2. Pharmacological Treatment

(1) Antacids (acid-neutralizing agents): The following medications may be used, preferably taken half an hour after meals or between meals, three times daily, with an additional dose before bedtime if necessary.

① Aluminum hydroxide gel, 10–15 ml each time; if constipation occurs, magnesium milk 3–5 ml can be taken concurrently.

② Magnesium trisilicate, 1 g each time.

③ Compound stomach-soothing tablets, 0.6–0.9 g each time.

(2) H₂ receptor antagonists: These drugs exert their antacid effect by blocking H₂ receptors, thereby inhibiting gastric acid secretion.

① Cimetidine (Tagamet), 200 mg each time, three times daily after meals, with an additional 400 mg before bedtime; continued use for more than one year can reduce recurrence rates. The main side effects of cimetidine include fatigue, elevated AST and ALT levels, as well as breast enlargement, impotence, and agranulocytosis; however, these usually resolve on their own after discontinuation. For patients with duodenal ulcer bleeding, if the amount of bleeding is substantial, cimetidine 400–600 mg can be added to 500 ml of 5%–10% glucose or normal saline solution for intravenous infusion once or twice daily.

② Ranitidine (Zantac), which has 5–10 times the potency of cimetidine, 150 mg twice daily (morning and evening), orally, with a treatment course of 4–6 weeks, can achieve good therapeutic results.

③ Famotidine is the latest product, with stronger and longer-lasting effects; 20 mg twice daily can achieve similar efficacy.

(3) Proton pump inhibitors: Omeprazole, also known as Losec, has a stronger effect than H₂ receptor antagonists in suppressing gastric acid secretion and is the newest type of antacid. It is now often recommended for the treatment of refractory ulcers, but is generally not used for first-time cases. Take 20 mg once before bedtime (single dose) or in the morning; for gastric ulcers, take for 8 weeks, and for duodenal ulcers, for 6 weeks. After 4–6 weeks, the ulcer healing rate can reach 80%–100%. However, this drug is expensive, so it should only be used when absolutely necessary.

(4) Gastric mucosal protectants:

① Sucralfate, 1 g each time, three times daily after meals; the ulcer healing rate is comparable to that of cimetidine, with a low recurrence rate.

② Dele granules, with an ulcer healing rate of 80%, and particularly effective for those infected with Helicobacter pylori, with an eradication rate of 80%.

③ Bismuth pectin, 2 g each time, three times daily, orally; a new type of gastric mucosal protector.

(5) Antibacterial therapy:

① Furazolidone, 0.1 g each time, four times daily, with a treatment course of 2 weeks.

② Trivalent bismuth subcitrate (Dele granules), 5 mg each time, four times daily, with a treatment course of 4 weeks.

In addition, berberine, gentamicin, norfloxacin, ampicillin, tetracycline** and other drugs can also be used, with a treatment course of 4 weeks.

(6) Symptom Self-Control Therapy (SSC): This is the latest measure introduced to prevent ulcer recurrence. Previously, preventing ulcer recurrence mainly involved maintaining treatment with anti-ulcer drugs for 0.5–1 year, which could significantly reduce the recurrence rate. However, long-term medication was inconvenient for patients, costly, increased the risk of side effects, and once maintenance treatment was stopped, the recurrence rate would rise again. Therefore, in recent years, SSC has been adopted as a substitute for traditional maintenance therapy. SSC involves preparing a certain amount of medication after a course of treatment that promotes ulcer healing; when patients feel symptoms about to appear, they take the medication, and when they feel normal, they stop taking it. Comparative studies have shown that this method is as effective as maintenance therapy in preventing ulcer recurrence, but at a much lower cost, making it particularly suitable for rural areas.

VI. Surgical Treatment

Indications for surgical treatment of peptic ulcers include:

① Massive bleeding that does not respond to emergency medical management;

② Acute perforation;

③ Pyloric obstruction (organic);

④ Suspected malignancy in gastric ulcers;

⑤ So-called "refractory gastric ulcers" that have received aggressive, standard medical treatment without improvement.

