3. Surgical Treatment

For both chronic atrophic and superficial gastritis, internal medicine treatment should be the mainstay, and surgery is generally not recommended. However, if chronic atrophic gastritis is accompanied by severe atypical hyperplasia, there is a risk of canceration, and surgical treatment should be considered immediately. For mild and moderate atypical hyperplasia, combined traditional Chinese and Western medical treatment can still reverse the condition, eliminating the need for surgery.

VI. Prognosis and Outcome

Chronic superficial gastritis can be cured, and after treatment, the gastric mucosa of chronic atrophic gastritis can also revert to superficial gastritis. However, severe atrophic gastritis, especially in elderly patients, is more difficult to treat. Patients with chronic atrophic gastritis accompanied by moderate or severe atypical hyperplasia should undergo gastroscopy and biopsy every six months. The canceration rate of atrophic gastritis in China is about 0.3%, with a canceration rate of about 1.8% for simple intestinal metaplasia, and up to 5.4% for intestinal metaplasia complicated by atypical hyperplasia.

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Chapter 4: Peptic Ulcer

Section 1: Overview

Peptic ulcer mainly refers to chronic ulcers occurring in the stomach and duodenum (accounting for about 95% of all ulcer diseases). The formation of ulcers is closely related to the digestive action of gastric acid and pepsin in gastric juice, hence the name "peptic ulcer." Duodenal ulcers have the highest incidence, about three times that of gastric ulcers. In addition, due to differences in location, etiology, and severity, peptic ulcers have several clinical names: when both the stomach and duodenum develop ulcers simultaneously, it is called a compound ulcer; when two to three ulcers exist at the same time, it is called a multiple ulcer; ulcers with a diameter greater than 2.0 cm are called giant ulcers; ulcers caused by acute gastrointestinal injury, bleeding, erosion, and necrosis resulting from stress factors such as trauma, major surgery, cranial diseases, severe infections, and medications are classified as stress ulcers; ulcers occurring at the anastomosis after gastric or duodenal surgery are called anastomotic ulcers; and ulcers caused by pancreatic β-cell tumors leading to hyperplasia of G cells in the gastric antrum and duodenum, resulting in excessive secretion of gastrin and causing multiple, refractory ulcers, are called pancreatic-origin ulcers.

Peptic ulcer is a common disease worldwide, affecting about 10% of the population at some point in their lives. It is also very common in China, with an incidence rate of 1.36%, including 0.78% for duodenal ulcers, 0.25% for gastric ulcers, and 0.06% for compound ulcers. Clinically, duodenal ulcers are more prevalent among young and middle-aged adults, while gastric ulcers tend to occur slightly later, about 10 years older than duodenal ulcer patients. Among duodenal ulcer patients, males outnumber females, whereas among gastric ulcer patients, the number of males and females is roughly equal, with no significant gender difference.

Regarding the causes and pathogenesis of peptic ulcers, generally speaking, the disease occurs when protective factors and damaging factors of the mucosa lose their relative balance. Specifically, the protective factors of the mucosa refer to the mucus layer and the intact epithelial cell membrane covering the surface of the gastric mucosa, together forming a defensive barrier known as the mucus-mucosal barrier; the most critical damaging factor is the digestive action of gastric acid and pepsin. Under normal circumstances, the digestive actions of gastric acid and pepsin are in relative balance with the mucus-mucosal barrier, keeping the gastric mucosa intact; however, under various pathogenic factors—such as emotional stress, increased gastrin secretion, food stagnation in the gastric antrum, stress factors, hormonal drug stimulation, and irritating foods—the secretion of gastric acid increases, disrupting the balance and weakening the protective function of the mucus-mucosal barrier, leading to disease. Some damaging factors, such as coarse, hard-to-digest foods, certain medications (aspirin, indomethacin), strong liquor, and bile reflux, directly damage the gastric mucosa. Once the gastric mucosa is damaged by these factors, hydrogen ions in gastric acid penetrate the mucosa, causing destruction of epithelial cells and inflammation of the mucosa, creating conditions for ulcer formation. On the other hand, the mucus-mucosal barrier can also be weakened by other factors, such as impaired blood supply to the mucosa, mucosal ischemia and necrosis, lack of prostaglandins—which enhance epithelial cell renewal and maintain mucosal integrity—and the presence of Helicobacter pylori, smoking, and genetic factors. The self-weakening of the mucus-mucosal barrier plays an important role in ulcer formation, because some ulcer patients do not have excessive gastric acid secretion; their levels are normal or even lower. In this case, even normal gastric acid and pepsin cannot block their digestive action, ultimately leading to ulcer formation. In short, ulcer formation is driven by adverse factors as well as by deficiencies within the mucosa itself. Just as Traditional Chinese Medicine says, "Where evil gathers, qi must be deficient; if righteous qi remains inside, evil cannot invade."

Section 2: Diagnosis