Finding the cause of infant pyloric stenosis

In the previous post I passed on something of the first part of a book in which the retired pediatric surgeon and emeritus professor Ian Rogers reviews what he has learnt about infant pyloric stenosis (“PS”) over a lifetime of interest and work with this condition.  This book, The consequence and cause of pyloric stenosis of infancy: Two personal stories, was a joint effort: in the first 20 pages I told something of “My Story”.

Communication04Dr Rogers continues his account, touching on a large number of medical facts and research findings that together have shaped his well-based and considered understanding of what causes PS.  To me they read a bit like a criminal case: What can we say immediately? Where and what are the clues? How do we put it all together to make a case that will stick?

Those with medical training and knowledge should refer to the book, as here I can only glean some of its main lines and those that can be explained in brief to the interested general reader.

Under the heading, My journey, Prof. Ian Rogers tells how his journey started when he found a 1941 article which documented the gastric acidity in newborn breast-fed babies.  It must be remembered that gastrin, the hormone that controls stomach acidity, was not identified until many years later.

In 1941 a researcher (Dr R A Miller) reported finding that babies’ stomach acidity was neutral at birth, probably  due to the swallowing of alkaline amniotic fluid, then rose very rapidly to an extreme level, and returned to normal levels after some 10 days, and the difference between minimum and maximum acidity also fell: clearly the baby’s body was taking control.  Miller concluded that the mother transmits a chemical to the infant to explain this pattern.

It is known that when birth is induced with the drug syntocinon the baby’s gastrin levels are not those of the spontaneously born child, probably because syntocinon affects the gastrin transfer.  It is now known that the mother’s placenta has a high level of gastrin at birth, and that rising gastrin levels parallel rising stomach acidity in babies from Day 4.

Ian Rogers then mentions several more points made by Dr Miller –

  • When acid enters the duodenum the pylorus contracts; antacid medication is therefore effective in treating some cases of adult PS.
  • When food enters the stomach several stages of relaxation occur, involving different parts of the stomach, various digestive movements, and preventing excessive discomfort.  The contraction and relaxation of the pylorus are integrated with this complex feeding process.
  • Repeated feeding results in repeated pyloric contraction, and this is amplified not only by hyperacidity but also by incompletely digested food and a stressed mother repeatedly feeding a desperately hungry baby.
  • More specifically in babies, milk accumulating behind a closed outlet increases alkalinity and the stretching of that part of the stomach, both triggering the release of gastrin and thus acid.  In addition to this, some people inherit their stomach walls secreting more acid than normal.  Dr Rogers proposes that it is the combination of high acid secretion, repeated pyloric contraction causing muscle over-work and over-development (hypertrophy) as well as further increasing gastrin levels, and too frequent feeding that together are the cause of PS.
  • When the pylorus of rats was artificially narrowed, it was found that the secretion of gastrin increased.

Dr Rogers then found the work of Dr John Dodge, who produced PS in 28% and gastric-duodenal ulcers in 16% of the puppies of 20 bitches injected with a synthetic form of gastrin.  It is known that gastrin crosses the canine placenta, increasing the gastrin level in her pups.

  • It is noted that the over-worked and over-developed pyloric muscle is also essential to PS: when it is divided it shrinks to its normal size, but when it is bypassed it does not.  But a working muscle does not usually over-develop: something else is causing this.
  • Cell studies of the pyloric tumour have confirmed that over-work causes the over-development of the pylorus of PS babies, and that no other abnormality causes the tumour.
  • Pregnant mothers and babies who take the macrolide antibiotic erythromycin see a 7-fold increase in the incidence of PS.  Macrolides increase the activity of the part of the stomach that is closest to the pylorus, as well as contracting the pylorus.
  • Another gastro-intestinal hormone, motilin, stimulates the emptying of the stomach.  It is believed to be linked with PS and may stimulate pyloric contraction; however the role of motilin is still incompletely understood.

Next post – some clinical aspects of pyloric stenosis

1 thought on “Finding the cause of infant pyloric stenosis

  1. Wendy

    This post really got me going! It underscored the reality that my pyloric stenosis was probably caused by my mother’s taking the drug erythromycin while pregnant with me. I can’t know for sure since Mom passed in 2007, but the fact that my dentist told me that the spots on my front teeth, and the discoloration of my teeth in general, was likely due to erythromycin is a huge clue. He’s the first dentist to mention this. My dentist growing up said that the spots were due to a lack of Vitamin C early on. I felt enormous rage reading your bullet point about erythromycin. I’ve known about this possibility years ago, but somehow I am just now really allowing myself to understand that this may have been the cause of my PS. In any case, back to the rest of your piece, thanks so much for deciphering Dr. Rogers’ work so that lay people can get the benefit. It is of enormous value. Thank you!


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