This large multicenter study confirms the safety and acceptable accuracy of ECE for the evaluation of esophageal varices. ECE might be proposed as an alternative to EGD for the screening of portal hypertension, especially in patients unable or unwilling to undergo EGD.

During phases II and III of the migrating motor complex, there is an increase in plasma motilin level that is synchronous with phasic and tonic contractile activity of the lower esophageal sphincter and of the stomach. The action of motilin on human lower esophageal sphincter is proposed to be mediated by cholinergic mechanisms. Recently, it has been shown that erythromycin was a motilin agonist. This study evaluated the pharmacological effects and the mechanisms of action of intravenous erythromycin on esophageal motility in humans. Healthy volunteers were studied three times at seven-day intervals in a randomized, double-blind fashion. Subjects were first studied for 10 min before drug administration. Afterwards, they received blindly and randomly an intravenous injection of placebo or atropine (12 micrograms/kg) followed by a 20-min continuous intravenous administration of placebo or erythromycin (150 mg). The difference (delta) between lower esophageal sphincter pressure and the duration, amplitude, and velocity of peristaltic contractions during the control period and after administration of drugs was compared. Erythromycin significantly increased (P < 0.05) the lower esophageal sphincter pressure (16.8 +/- 4.7 mm Hg) compared to placebo (-0.029 +/- 1.4 mm Hg). Erythromycin significantly decreased peristaltic contraction velocity compared to placebo (P < 0.05). The effects of erythromycin on lower esophageal sphincter pressure were completely blocked by previous administration of intravenous atropine. Erythromycin increased the number of fundic contractions compared to the placebo, but this effect was not blocked by the previous administration of atropine.(ABSTRACT TRUNCATED AT 250 WORDS)

Terlipressin (Glypressin), a vasopressin analog, may be administered to patients with cirrhosis receiving a beta-adrenergic antagonist. Since terlipressin alone and beta-blockers alone both decrease portal pressure, a combination of these substances may have additional portal hypotensive effects. However, the negative side effects of terlipressin may be accentuated by long-term beta-blockade. Thus, the present study examined hemodynamic and metabolic responses to terlipressin in 12 patients receiving nonselective beta-blockers (propranolol or nadolol). Hemodynamics and oxygen (O2) -derived variables were measured prior to and 30 min after the administration (intravenous bolus) of terlipressin (1 to 2 mg, according to body weight). The hepatic venous pressure gradient and azygos blood flow significantly decreased (from 15.3 +/- 1.1 to 12.5 +/- 1.1 mm Hg, and from 0.6 +/- 0.1 to 0.5 +/- 0.1 liters/min, respectively). Arterial and pulmonary wedged pressures significantly increased. Heart rate, cardiac index, and O2 consumption were not significantly affected by terlipressin. In conclusion, in patients with cirrhosis being treated with a nonselective beta-blocker, terlipressin administration decreased portal pressure. Moreover, terlipressin induced only mild systemic hemodynamic effects in these patients. These results suggest that terlipressin can be administered in patients receiving a beta-adrenergic blocker.