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Alcohol and gastrointestinal bleeding.
Emerg Med Clin North Am. 1990 Nov; 8(4):859-72.EM

Abstract

Ethanol has experimentally been shown to be "ulcerogenic," independent of gastric intraluminal pH. Ethanol remains ulcerogenic despite antisecretory doses of H2-receptor antagonists. Low-dose alcohol stimulates acid secretion in man, an effect possibly mediated by histamine or gastrin. High-dose alcohol reduces intraluminal acid by damaging mucosa, thereby enhancing back diffusion of hydrogen ion, and also by direct damage to oxyntic (parietal) cells. Ethanol is capable of increasing gastric mucosal permeability as evidenced by the increase in back diffusion (increases intraluminal pH) and by the characteristic fall in transmucosal potential difference which reflects surface cell layer exfoliation. This exfoliation may offer an explanation for the potentiating effect of alcohol on gastric mucosal injury when it is ingested simultaneously with other gastric irritants. Ethanol of greater than 20% concentration can rapidly destroy the gastric mucus-bicarbonate layer, which may be a defense layer for both the inhibition of back diffusion and bicarbonate neutralization of existing acid. Ethanol depletes sulfhydryl compounds in gastric mucosa. These sulfhydryls may be necessary for stabilization of cell membranes as well as for binding free radicals. Ethanol is damaging to the mucosal microcirculation. The rapidity of ethanol-induced damage makes it unlikely that the process is purely ischemic. The cytoprotective phenomenon, as this brief literature review suggests, is a multifactorial, dynamic process. The complex interplay of mucosal defense factors, endogenous and exogenous stimuli, induction of humoral responses, and ultimately the success or failure of cellular repair, is unlikely to be solely mediated by endogenous prostaglandins. Although prostaglandins are unquestionably significant to cytoprotection, the supporting and, perhaps, major roles of leukotrienes, sulfhydryls, histamines, and like substances cannot be ignored. Several innovative therapeutic agents directly derived from these research efforts have already entered the clinician's formulary. The significance of the concept of cytoprotection is only now being realized in clinical applications. Alcoholic hemorrhagic gastritis, although a significant clinical entity, remains a rather elusive diagnosis for the emergency physician. As a diagnosis of suspicion, therapeutic trials of antacids, sucralfate, or perhaps synthetic prostaglandin analogues are acceptable, pending endoscopic verification or short-term resolution of symptoms. All patients presenting with true hemorrhage or with persistent symptoms should undergo gastroenterologic referral and endoscopic evaluation. The Mallory-Weiss syndrome has long been associated with acute and chronic alcohol abuse.(ABSTRACT TRUNCATED AT 400 WORDS)

Authors+Show Affiliations

Department of Surgery, University of Florida Health Science Center/Jacksonville.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

2226291

Citation

MacMath, T L.. "Alcohol and Gastrointestinal Bleeding." Emergency Medicine Clinics of North America, vol. 8, no. 4, 1990, pp. 859-72.
MacMath TL. Alcohol and gastrointestinal bleeding. Emerg Med Clin North Am. 1990;8(4):859-72.
MacMath, T. L. (1990). Alcohol and gastrointestinal bleeding. Emergency Medicine Clinics of North America, 8(4), 859-72.
MacMath TL. Alcohol and Gastrointestinal Bleeding. Emerg Med Clin North Am. 1990;8(4):859-72. PubMed PMID: 2226291.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alcohol and gastrointestinal bleeding. A1 - MacMath,T L, PY - 1990/11/1/pubmed PY - 1990/11/1/medline PY - 1990/11/1/entrez SP - 859 EP - 72 JF - Emergency medicine clinics of North America JO - Emerg Med Clin North Am VL - 8 IS - 4 N2 - Ethanol has experimentally been shown to be "ulcerogenic," independent of gastric intraluminal pH. Ethanol remains ulcerogenic despite antisecretory doses of H2-receptor antagonists. Low-dose alcohol stimulates acid secretion in man, an effect possibly mediated by histamine or gastrin. High-dose alcohol reduces intraluminal acid by damaging mucosa, thereby enhancing back diffusion of hydrogen ion, and also by direct damage to oxyntic (parietal) cells. Ethanol is capable of increasing gastric mucosal permeability as evidenced by the increase in back diffusion (increases intraluminal pH) and by the characteristic fall in transmucosal potential difference which reflects surface cell layer exfoliation. This exfoliation may offer an explanation for the potentiating effect of alcohol on gastric mucosal injury when it is ingested simultaneously with other gastric irritants. Ethanol of greater than 20% concentration can rapidly destroy the gastric mucus-bicarbonate layer, which may be a defense layer for both the inhibition of back diffusion and bicarbonate neutralization of existing acid. Ethanol depletes sulfhydryl compounds in gastric mucosa. These sulfhydryls may be necessary for stabilization of cell membranes as well as for binding free radicals. Ethanol is damaging to the mucosal microcirculation. The rapidity of ethanol-induced damage makes it unlikely that the process is purely ischemic. The cytoprotective phenomenon, as this brief literature review suggests, is a multifactorial, dynamic process. The complex interplay of mucosal defense factors, endogenous and exogenous stimuli, induction of humoral responses, and ultimately the success or failure of cellular repair, is unlikely to be solely mediated by endogenous prostaglandins. Although prostaglandins are unquestionably significant to cytoprotection, the supporting and, perhaps, major roles of leukotrienes, sulfhydryls, histamines, and like substances cannot be ignored. Several innovative therapeutic agents directly derived from these research efforts have already entered the clinician's formulary. The significance of the concept of cytoprotection is only now being realized in clinical applications. Alcoholic hemorrhagic gastritis, although a significant clinical entity, remains a rather elusive diagnosis for the emergency physician. As a diagnosis of suspicion, therapeutic trials of antacids, sucralfate, or perhaps synthetic prostaglandin analogues are acceptable, pending endoscopic verification or short-term resolution of symptoms. All patients presenting with true hemorrhage or with persistent symptoms should undergo gastroenterologic referral and endoscopic evaluation. The Mallory-Weiss syndrome has long been associated with acute and chronic alcohol abuse.(ABSTRACT TRUNCATED AT 400 WORDS) SN - 0733-8627 UR - https://www.unboundmedicine.com/medline/citation/2226291/Alcohol_and_gastrointestinal_bleeding_ L2 - https://medlineplus.gov/alcoholusedisorderaud.html DB - PRIME DP - Unbound Medicine ER -