Some 40 years ago, one of my uncles had surgery for a gastric ulcer. When he visited us I found that his scar from that operation was not unlike mine from pyloric stenosis (PS) surgery when I was a newborn. But little did I think there might be much more of a connection.
In the first sections of his part of the book to which I devoted last week’s post, and which Dr Ian Rogers and I have co-written, Ian lays the foundations for understanding the link between infant PS and a duodenal ulcer. Here is the first part of my summary of Dr Rogers’ comprehensive report – for the medically untrained (and isn’t that most of us reading this?) And do get a copy of our book if you’re interested in more details.
This is information I want everybody with an interest in PS to have!
Personal history, gastrin and acid
When Scottish medical student Ian Rogers graduated and started his work in 1970, duodenal ulcers (DU) were common and dangerous, and related research was prominent. At that time it had become well-known that the ulcers were caused by over-acidity in the stomach which was triggered by the hormone gastrin, the release of which was in turn caused by food reducing the acidity of the stomach. When acidity rises, the release of gastrin stops, and thus balance is maintained.
It was also known that DU patients produced more gastrin than usual after a meal (especially when the gastric acid had scarred the stomach’s outlet or pyloric passage), that males produced more gastrin than females, and that 5 male DU patients presented for every one female. It was found that the vagus nerve (the hunger messenger) also raised gastrin secretion. In those days the role of Helicobacter pylori (or H. pylori) bacteria and the possibility of antacid treatment were unrecognised, and surgery was the accepted answer to a DU: the vagus nerve was immobilised and/or the lower part of the stomach was removed.
Because the drug atropine blocks the vagus nerve it was used to test whether a vagotomy would be effective in reducing stomach acidity.
All the above classical features of a DU are similar to those of infant pyloric stenosis (PS), including what was already described in 1921 as the PS baby’s “voracious appetite”: being ravenously hungry immediately after vomiting (not normal behaviour after bringing up a meal!).
The important role of the bacterium Helicobacter pylori was not yet recognised in 1970: it has infected 80% of DU patients, creating an alkaline environment in the lower stomach to protect itself from acid and also stimulating acidity.
Ian Rogers lists 11 telling clues about babies who present with PS, and yet the cause of the condition remains (it is claimed by most) unknown today.
In 1921 Dr John Thompson reviewed what was then known and done about PS – the details are most significant but too many to detail here. Most importantly he (1) identified 3 common levels of PS, the acute, the ordinary and the very mild, and (2) reported on how PS could often be managed medically (and without surgery).
Dr Thompson also mentioned two theories about the cause of PS: (1) that is was caused by an abnormality of the pylorus, and (2) that the pylorus was being stimulated to malfunction. He favoured the 2nd theory, citing the work of an 18th century anatomist on what causes muscles to hypertrophy (over develop).
Next: My journey
Whenever I asked my parents about the weird marks on my stomach their answer was limited to “A doctor did that because you were a little bit sick when you were a baby”. Yikes, I hoped I wouldn’t get “a little bit sick” ever again. So as a child and ever since, I’ve been in the hunt for a better answer. But apart from one-paragraph entries about pyloric stenosis in encyclopedias and medical handbooks, there was nothing. So in recent years I’ve been passing on what I’ve learnt about PS issues by blogging (“Surviving Infant Surgery”). And when the British professor of pediatric surgery Dr Ian M Rogers invited me to contribute “My Story” to a small book he was publishing about his conclusion after a lifetime of work – that all the symptoms of PS agree with it being caused by over-production by mother and baby of a gastric hormone, the result was: “The consequence and cause of infant pyloric stenosis: two personal stories”. I hope that this modest book will go viral and make it onto many bookshop, library, and doctors’ shelves. Interested PSers, parents and others can find out more about the book by googling for the title – and get a copy if you have a spare €24 for a medically priced publication – lol. Anything I get will go to medical research into the diseases of infancy.