In the previous two posts I have “translated” several parts of the larger share of the small book I have co-written with the emeritus Prof. Dr Ian Rogers, titled The consequence and cause of pyloric stenosis of infancy: Two personal stories. My co-author has addressed his section to the medical profession but gives much information that is of no small interest to many of us who have been touched by infant pyloric stenosis (“PS”). It has certainly helped me to understand much more of the what, how and why of this rather enigmatic condition, something I have longed for ever since I became aware of the strange markings on my belly!
In this post I want to revisit (in more detail than my initial post) the first pages of Dr Rogers’ section, in which he writes about the function of the hormone gastrin in digestion. He mentions that the Glasgow academics under whom he trained specialised in the physiology (working) of the stomach and intestines, clearly because duodenal ulcers were a major cause of illness at the time.
When Ian Rogers finished his surgical training in the early 1970s, it was known that –
- hyper- (or over-) acidity could be constitutional or acquired, and was the major cause of duodenal ulcers;
- hydrochloric acid release is triggered by the vagus nerve and/or the hormone gastrin;
- the upper (proximal or first) part of the stomach secretes the hydrochloric acid;
- gastrin occurs in the mucosa (lining) of the distal (or end) part of the stomach;
- food in the stomach causes chemical change which releases gastrin into the bloodstream and this as well as stomach activity triggers the release of acid into the stomach contents;
- acid is essential to digestion as well as sterilising food;
- normally, gastrin controls acidity, not allowing its level to become too high or low;
- duodenal ulcers were thought to be caused by hyper-acidity, most common in anxious men; often this could be controlled by cutting the vagus nerve, and otherwise by a gastro-enterostomy (which involves more radical surgery).
It has only become known in more recent decades that Helicobacter pylori bacteria are also involved in hyper-acidity and cause some 80% of duodenal ulcers, and also that antibiotic treatment and/or suppression of vagus nerve activity with atropine could control acidity, almost eliminating the need for surgery to relieve gastric ulcers.
Although both men and women have rates of H. pylori infection that rise during their lives and are almost similar at age 70, the acid-secreting stomach cells are more numerous in adult men than women.
Thus there are some interesting parallels between patients with PS of infancy and those with gastric ulcers in adulthood –
- a 5:1 male preponderance;
- high acidity;
- a good appetite;
- other family members affected.
The above facts represent what was commonly known in the early 1970s when Ian Rogers completed his surgical training in London and returned to Glasgow.
In later pages Dr Rogers continues by describing the “clinical (observable) signs” of PS – as they give many clues to its cause.
- it arises very early in a baby’s life;
- it affects many more boys than girls;
- it cures itself in time if the patient can be treated medically;
- it can have a strong family link;
- if the pyloric tumour is split surgically the swelling soon disappears;
- the swelling does not disappear if the blockage is surgically by-passed;
- the high acidity in the stomach cannot be explained as accumulation due to the pylorus being closed;
- survivors continue to secrete higher than usual acid;
- PS babies have a ravenous appetite;
- they are often first-born babies;
- some PS babies are found to have a superficial duodenal ulcer.
Despite these clear pointers, the medical community still finds the cause of PS a mystery more than 120 years after it was first fully described.
Dr Rogers then refers to the significant 1921 paper of the Scottish Dr John Thompson who observed that –
- the “pyloric tumour” is in fact over-developed muscle;
- PS is self-limiting (see #3 above);
- PS can be managed with small feeds, daily stomach wash-outs, and if feeding has been unsuitable, with IV feeding;
- there are 3 kinds of PS: the acute (with sudden and violent symptoms), ordinary, and very mild.
Thompson accepted the theory that PS is caused by a functional abnormality, referring to an 18th century anatomist who found that all muscles develop with use, but involuntary muscles (ones like the pylorus over which we have no control) more than others. However, this theory was not further explored, even though PS occurs also in other mammals.
Dr Rogers has now laid the foundations for his conclusions about the cause of PS, and in the next post we’ll see how what he has been mentioned in these three posts applies to gastrin, hyper-acidity and PS in the newborn.