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Quote gladiolus Replybullet Topic: Endoscopy every 3 years after Barretts diagnosis?
    Posted: 19 Jun 2018 at 6:17pm
I was diagnosed with Barrett's in November of 2016. It is a small segment (under 1cm) in my lower oesophagus. After I had the endoscopy, one of the nurses said I would be sent for another endoscopy in 3 years. I am wondering if it's normal to have an endoscopy 3 years later after diagnosis. It seems like a long time considering I have Barrett's cells just sitting there. I have read that in some countries, they do ablation as soon as possible after Barrett's is diagnosed. On the NHS it seems the standard practice is to only observe and do endoscopies until further changes are found. I am currently on 150mg Ranitidine twice a day. I was previously on Omeprazole. I do not take anything else. I also try not to eat within 2 hours of going to sleep as that seems to worsen my gastric reflux. Can anyone reassure me please? I worry about my Barrett's a lot.
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Quote chrisrob Replybullet Posted: Yesterday at 10:36am
Hi Glad,

Barrett's is actually very common. There could be as many as 3 million with it in the K though fewer than 100,000 may know. (Indeed in a discussion I read recently, a top international gastroenterologist suggested everyone has a few Barrett's cells dotted throughout their oesophagus ready to proliferate if required.) Barrett's is nothing to be frightened of and those of us identified with t are the lucky ones as we'll receive the best medication and surveillance to look for any possibility of progression towards cancer whence it can be eradicated.

The UK guidelines are roughly in alignment with the guidelines used elsewhere in the world. The UK, US, EU and Aus guidelines are linked to on this page of the Barrett's UK ( site.

This flow chart shows the scoping recommendation:

(You will find a better image on this page of Barrett's Wessex website.)

Frequency of surveillance scoping is an oft discussed issue and is dependent on so many different things.
Since 98% of surveillance scopes show no significant change, the argument is, we scope too much - and there is, of course, risk always associated in scoping. (Approx 1 in 2000 will cause damage to the oesophagus.)

It also depends the type and size of the Barrett's and other factors like the patient's age, sex, body build, familial history etc.

In UK and many other parts of the world, Barrett's is defined as being columnar cells lining the oesophagus. (Think of it as armour plating produced by the body as a protection against acid erosion.) Columnar cells are typically gastric (or cardial) in nature or intestinal. (The difference being whether the existence of "goblet cells" is detected between the columna cells.)
So in UK, Barrett's may be "gastric metaplasia" or "intestinal metaplasia".
In US, gastric metaplasia is not recognised as Barrett's, their definition requires the existence of intestinal metaplasia.

Whereas we do not know the role of goblet cells, and intestinal metaplasia carries a higher risk of progression than gastric, it is always possible goblet cells may exist undetected within gastric columnar cells.

I have had my Barrett's (presently defined as c4m6 = a 4 cm ring with tongues extending to 6 cm) for at least 24 years and probably much longer and it hasn't changed in that time.

We really need to identify those who are most at risk to enable surveillance to be better targetted.

Ablation is not recommended unless dysplastc changes are ever seen. The procedure can cause damage to the oesohagus. (One London professor who is considered something of an expert at Radio Frequency Ablation, confided in me once, he had had two perforations in a year.)
Ablation will get rid of the Barrett's cells but, having developed Barrett's previously, you would probably develop it again if the causes remained - not just reflux of acid and bile but genetic propensity, body build, lifestyle and other factors we have yet to identify. So post ablation, patients still require surveillance scoping and acid suppressant medication regimen.

You ae on a total of 300mg of a Histamine H2 receptor antagonist that stops some of the receptors for histamine signals from the brain to the stomach to produce acid. These will result in a slightly less acid being available to cause damage if it refluxes. The other, more powerful acid suppressants are the Proton Pump Inhibitors that prevent some of the cells lining the stomach becoming "proton pumps" that produce acid.

Research has confirmed that acid suppressants will reduce the risk of progression of Barrett's towards cancer.

Please visit the website of the free, fully researched and referenced encyclopaedia in layman's language, "Down With Acid" ( whish you will find contains most of what you may wish to know about acid and reflux, complicationa and management. If you wish to message me with a postal address, I can send you a printed copy.

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