < .005). The glomerular filtration rate was decreased in the 11 patients with ascites (57 +/- 9 vs. 68 +/- 12 mL/min, P < .05), and plasma renin activity was increased in 4 ascitics. Twenty-one patients (16 from the acute study + 5 other patients) were given Is-5-Mn for 3 months at the dose of 80 mg/d. This did not affect blood pressure and renal function in patients without ascites, but reduced mean blood pressure (91.9 +/- 3.4 vs. 89.6 +/- 3 mm Hg, P < .05), urine volume (5.8 +/- 1.1 vs. 3.4 +/- 0.9 mL/min, P < .05), and urine sodium excretion (205 +/- 38 vs. 99 +/- 16 muEq/min, P < .01) in those with ascites. There were no changes in glomerular filtration rate and renal plasma flow, while plasma renin activity increased in only 3 patients with ascites and 1 without. Systemic hemodynamics and renal function of cirrhotic patients, especially those with ascites, are affected adversely by acute administration of Is-5-Mn. Long-term administration of the drug is well tolerated by compensated patients and does not affect renal plasma flow nor glomerular filtration rate, but can induce hypotension and sodium retention in patients with ascites.