Rogers Ian Munro
Acta Paediatr. 2006 Feb;95(2):132-6. doi: 10.1080/08035250500431385.
Pyloric stenosis (PS) has no known cause. A testable theory of cause is proposed, based on the inheritance of a parietal cell mass (PCM) at the upper end of the normal range. It is proposed that, until 3-4 wk of age, the obligatory high fasting gastrins are at maximal levels and not able to be diminished by increasing antral acidity. Hence, rising acidity is not reduced by a lowered gastrin during this time, and very high acidity occurs.
Persisting duodenal hyperacidity is created by an inherited high PCM and loss of gastrin control. These two factors produce pyloric stenosis through work hypertrophy from repeated pyloric contraction in response to hyperacidity.
幽门狭窄(PS)的病因尚不清楚。基于正常范围上限的壁细胞量(PCM)的遗传,提出了一种可检验的病因理论。有人提出,在3 - 4周龄之前,空腹时胃泌素必然处于最高水平,且无法通过增加胃窦酸度而降低。因此,在此期间,酸度升高不会因胃泌素降低而降低,从而出现极高的酸度。
遗传性高PCM和胃泌素控制丧失导致十二指肠持续高酸度。这两个因素通过对高酸度的反复幽门收缩引起的工作性肥大导致幽门狭窄。