Ulcer Treatment, Then and Now

How the Stomach Sets the Stage for Ulcer-Causing Bacteria

Zantac. Wikimedia Commons

Sufferers describe an ulcer as a burning, cramping, gnawing, or aching in the abdomen that comes in waves, for three to four days at a time, but may subside completely for weeks or months. Pain is worst before meals and at bedtime, when the stomach is usually empty. The ulcer itself is an open sore in the lining of the stomach (gastric ulcer) or in the upper part of the small intestine, or duodenum (duodenal ulcer).

Both types are also called peptic ulcers.

The Acidic Stomach: Setting the Stage for Ulcers

The stomach is the most acidic part of the body, setting the stage both for ulcer development and infection. Three types of cells pump out the ingredients of gastric juice: mucous-secreting cells, chief cells that release digestive enzymes, and parietal cells that produce hydrochloric acid. The mucous-secreting cells also produce histamine, which stimulates the parietal cells to release acid. The stomach needs the acid environment for the digestive enzyme pepsin to break down proteins in foods.

Acidity is measured using the pH scale. A neutral pH is neither acid nor base--it has a value of 7; acids are less than 7, and bases (also called alkaline substances) are greater than 7. Many body fluids, including blood, tears, pancreatic juice, and bile, are in the 7 to 8 pH range. Gastric juice, in contrast, has a pH of 1.6 to 1.8.

That's more acidic than lemon juice, cola drinks, and coffee. The environment in the small intestine is far less acidic than in the stomach, but because it receives the acidic mixture of semi-digested food from the stomach, it is prone to ulceration too.

The stomach's innermost lining, the mucosa, protects it from digesting itself.

The mucosa consists of lining cells, connective tissue, and muscle. An ulcer hurts when it penetrates the mucosa into the underlying submucosa, which is rich in nerves and blood vessels.

Ulcer-Causing Bacteria

A vat of churning acidic goop may not seem a hospitable place for a microbe, but the type that causes ulcers (H. pylori) thrives in the low pH environment. "They have outgrowths called flagella that allow them to penetrate the mucus layer of the stomach, where the pH is more tolerable. Eradicating these bacteria is not simple," says Dr. Gallo-Torres. The antibiotic drug must be able to kill the bacteria, yet also resist breakdown in the acidic surroundings.

Researchers aren't certain how people acquire the bacteria. However, person-to-person transmission is believed to be the most likely route in developed countries. In developing countries, fecal-oral transmission may play a more important role, similar to the way a person contracts cholera and hepatitis A.

Treating Ulcers, Then and Now

Early in the 20th century, the prescription for an ulcer was bed rest and a bland diet, in a hospital if the patient could afford it.

Antacids were added to the treatment regimen when researchers learned that ulcer patients produce excess stomach acid. By 1971, the control site of acid secretion was identified-- histamine (H2) receptors on the parietal cells.

When histamine binds such receptors, acid output increases. Four approved ulcer drugs--Zantac (ranitidine), Tagamet (cimetidine), Pepcid (famotidine), and Axid (nizatidine)--block H2 receptors, thwarting the signal to secrete acid. A second type of ulcer drug, called an acid- or proton-pump inhibitor, works at a different point in digestion, blocking parietal cells from releasing acid. Prilosec (omeprazole) is the only acid-pump inhibitor approved in the United States at this time for the treatment of ulcers.

The problem with existing drugs is that they only temporarily improve symptoms; the ulcer is likely to return. That's why antibiotics are the first line of defense for ulcers. If bacteria causing some ulcers are eradicated, however, the likelihood of ulcer recurrence is much less because the problem is attacked at its source. 

What Do I Need to Know About Peptic Ulcers? National Digestive Diseases Information Clearinghouse (NDDIC) - NIH Publication No. 11–5042 - Updated Oct 2012

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