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Article: Alcohol drinking and cigarette smoking: a 'partner' for gastric ulceration

TitleAlcohol drinking and cigarette smoking: a 'partner' for gastric ulceration
Authors
Issue Date2000
PublisherChinese Medical Association (Taipei). The Journal's web site is located at http://www.cmj.org/
Citation
Chinese Medical Journal, 2000, v. 63 n. 12, p. 845-854 How to Cite?
AbstractAlcohol consumption and cigarette smoking are two etiologic factors that have a close relationship with peptic ulcer diseases. Chronic active gastritis is reportedly associated with chronic alcohol ingestion. Nonetheless, the inflammatory changes are likely to be related to concurrent Helicobacter pylori infection that is common among alcoholics. Moreover, chronic alcoholism is also correlated with the presence of gastric metaplasia. Both clinically and experimentally, alcohol had been shown to affect the mucosal barrier and histology. These ulcerogenic effects play a crucial role in altering gastric mucosal defense mechanisms. Cigarette smoking is coupled with the initiation and prolongation of gastric ulcers. Epidemiologic data show that cigarette smoking increases both the incidence and relapse rate of peptic ulcer diseases and also delays ulcer healing in humans. Retrospective studies also indicate that cigarette smoking is a key factor in inducing ulcer diseases rather than a linked behavior. The general detrimental effects of cigarette smoking in the gastric mucosa include reduction of circulating epidermal growth factor, increase in tissue free radical production and the presence of free radicals in smoke, together with reduction of mucosal constitutive nitric oxide synthase activity. Furthermore, the alteration of normal gastric mucosal blood flow and angiogenesis and the suppression of cell proliferation contribute largely to the delay in ulcer healing in cigarette smokers. Concurrent consumption of alcohol and cigarette smoking significantly increases the risk of gastric ulcers. In animal experiments, cigarette smoking potentiated ethanol-induced gastric mucosal damage. The reduction of mucus secretion, increase in leukotriene B4 level, increased activities of inducible nitric oxide synthase, xanthine oxidase and myeloperoxidase, and the expression of adhesion molecules in the gastric mucosa accompanied such potentiating effects. Substances other than nicotine in cigarette smoke may also contribute to the above effects.
Persistent Identifierhttp://hdl.handle.net/10722/222899
ISSN

 

DC FieldValueLanguage
dc.contributor.authorKo, JKS-
dc.contributor.authorCho, CH-
dc.date.accessioned2016-02-11T08:23:38Z-
dc.date.available2016-02-11T08:23:38Z-
dc.date.issued2000-
dc.identifier.citationChinese Medical Journal, 2000, v. 63 n. 12, p. 845-854-
dc.identifier.issn0578-1337-
dc.identifier.urihttp://hdl.handle.net/10722/222899-
dc.description.abstractAlcohol consumption and cigarette smoking are two etiologic factors that have a close relationship with peptic ulcer diseases. Chronic active gastritis is reportedly associated with chronic alcohol ingestion. Nonetheless, the inflammatory changes are likely to be related to concurrent Helicobacter pylori infection that is common among alcoholics. Moreover, chronic alcoholism is also correlated with the presence of gastric metaplasia. Both clinically and experimentally, alcohol had been shown to affect the mucosal barrier and histology. These ulcerogenic effects play a crucial role in altering gastric mucosal defense mechanisms. Cigarette smoking is coupled with the initiation and prolongation of gastric ulcers. Epidemiologic data show that cigarette smoking increases both the incidence and relapse rate of peptic ulcer diseases and also delays ulcer healing in humans. Retrospective studies also indicate that cigarette smoking is a key factor in inducing ulcer diseases rather than a linked behavior. The general detrimental effects of cigarette smoking in the gastric mucosa include reduction of circulating epidermal growth factor, increase in tissue free radical production and the presence of free radicals in smoke, together with reduction of mucosal constitutive nitric oxide synthase activity. Furthermore, the alteration of normal gastric mucosal blood flow and angiogenesis and the suppression of cell proliferation contribute largely to the delay in ulcer healing in cigarette smokers. Concurrent consumption of alcohol and cigarette smoking significantly increases the risk of gastric ulcers. In animal experiments, cigarette smoking potentiated ethanol-induced gastric mucosal damage. The reduction of mucus secretion, increase in leukotriene B4 level, increased activities of inducible nitric oxide synthase, xanthine oxidase and myeloperoxidase, and the expression of adhesion molecules in the gastric mucosa accompanied such potentiating effects. Substances other than nicotine in cigarette smoke may also contribute to the above effects.-
dc.languageeng-
dc.publisherChinese Medical Association (Taipei). The Journal's web site is located at http://www.cmj.org/-
dc.relation.ispartofChinese Medical Journal-
dc.subject.meshAlcohol Deterrents - adverse effects-
dc.subject.meshGastric Mucosa - pathology-
dc.subject.meshHumans-
dc.subject.meshSmoking - adverse effects-
dc.subject.meshStomach Ulcer - etiology - pathology-
dc.titleAlcohol drinking and cigarette smoking: a 'partner' for gastric ulceration-
dc.typeArticle-
dc.identifier.emailKo, JKS: jksko@hkucc.hku.hk-
dc.identifier.emailCho, CH: chcho@hkusua.hku.hk-
dc.identifier.pmid11195134-
dc.identifier.hkuros58818-
dc.identifier.volume63-
dc.identifier.issue12-
dc.identifier.spage845-
dc.identifier.epage854-
dc.publisher.placeTaiwan, Republic of China-

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