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Why does acid secretion go up in duodenal ulcers but down in gastric ulcers?

Posted Jun 15 2010 8:05am



Q. I would be highly obliged if you can help me out on one thing. Being an average student, I refer to a textbook by a local author. He writes, “in gastric ulcer the value of basal acid output (BAO) and maximal acid output (MAO) are usually normal or slightly below normal” and “higher values are found in duodenal ulcer.” I am confused on both statements. Shouldn’t the level be higher in gastric ulcers? And if it’s low in gastric ulcer why is it higher in duodenal ulcer?

A. Great question! Before I get to the answer to your question, we’ll briefly review stomach anatomy and physiology, and then take a look at H. pylori infection. Then we’ll look at the effect of H. pylori on acid secretion in different types of gastritis, which will explain the mysterious statements in your book.

Stomach anatomy and physiology
The stomach consists of two distinct regions that differ morphologically and functionally. The proximal two thirds of the stomach is referred to as the body region; it contains acid-secreting parietal cells. The distal one third of the stomach is referred to as the antrum; it does not contain any acid-secreting cells but it does contain G cells, which release the hormone gastrin.

Acid secretion is increased whenever you think of, see, smell or taste food. This acid secretion is regulated by gastrin. When you eat protein, the G cells in the antrum release gastrin, which circulates and causes the body region of the stomach to secrete acid (it actually does this by stimulating release of histamine from enterochromaffin-like (ECL) cells that then activates the H2 receptors on the acid producing parietal cells, if you are into that kind of detail). Gastrin secretion itself is kept in check by the pH of the stomach; the lower the pH of the stomach, the less gastrin is secreted (good idea).

H. pylori
As you probably know, gastric ulcers (as well as gastritis, gastric cancer and a particular kind of lymphoma called mucosa-associated lymphoid tissue – MALT – lymphoma) are caused by H. pylori infection. H. pylori causes damage by eliciting a strong, tissue-damaging inflammatory response in the infected tissue. Weird: everyone used to think ulcers were caused by high acid levels, but it turns out they’re caused by the host’s own inflammatory response.

Anyway, for H. pylori to live in the naturally highly-acidic stomach, it has to have some way to combat the acid. It does this with a special enzyme called urease, which converts urea (which is sitting around in the stomach) to carbon dioxide and ammonia. Ammonia raises the pH (lowers the acidity), making the stomach just hospitable enough for H. pylori to take up residence.

So you’d think that if you have H. pylori infection (which all people with ulcers do), you’d automatically have an increased gastric pH. It turns out that it’s not that simple. Depending on the pattern of gastritis induced by H. pylori, gastric acid secretion can be increased, decreased, or unchanged!

Increased acid secretion
In patients with duodenal ulcers, H. pylori colonizes the entire stomach. However, the inflammation of the stomach mucosa is more marked in the distal (antral) region, with relative sparing of body (acid-secreting) region. This pattern results in increased gastrin release, which makes the acid secretion in the stomach go up. This is what the author of your book meant when he said that “higher [acid] values are found in duodenal ulcer.”

Decreased acid secretion
Patients with gastric ulcers usually have an underlying pangastritis (involving the whole stomach – body and antrum). In addition, in contrast to the gastritis in patients with duodenal ulcers, the gastritis in patients with gastric ulcers is usually atrophic (meaning that the mucosa is thinned and less capable of doing what it’s supposed to do). As a result, the body is less able to secrete acid (since the mucosa is atrophic), so the acid levels in the stomach go down. This is what the author meant when he said “in gastric ulcer, the value of BAO and MAO are normal or slightly below normal.”

Unchanged acid secretion
Most patients with H. pylori infection, however, do not have ulcers. These patients have a non-atrophic gastritis which involves both the antrum and the body. This pattern of gastritis results in no overall change in gastric acid secretion.

In real life, the most important thing to do in a patient with either type of ulcer is to give antibiotic therapy. You can bring down the level of acid all you want, but if you don’t get rid of H. pylori, the ulcer will just come back! If you want to read more on this, a good article is: McColl KE, El-Omar E, Gillen D. Helicobacter pylori gastritis and gastric physiology. Gastroenterology Clinics of North America 2000; 29(3):687-703.

The nice EM of H. pylori is from Wikimedia Commons: http://commons.wikimedia.org/wiki/File:Helicobacter_pylori,_Gastric_
Mucosa,_Giemsa_stain_(390307643).jpg

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