Barrett's Oesophagus
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Quote Caoimhinn Replybullet Topic: B.E...or not B.E.
    Posted: 18 Jan 2020 at 6:59am
I’m in my mid 30s, and have had reflux for nearly ten years. I sought treatment after I had some severe difficulty swallowing. My GI dilated my esophagus and put me on pantoprazole 40mg daily, and nizatidine 300mg before bed. I go for annual EGDs. I’ve had a few linear ulcers, all of which have healed—but inflammation and esophagitis is invariably a finding on my procedure reports.

A few months ago, my doctor notes that endoscopically, he had observed Barrett’s, but that the biopsies were negative for IM. If you haven’t ascertained by my spelling, I am in the US.

I read his procedure notes, and he quite conclusively wrote “Barrett’s Esophagus” as an impression, and noted seeing “mucosal tongues”. No dimensions, locations, or other information was given. He noted that he took biopsies “from the appropriate quadrants”. He took three from the GE junction, as noted on the pathology report. They were each negative for IM.

Still, he has performed my endoscopies for years. He’s never observed an abnormal z-line in the past. So I assume he saw something clearly enough to conclude it was BE. I’ve had the endoscopies performed on occasion by other physicians depending on where I was living, including in Ireland. This is the first I’ve had BE noted.

He assured me that there was no need for concern, based on the pathology.

I was still concerned, and had an EGD repeated in a Russian clinic while visiting my wife’s family this past week. I’ll quickly note that, notwithstanding the higher cost, I prefer the US approach of sedation. I didn’t inform the endoscopist that I had a suspected Dx of Barrett’s, but indicated that I had a history of ulcers around the GEJ.

He performed the gastroscopy, while I watched the monitor, fully conscious. He didn’t observe anything suspicious. He added that there wasn’t anything remotely suspicious for him to biopsy.

Following the endoscopy, I met with the gastroenterologist, who read the endoscopy notes and provided general lifestyle adjustments to make.

She strongly disapproved of the pantoprazole dose and suggested that I stop in favor of a one month course of a newer PPI that I don’t believe is available in the US.

Any thoughts on what may have caused the original US GI’s visualization of BE? I’ll add another factor: years ago, I had been Dx with a small hiatal hernia during a barium swallow fluoroscopy. It was never noted on an endoscopy. I always wondered what happened to it.

Also, in looking at the video of my Russian EGD, there is the strong appearance of what looks like Schatzki’s Ring before the GEJ. In nearly ten years, nobody has mentioned this.

Finally, what are the thoughts on the Russian doctor’s aversion to pantoprazole? She seemed to think that an otherwise healthy person should not be managing acid with medication, but rather only through lifestyle. Based on my understanding of GERD, her faith in the efficacy of dietary changes seems misplaced...but what do I know?
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Quote chrisrob Replybullet Posted: 18 Jan 2020 at 2:33pm
Hi Caoimhinn and welcome to the forum.

Whether you have Barrett's or not may depend upon the definition pertaining to where you were scoped.
In US, Barrett's is defined as Intestinal Metaplasia, ie the presence of goblet cells must be found on histology. In many countries, eg UK, Barrett's is defined as columnar cells lining the mucosa.
I think the difference is, in US, they wish to exclude stomach cells that may have accidentally been harvested by biopsies taken below the z-line. In UK, they say although goblet cells are not found, they may still be there, so UK definition permits gastric cardia metaplasia (eg resembling stomach lining) to be counted as Barrett's as well.
The role of goblet cells isn't known and studies have shown, although reduced likelihood, gastric metaplasia may also mutate to oesophageal adenocarcinoma.
This image from Johns Hopkins shows what histopathologists look for:

But Barrett's has to be confirmed by histopathology. Although visually Barrett's cells may appear to be present, they may be confused with oesophagitis(usually redder and possibly bloody) or, commonly, hiatus hernia - which would, of course, be lined with columnar gastric cells.

I don't know why the Russian GI is against pantoprazole. Too many with "just ordinary" acid reflux are taking PPI medication inappropriately as an "easy option" whilst ignoring lifestyle modification and other ideas. Those of us with Barrett's, however, are advised to take them daily for life.
The drug he may have been referring to could possibly be Vonoprazan, a new potassium-competitive acid blocker introduced in Japan a few years ago. I don't think it is (yet) available in US or UK.
A review published in the Journal of Gastroenterology & Hepatology last August,
Vonoprazan versus proton-pump inhibitors for healing gastroesophageal reflux disease: A systematic review concluded: "This analysis shows that the GERD healing effect of vonoprazan is higher than that of rabeprazole (20 mg) but not higher than other PPIs. Subgroup analysis indicated that vonoprazan is more effective than most PPIs for patients with severe erosive esophagitis."
Although there are newer PPIs than pantoprazole, particularly esomprazole/Nexium or dexlansoprazole/Dexilant, they have been shown to be no better in reducing acid than the older drugs they are based on (omeprazole and lansoprazole) - just more expensive.

Regarding hiatus hernia. The majority are "sliding hernias" whereby part of the stomach has herniated into the thorax via the hiatus hole in the diaphragm. It is possible for the stomach to slide back into the abdomen. Hiatus hernia is what's the most frequently mistaken visually as Barrett's Oesophagus. Of course, biopsies from it would appear to show gastric metaplasia.
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Quote Caoimhinn Replybullet Posted: 19 Jan 2020 at 5:07pm

Thanks for yet another thoroughly detailed post. This was the first time I’ve seen a graphic of the histologic progression of Barrett’s. Very fascinating stuff.

The Russian GI was of the mindset that reflux could be competently managed exclusively through dietary changes and lifestyle modification. I’ve read many times on this forum (and, of course, on the Down with Acid materials), that for a number of physiological reasons, this is not a realistic expectation. If an anatomical defect, like a weak lower esophageal sphincter, permits stomach acid to enter the esophagus, no lifestyle modification can be curative absent surgical intervention. So, as you and others have said, PPIs will make the inevitable acid incursion less corrosive. The risks associated with long term PPI use appear to be overstated or are otherwise benign (fundic polyps).

I go for follow up with my US GI in about five months. I’ll raise the questions about a hiatal hernia. You mentioned that the biopsy of the columnar cells would appear to show gastric metaplasia. I wonder, however, if the US biopsy protocols would indicate gastric metaplasia at all, even if it were present, given that it is not relevant to the US definition of Barrett’s. The pathology report narrowly said “Negative for intestinal metaplasia”, which on its face doesn’t seem to preclude the presence of gastric cells.

In the end, whether I have Barrett’s or not is irrelevant from one perspective. Either I have it or I don’t—and if I don’t, I very well may do in the future. I go annually for follow up EGDs, which usually include dilation of the esophagus when the difficulty swallowing becomes more troublesome. At that interval, I’m well within the recommended surveillance schedule anyway. So, if IM is ever confirmed I’ll manage in accordance with the standard of care at the time and...will hope for the best!

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Quote Ulaman Replybullet Posted: 21 Jan 2020 at 9:38pm
Hi Caoimhinn. Im in a similar situation. They suspected I had BE, but the biopsies came back negative for any metaplasia.

I'm considering a repeat scope in a few years to rule out IM.
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