When I Escalated His GERD Treatment, My Patient Got Worse. Now I Know Why

Not all dyspepsia is due to acid excess or reflux

Pierre Patenaud had a long history of dyspepsia with fair control on 20 mg of omeprazole. A few months ago, he started getting worse. My first response was to check for changes in his lifestyle and increase his dose to 40 mg. When that didn’t work, I added famotidine 40 mg twice a day. He felt worse and even developed hoarseness. I prescribed sucralfate before meals and at bedtime and made a referral to one of our general surgeons for an upper endoscopy.

The other day I got a call from the surgeon.

“Mr. Patenaud’s endoscopy looked atrophic and I just got a call from the pathologist. The biopsies were negative for helicopabter pylori, but he’s got giardia in his stomach.”

“I’ve never heard of that”, I said, “and he hasn’t had any lower GI symptoms.”

My literature search yielded mostly old articles, like an Italian one from 1992 linking it to helicobacter pylori, a 1994 piece in the BMJ linking it to achlorhydria (which may be why Mr. Patenaud got worse with more acid suppression) and bile reflux (bile is alkaline). The most recent piece I read was from 2009 by the WHO, reporting Egyptian data on helicobacter pylori and giardia, which often coexist as they are transmitted in the same fashion between individuals.

The lesson here is: Not all dyspepsia is due to acid excess or reflux, or even bile reflux in and of itself. And the ones that are neither of those aren’t necessarily irritable bowel related “nonulcer dyspepsia” – a strong case for scoping and biopsying difficult dyspepsia.