Is this the link between PPIs and OAC? A patient's perspective.

A tale of tribulation, victory and eventual explanation.

Late in 2007 I was diagnosed with a hiatal hernia, long segment Barrett's oesophagus and severe ulceration above the Barrett's. I was put on 40mg omeprazole uid. 5 weeks later at a second endoscopy the consultant asked me what medication I was on and in response said "40mg isn't enough. That lasts about 20 hours - you need to take two of those a day."

So I learnt that PPI dosage was a bit suck-it-and-see. I experimented. I found that 40mg did indeed last "about 20 hours". I halved the dose - and learnt about the effective half life of omeprazole - further dosage experiments showed me that my effective half-life at that time was around 2 1/3 hours. Somewhat longer than the generally stated half-life.

But what disturbed me most during these experiments was the sequence of symptoms that developed as a dose wore off.

The bile I tasted was very concerning. I had previously only had bile after heavy vomiting. It was not normal. But trying to discuss it with my consultant, I got the brush-off with comments such as "I'm surprised you can tell the difference." or "We can't control bile."

But my experiments with dosage and half-life continued:

Naturally I wondered how long 5mg would last. Most PPIs being granules in a gelatine capsule, the experiments were easy to do - even if the results were difficult to interpret! for by this time, after 2 ½ years on PPIs, I had lost several Kg (not due to the PPIs!) and it wasn't so easy to test the taste of the refluxate!

I thought 5mg worked. But I started getting a series of bad nocturnal bile reflux events: 37 days, 46, 53, 90 and 108 days after changing to 5mg doses. These were extremely unpleasant I would far, far prefer an acid reflux! I did not then realise the implications!

Then in November 2011 I had ambulatory pH monitoring. My dosage clearly was not working. I fiddled about with the dosage. My notes say 10mg lasted 9 hours - initially the figure was 15! But subjective measurement was difficult. Reluctantly I went back to 20mg doses.

One day I decided to test exactly how long a 20mg dose lasted. First, experiment to see what symptoms I actually got when the dose started to wear off, so that I would know what to look for when I started timing.

The first symptom that the dose was wearing off was that the almost permanent tickly cough I had abated!

I never took another PPI so the experiment was aborted, But I had the distinct impression that a measure of drug tolerance had set in. Tolerance to PPIs does not seem to be mentioned anywhere I can find in the on-line literature, but the fact that the liver learns to faster metabolise xenotoxins over time indicates that tolerance could be a real problem.

Oops! Again, just as I has experienced before when reducing to 5mg doses, I experienced a series of severe, nocturnal bile reflux events. 49, 59 and 104 days after withdrawal. So exactly how many of the reported acid rebound events are, in fact, bile. The symptoms are apparently the same - unless you regurgitate it when, brother - do you know the difference! Just for this effect alone I would make all doctors take a course in PPIs! Believe me, such serious bile reflux simply is not funny!

So I was left with a strong need to explain what had happened. I spent hours searching the internet. Eventually I found two papers:

Here was real scientific proof that whatever had been happening to me was not a unique quirk in my own physiology, but was normal. Although the second test was on a small sample of only 19, 15 had showed the effect. 80% of a small sample may be a small group but it shows a very high probability. In my case a near certainty as it explained my symptoms!

So what happens if the gall bladder cannot properly release bile when it should under the influence of CCK? I see 3 possibilities: it forms gallstones (and yes, I have been in contact with people who blame their cholecysectomies on PPIs), or it leaks into the duodenum when it should not. Or thirdly, the bile goes into hyperspace. If any doctor believes that - can I consult you about fairies?

Surely if bile is leaking into the duodenum when the pylorus is relaxed -that is how it enters the stomach. The pyloric sphincter is active and has evolved to control a one-way flow of chyme. Bile is released into that chyme. If bile is released when the pyloric sphincter is not passing chyme - then there is your bile reflux.

So I find the case very nearly proven that PPIs, far from stopping OAC, are in fact causing it. The statistics on Barrett's, OAC and PPI useage very strongly support this.

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Page first published: Sunday the 1st of January, 2017
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