Specific Causes of Peptic Ulcer in the Human Being

Specific Causes of Peptic Ulcer in the Human Being

Bacterial Infection by Helicobacter pylori Breaks Down the Gas- troduodenal Mucosal Barrier. Many peptic ulcer patientshave been found to have chronic infection of the ter-minal portions of the gastric mucosa and initial portions of the duodenal mucosa, infection most often caused by the bacterium Helicobacter pylori. Once this infection begins, it can last a lifetime unless it is eradicated by antibacterial therapy. Furthermore, the bacterium is capable of penetrating the mucosal barrier both by virtue of its physical capability to burrow through the barrier and by releasing bacterial digestive enzymes that liquefy the barrier. As a result, the strong acidic digestive juices of the stomach secretions can then pen-etrate into the underlying epithelium and literally digest the gastrointestinal wall, thus leading to peptic ulceration.

Other Causes of Ulceration. In many people who havepeptic ulcer in the initial portion of the duodenum, the rate of gastric acid secretion is greater than normal, sometimes as much as twice normal. Although part of this increased secretion may be stimulated by bacterial infection, studies in both animals and human beings have shown that excess secretion of gastric juices for any reason (for instance, even in psychic disturbances) may cause peptic ulceration.

Other factors that predispose to ulcers include (1) smoking, presumably because of increased nervousstimulation of the stomach secretory glands; (2) alcohol, because it tends to break down the mucosal barrier; and (3) aspirin and other non-steroidal anti-inflammatory drugs that also have a strong propensity for breaking down this barrier.

Physiology of Treatment. Since discovery of the bacterialinfectious basis for much peptic ulceration, therapy has changed immensely. Initial reports are that almost all patients with peptic ulceration can be treated effectively by two measures: (1) use of antibiotics along with other agents to kill infectious bacteria and (2) administration of an acid-suppressant drug, especially ranitidine, an antihistaminic that blocks the stimulatory effect of his-tamine on gastric gland histamine₂ receptors, thus reducing gastric acid secretion by 70 to 80 per cent.

In the past, before these approaches to peptic ulcer therapy were developed, it was often necessary to remove as much as four fifths of the stomach, thus reducing stomach acid–peptic juices enough to cure most patients. Another therapy was to cut the two vagus nerves that supply parasympathetic stimulation to the gastric glands. This blocked almost all secretion of acid and pepsin and often cured the ulcer or ulcers within 1 week after the operation was performed. However, much of the basal stomach secretion returned after a few months, and in many patients the ulcer also returned.

The newer physiologic approaches to therapy may prove to be miraculous. Even so, in a few instances, the patient’s condition is so severe—including massive bleeding from the ulcer—that heroic operative proce-dures often must still be used.