Dr. Qaadri

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Acid Reflux and Ulcers

By Dr. Shafiq Qaadri, MD

How common are ulcers in the Canadian population?
We do not have exact numbers, but figures from the United States suggest the lifetime incidence of peptic ulcer disease is about 10 percent.

Are ulcers part of the continuum of heartburn, acid reflux, esophagitis, or are ulcers distinct?
They are quite often distinct. Generally, ulcers are lesions in the stomach or duodenum, but they are acid-related.

Do stress, alcohol, coffee, and going on an empty stomach all day—do these cause ulcers?
Stress and coffee may be aggravating factors, but none of these really have been major causes, even though they may result in heartburn.

What is the official story on Helicobacter pylori—is it a pathogen or a normal commensual. Is it supposed to be treated or not?
Individuals with H. pylori have a higher incidence of developing peptic ulcer disease. Without H. pylori, unless someone is taking a nonsteroidal anti-inflammatory, it is very rare to get an ulcer…In fact, H. pylori is the commonest cause of peptic ulcer disease other than nonsteroidal anti-inflammatory medications.

What precisely is the mechanism of NSAID-induced ulcers? Are NSAIDS direct irritants, or is it a prostaglandin effect?
Consider aspirin. Aspirin plays a dual role in the causation of ulcers. First, there is direct injury to stomach mucosa. Aspirin also inhibits prostaglandins in the stomach, which is one of the important protective mechanisms.

If you think about the stomach itself, there is always acid present. What prevents the development of ulcers is the bicarbonate and mucus layers—these are both produced in response to prostaglandins.

How much more ulcerogenic is plain aspirin compared to EC ASA, enteric-coated aspirin?
We see many ulcer patients who were taking enteric-coated aspirin. The enteric coating prevents the medication from dissolving in the stomach. But once it passes the stomach, reaching the duodenum, it does dissolve, potentially causing an ulcer.

The enteric coating may be protective to the stomach. But there is also a systemic effect. Even if you took aspirin intravenously, entirely bypassing the stomach, you would still inhibit the prostaglandin-mediated protection.

Are you seeing an increased incidence of bleeding ulcers given that family doctors widely prescribe coated aspirin for cardiac prophylaxis?
No, we do not see an increased burden. Most of the time 81 mg of aspirin is used, a very small dose. While even this small dose can lead to stomach damage, it is not as problematic as a higher dose.
The number of people who develop ulcers continues to be about 3 to 10 percent of the population.

Would you say that NSAIDs are overused in Canada?
A lot of nonsteroidal anti-inflammatories are prescribed more often than we would like them to be used. Let’s say you are playing hockey, you fall or get hit with a puck. You see your family doctor. Quite often you are prescribed an anti-inflammatory. Yet basic analgesics like acetaminophen are quite effective, and you didn’t need the anti-inflammatory effect.

On the other hand, if you have an inflammatory disease like rheumatoid arthritis, you need an anti-inflammatory medication.

How does age impact ulcer risk?
The age of 60 is a risk factor, especially with multiple medical conditions, which usually leads to taking multiple medications.

Does an NSAID-induced ulcer stay silent, lead to an overwhelming bleed, or just a smallish bleed that comes to attention? Is there any way to predict this?
Thirty percent of people with an ulcer do not even know they have it. These patients present with black stools, having lost blood; some even present to the E.R. in shock.

The other two thirds of patients may have minimal symptoms—perhaps nausea, maybe epigastric pain, or feeling unwell. So the concern, of course, is that 30 percent of patients have no symptoms.

Could you summarize our understanding of the COX2 inhibitors? Were these kinder and gentler on the GI tract? How has their withdrawal impacted ulcer treatment?
The COX2 inhibitors caused concern with the increased incidence of cardiovascular disease such as myocardial infarction. That was the negative.

What COX2 inhibitors have done is decreased the incidence of bleeding peptic ulcers by about half—not totally, but by about half. We still see people who are taking COX2 inhibitors who bleed, so there is not a full gastric protective effect.

