A concept of the etiology of gastric and duodenal ulcers.
A concept of the etiology of gastric and duodenal ulcers.
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胃和十二指肠溃疡病因学的概念。
DOI：
10.1016/s0016-5085(56)80128-5
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发表时间：
1956
期刊：
影响因子：
--
通讯作者：
L. Dragstedt
中科院分区：
文献类型：
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作者：
L. Dragstedt
最近在实验室和临床上的研究已经允许一个新的概念，胃和十二指肠溃疡的病因，似乎有助于解释这些病变的一些差异，特别是在他们的反应手术治疗。这种疾病通常被称为消化性溃疡，因为它被认为是由胃内容物的腐蚀或消化作用以某种方式引起的。病变仅发生在暴露于胃液的粘膜中，这是支持这一观点的有力证据，并且对低等动物进行的大量实验已经确定了这样的事实，即纯胃底分泌物可以消化掉胃和肠的正常粘膜，产生一种非常类似于人类溃疡的缺陷。在正常情况下，胃壁不会被胃消化破坏，但是，如果粘膜的抵抗力保持正常，则粘膜的消化和溃疡的形成可能是由于局部区域对胃内容物的消化作用的抵抗力降低，或者是由于胃内容物的腐蚀性增加。如果要根据消化性消化来解释溃疡，那么正常人的胃和十二指肠粘膜未能被消化掉，似乎需要局部抵抗力下降的假设。这一要求自然导致了这样的观点，即溃疡是由于血管损伤、保护性粘液缺乏、局部过敏、细胞缺氧或其他因素引起的粘膜抵抗力的局部降低。十二指肠溃疡局部切除后溃疡迅速复发，这使人们对局部抵抗力下降是该病的致病因素这一观点产生了严重怀疑，对切除的胃进行仔细检查也通常未能发现血管病理学的证据。等式的另一边是更有希望的，有很多证据表明，溃疡患者胃内容物的腐蚀性和消化性比正常人大得多。腐蚀性道具-
Recent studies in the laboratory and the clinic have permitted a new concept of the etiology of gastric and duodenal ulcers that appears to be helpful in explaining some of the differences in these lesions, particularly in their response to surgical treatment. The disease is commonly termed peptic ulcer for it is believed to be caused in some way by the corrosive or digestive action of the gastric content. The occurrence of the lesions only in mucous membrane that is exposed to gastric juice is strong evidence in favor of this opinion, and a large variety of experiments on lower animals has established the fact that the pure fundic secretion can digest away the normal mucosa of the stomach and intestines, producing a defect that closely resembles the ulcer seen in man.Under normal conditions the wall of the stomach is not damaged by gastric digestion, but it appears possible that digestion of the mucous membrane with ulcer formation might result either from a decrease in the resistance of a local area to the digestive action of the gastric content or from an increase in the corrosive properties of the gastric content, assuming that the resistance of the mucous membrane remains normal. The failure of the gastric and duodenal mucosa to be digested away in normal individuals appeared to demand the postulate of a local decrease in resistance if ulceration was to be accounted for on the basis of peptic digestion. This requirement leads naturally to the view that ulcers are due to a local decrease in the resistance of the mucosa brought about by vascular impairment, deficiency of protective mucus, local allergy, anoxia of the cells or to other factors. The prompt recurrence of ulceration after the local excision of duodenal ulcers casts grave doubt on this view of a local decrease in resistance as being the causative factor in the disease, and careful examination of resected stomachs has also usually failed to reveal evidence of vascular pathology. The other side of the equation is more promising, and there is much to suggest that in ulcer patients the corrosive and digestive properties of the gastric content are much greater than in normal people. The corrosive prop-