Approximately 5% to 12% of the population is affected by peptic ulcers. Most cases of peptic ulcer are apparently due to the infection of a specific bacterium Helicobacter pylori. It is also thought that the bacterium is involved in many cases of gastritis and gastric cancer. Conventional wisdom has focused for years on the notion that stress, diet, smoking, and/or alcohol cause excess acid secretion in the stomach, resulting in ulcers. Even today, antacids are used to treat 90% of all ulcers, with $4.4 billion spent on antacids in the United States during 1992. Antacid therapy does relieve the ulcer in most cases. However, with antacid treatment, there is a 50% incidence of relapse within 6 months and a 95% incidence of relapse after 2 years. On the other hand, studies using antibiotic therapy in addition to bismuth and ranitidine have demonstrated a 95% eradication of gastric ulcers and 74% of duodenal ulcers within 2 months.

Dramatically reduced relapse rates have also been obtained. One such study reported a recurrence rate of 8% following antibiotic therapy, compared to recurrence rate of 86% in controls.

The infection rate from H. pylori in the United States population is about 1% per year of age: 30% of people that are 30 years old have the bacterium and 80% of those age 80 are infected. In third-world countries, as many as 100% of people age 25 or older are infected. This may relate to the high rates of stomach cancer in some of those countries. We still have much to learn in understanding this bacterium. Very little is known concerning how people become infected. Also, with such high rates of infection it is not known why only a small fraction of those infected actually develop ulcers. It may be that the factors listed predispose a person who is infected by the bacterium to actually develop an ulcer.

Peptic ulcer is classically viewed as a condition in which the stomach acids digest the mucosal lining of the GI tract itself. The most common site of a peptic ulcer is near the pylorus, usually on the duodenal side (that is, a duodenal ulcer; 80% of peptic ulcers are duodenal). Ulcers occur less frequently along the lesser curvature of the stomach or at the point at which the esophagus enters the stomach. The most common presumed cause of peptic ulcers is the oversecretion of gastric juice relative to the degree of mucous and alkaline protection of the small intestine. One reason that bacterial involvement in ulcers has been dismissed for such a long time is that it was assumed that the extreme acid environment would not allow bacteria to survive. Apparently not only can H. pylori survive in such an environment, but it may even thrive there.

People experiencing severe anxiety for a long period of time are the most prone to develop duodenal ulcers. They often have a high rate of gastric secretion (as much as 15 times the normal amount) between meals. This secretion results in highly acidic chyme entering the duodenum. The duodenum is usually protected by sodium bicarbonate (secreted mainly by the pancreas), which neutralizes the chyme. However, when large amounts of acid enter the duodenum, the sodium bicarbonate is not adequate to neutralize it. The acid tends to reduce the mucous protection of the duodenum, perhaps leaving that part of the digestive tract open to action of H. pylori, which may further destroy the mucous lining.

In one study, it was determined that ulcer patients prefer their hot drinks extra hot, 62 degrees C compared to 56 degrees C for a control group without ulcers. The high temperatures of the drinks may cause thinning of the mucous lining of the stomach, making those people more susceptible to ulcers, again perhaps by increasing their sensitivity to H. pylori invasion.

In some patients with gastric ulcers, there are often normal or even low levels of gastric hydrochloric acid secretion. However, the stomach has a reduced resistance to its own acid. Such inhibited resistance can result from excessive ingestion of alcohol or aspirin.

Reflux of duodenal contents into the pylorus can also cause gastric ulcers. In this case, bile, which is present in the reflux, has a detergent effect that reduces gastric mucosal resistance to acid and bacteria.

An ulcer may become perforated (a hole in the stomach or duodenum), causing peritonitis. The perforation must be corrected surgically. Selective vagotomy, cutting branches of the vagus (X) nerve going to the stomach, is sometimes performed at the time of surgery to reduce acid production in the stomach.

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