The second major problem is the combination of COX2 inhibitors with aspirin, especially in elderly patients. The problem is that if you take a COX2 inhibitor, as well as baby aspirin, you nullify the protective effect of the COX2. This leads to a risk of bleeding that is no different than if you are taking higher-dose aspirin.

How do you counsel patients who actually demand generic ranitidine or famotidine, or who self-treat ulcers with over-the-counter medications?
One of the concerns with these medications is this: if you have no symptoms taking H2 receptor-blockers does not mean your ulcer has been healed. You may not feel it, but ulcers can still be present, leading to complications such as bleeding or perforation.

As well, over-the-counter medications are often taken only for short periods, just for symptomatic relief, maybe for a few days or intermittently. But ulcers take much longer to heal.

How sensitive is gastroscopy? Why do patients with significant longterm symptoms often have normal endoscopies?
Gastroscopy is the goal standard for finding ulcers. If I do perform a gastroscopy and I do not find an ulcer, it is very unlikely that the patient has an ulcer. That is number one.
Number two, there is a condition that what we call non-ulcer dyspepsia—you get symptoms of an ulcer but you do not have an ulcer.

A lot of individuals who are taking NSAIDs may suffer from this condition—they do not have an ulcer. So it is not uncommon to have a lot of patients who have symptoms highly suggestive of an ulcer, yet you find nothing on endoscopy.

What is the pathophysiology of non-ulcer dyspepsia?
An answer to that question would lead to a Nobel Prize. Nobody knows precisely. For example, H. pylori was thought to be a major factor in this condition. Yet even eliminating the Helicobacter did not remove symptoms.

How much stronger in terms of acid reduction are the PPIs compared to say H2 blockers, or even a Maalox tablet?
It’s the difference between a single bullet versus a machine-gun. There is a big difference. The acid reduction that you get with a PPI you can rarely ever get with an H2 receptor antagonist…A PPI blocks acid production almost totally, not 100 percent, but far more than with an H2 receptor antagonist.

What are the ideal qualities of a PPI and what should we look for?
All the PPIs available are quite effective for acid reduction, and they are similarly effective. Some claim to be more protective against NSAID-induced ulcers than others, but we are not totally clear about this.
The indication for a PPI, for example, in patients who take NSAIDs can be different. For example, some manufacturers say that their drugs work within 24 hours, 36 hours, or 48 hours. But within about 3 to 5 days, most PPIs are the same.

However, we do note that some people may respond to one PPI better than another, and the reason for this is not clear.

What is the difference between symptom relief and tissue-healing? Is there that great a separation between the two?
Esophagitis is a better example than peptic ulcer disease. The patients with esophagitis get burning, pain with swallowing, and discomfort every time they eat. They start taking a PPI and feel very well. Yet quite often when we endoscope these patients, we find severe esophagitis. Similarly, they may take H2 receptor antagonists like Zantac and feel good. Yet when we look inside they have inflammation.

So there is often no relationship between symptoms and healing. Just feeling better may not be enough.

There is a recommendation that if an arthritis patient is going to be regularly using an NSAID, then they should be on a PPI such as Prevacid as prophylaxis from day one. Can you comment?
Well, this is a Pandora's box for which we do not have the exact answer. We do know that people who are taking NSAIDS but no PPI, are more likely to develop ulcers.

What is your own practice or clinical approach in terms of NSAID-induced ulcer disease? Should arthritis patients who regularly use NSAIDs be on a PPI to cut down their ulcer risk?
Essentially, it is an academic question, but this what we do clinically right now.

What should family doctors remember about the management of ulcer and acid-related diseases?
The message I would give is this: if a patient has an ulcer, try to heal it first. If a patient has an ulcer and is H. pylori positive, treat the H. pylori and then start other medications. If you need to use COX2 inhibitors, avoid using any aspirin or other nonsteroidal anti-inflammatory medication in combination. If the patient has a peptic ulcer disease history, use a PPI in combination with the NSAID as protection.

Dr. Shafiq Qaadri is a Toronto family physician and Continuing Medical Education lecturer. www.doctorQ.ca

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