婴儿幽门狭窄的病因:原发性胃酸过多和生化联合

I. Rogers
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引用次数: 2

摘要

婴儿幽门狭窄(PS)的病因目前尚不清楚。一个理论的因果关系提出,这是一致的所有已知的临床特点,这种情况。这是基于这样的知识,即患有PS的婴儿分泌过多的酸,这早于PS的发展,是一种遗传的体质特征。由于在生命的最初几周内胃泌素和胃酸之间的负反馈暂时不敏感,这种酸度变得危险的高。正常酸度水平的正常婴儿也会在那个时候经历酸度峰值,但并不危险。酸进入十二指肠引起幽门括约肌收缩。胃酸过多自然会导致幽门括约肌反复收缩,从而导致括约肌和PS的工作性肥大。如果患有PS的婴儿存活超过大约6周,胃泌素和胃酸之间成熟的负反馈将确保危险的胃酸过多得到控制。因此,随着时间的推移,生理上可以控制高酸性。当伴有与年龄相关的幽门管控制扩宽时,长期治愈是自然的结果。这一理论令人满意地解释了这种情况的所有已知的和迄今尚未解释的特征。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Cause of Pyloric Stenosis of Infancy: Primary Hyperacidity and Biochemistry Combined
Abstract The cause of pyloric stenosis (PS) of infancy is at present unknown. A theory of causation is proposed, which is consistent with all the known clinical features of this condition. It is based on the knowledge that babies with PS are hypersecretors of acid, which predates the development of PS and is an inherited constitutional feature. This acidity becomes dangerously high due to a temporary insensitivity of the negative feedback between gastrin and gastric acidy within the first few weeks of life. Normal babies with normal acidity levels will also experience peak acidity at that time but not dangerously so. Acid entering the duodenum causes contraction of the pyloric sphincter. Hyperacidity will naturally lead to repeated pyloric sphincter contractions with resulting work hypertrophy of the sphincter and PS. Should the baby with PS survive beyond the age of approximately 6 weeks, the matured negative feedback between gastrin and acid will ensure that dangerous hyperacidity is kept in check. Thus, the passage of time allows the physiological control of hyperacidity. When associated with an age-related widening of the pyloric canal control, a long-term cure is the natural outcome. This theory explains satisfactorily all the known and hitherto unexplained features of this condition.
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