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[消化性溃疡:胃十二指肠黏膜防御机制的失效?]

[Peptic ulcer: a failure of the defense mechanisms of the gastroduodenal mucosa?].

作者信息

Chacín J

机构信息

Instituto de Investigaciones Biológicas, Facultad de Medicina, Universidad del Zulia.

出版信息

G E N. 1990 Apr-Jun;44(2):163-70.

PMID:2152272
Abstract

Peptic ulcer is an heterogeneous and multifactorial disease. Secretion of acid/pepsin is a critical permissive factor in gastroduodenal peptic ulceration. Therapy of this disease has been based mostly on this principle. The sole presence of the aggressive factor, acid/pepsin, is not enough to explain peptic ulceration. Mucosal defense (resistance) is another critical factor involved in pathogenesis of this disease. Defects in some gastroduodenal defense mechanisms have been found in patients with peptic ulcer disease, such as: synthesis and release of prostaglandins, mucus and bicarbonate secretions, and the luminal hydrophobic layer. Both the dictum "no acid-no ulcer" and the coroliary "normal healing-no ulcer" seems to be valid. Correction of a possible deficiency in mucosal defense/resistance may be a useful and practical principle is management of patients with peptic ulcer disease.

摘要

消化性溃疡是一种异质性的多因素疾病。胃酸/胃蛋白酶的分泌是胃十二指肠消化性溃疡形成的一个关键促成因素。该疾病的治疗大多基于这一原则。仅仅存在侵袭性因素胃酸/胃蛋白酶不足以解释消化性溃疡的形成。黏膜防御(抵抗力)是该疾病发病机制中另一个关键因素。在消化性溃疡病患者中发现了一些胃十二指肠防御机制的缺陷,如:前列腺素的合成与释放、黏液和碳酸氢盐分泌以及腔内疏水层。“无酸无溃疡”这一格言以及其推论“正常愈合无溃疡”似乎都是正确的。纠正黏膜防御/抵抗力可能存在的缺陷可能是治疗消化性溃疡病患者的一个有用且实用的原则。

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