Keshavarzian A, Polepalle C, Iber F L, Durkin M
Department of Medicine, Loyola University Medical Center, Maywood, Illinois 60153.
Alcohol Clin Exp Res. 1990 Aug;14(4):561-7. doi: 10.1111/j.1530-0277.1990.tb01200.x.
Both acute and chronic ethanol consumption may cause esophageal dysmotility. In order to systematically evaluate the effect of ethanol on esophageal motility, we studied esophageal motility in 13 healthy subjects before and following acute intravenous administration of 0.8 g/kg ethanol and in chronic alcoholics within 6 hr of their last drink (n = 6) and following 24 to 48 hr of abstinence when signs of withdrawal were present (n = 13). Withdrawing alcoholics were also restudied after intravenous administration of 0.8 g/kg ethanol. Ethanol transiently decreased lower esophageal sphincter pressure (LESP) and inhibited LES relaxation in all control subjects; this inhibitory effect of ethanol on LESP in alcoholics was significantly less, indicating the development of tolerance. Ethanol moderately decreased esophageal contraction amplitude (ECA) in 10 of 13 controls and prolonged duration of contractions in all but had no effect on velocity of esophageal contractions. In contrast, ECA was significantly elevated in both groups of alcoholics, but this was significantly more marked in withdrawing alcoholics. Ethanol infusion returned ECA toward normal values in withdrawing alcoholics. Abnormal motility was noted in three intoxicated alcoholics and 10 (77%) withdrawing alcoholics. This included nutcracker esophagus in five and hypertensive LES in two. These data indicated that (1) esophageal motor dysfunction is common in alcoholics; (2) acute ethanol administration decreases LESP and esophageal contraction amplitude, whereas chronic ethanol consumption and withdrawal from ethanol increases ECA. This suggests development of a compensatory mechanism in chronic alcoholics leading to high pressure esophageal contractions during withdrawal.