VII. Prognosis and Outcome

Peptic ulcers, whether treated with traditional Chinese medicine or Western medicine, are generally easy to treat but also prone to recurrence. Within two years after initial cure, the recurrence rate can reach 60%–80%, with varying durations of remission between attacks. Generally, gastric ulcers have a lower recurrence rate than duodenal ulcers. The mortality rate of this disease is relatively low, typically around 2%–3%. The mortality rate is zero for those under 25, increasing with age. The main causes of death are complications, especially massive bleeding and acute gastric perforation. Duodenal ulcers are less likely to become malignant, while gastric ulcers have a higher chance of malignant transformation, though the rate remains low, below 1%.

Chapter 5: Stomach

Section 1: Overview

Gastric cancer is the most common malignant tumor of the digestive tract, ranking third among all common malignant tumors in terms of incidence, yet it ranks first in mortality from malignant tumors, accounting for 23.02%. In China, the incidence of gastric cancer is higher in the north than in the south, lower along the coast than inland, with the highest rates in Qinghai, Gansu, and Ningxia in the northwest, followed by Northeast China and Inner Mongolia, then North and East China, while Central and South China (Hunan, Guangdong, Guangxi) and Southwest China (Sichuan, Yunnan, Guizhou) have the lowest rates. The majority of patients are male, with a male-to-female ratio of approximately (2–3):1. The onset is most common in middle-aged and elderly individuals, with those aged 41–60 accounting for two-thirds, and those under 40 about one-quarter. In recent years, the proportion of young people under 30 diagnosed with gastric cancer has gradually increased, rising from 1.7% in the 1970s to 3.3%, possibly due to unhealthy lifestyle habits such as smoking, excessive drinking, consumption of spicy and stimulating foods, irregular living patterns, and excessive mental stress.

The exact causes of gastric cancer remain unclear, but since the stomach is constantly in contact with food, carcinogenic exogenous substances (external carcinogens) can only come from the diet. Research shows that gastric cancer is closely related to high consumption of pickled cabbage, salted fish, and smoked foods; conversely, milk, fresh vegetables, fruits, vitamin C, and refrigerated foods can reduce the risk of gastric cancer. Excessive intake of salt may also contribute to the development of gastric cancer. How do these phenomena occur? Studies have found that nitrosamines are the primary culprits behind gastric cancer, and the precursor substances that form nitrosamines, such as nitrites, are widely present in pickled cabbage, salted fish, and cured meats. Chronic atrophic gastritis, due to low gastric acid levels, creates favorable conditions for the proliferation of nitrate-reducing bacteria, converting nitrates into nitrosamines. If the nitrate content in local soil and drinking water increases, along with higher salt intake, total nitrate consumption rises, increasing the amount of carcinogenic substances. Scientific research has also shown that vitamin C can inhibit the combination of nitrites and amines, thereby blocking the formation of nitrosamines; thus, foods rich in vitamin C, such as milk, fresh vegetables, and fruits, can reduce the risk of gastric cancer. Additionally, low temperatures can inhibit the conversion of nitrates into nitrosamines, which may explain why the incidence of gastric cancer has declined significantly in countries like the United States and Japan in recent years—widespread use of refrigerators may be one contributing factor. Another culprit is benzopyrene. Foods that undergo baking, grilling, frying, or smoking have significantly higher levels of benzopyrene. In the past, residents of Iceland favored smoked fish and meat, resulting in a high incidence of gastric cancer; later, reducing consumption of smoked products and improving smoking methods greatly lowered the incidence. A third culprit is aflatoxin, found in food that has been stored too long and become moldy. All these facts indicate that dietary preferences, nutritional imbalances, environmental factors, and fungal infections create favorable conditions for the formation of carcinogenic substances, serving as external factors in the development of gastric cancer; internal factors refer to genetic predisposition, with relatives of gastric cancer patients having a fourfold higher incidence than the general population, suggesting that carcinogenic substances are more likely to cause cancer in individuals with genetic susceptibility.

Currently, it is widely accepted that gastric cancer develops gradually from certain benign gastric diseases, referred to as precancerous conditions or pre-cancerous states, including chronic atrophic gastritis, gastric polyps, residual stomach, and gastric ulcers.

(1) Chronic atrophic gastritis: Particularly chronic atrophic gastritis of the antrum can progress to gastric cancer, but this is a long process, usually taking more than 10 years. Foreign studies have followed patients diagnosed with chronic atrophic gastritis for 10–20 years, or even 22–26 years, finding that 8%–10% eventually developed gastric cancer. In China, a follow-up study of 1,610 patients over 2–8 years showed a gastric cancer incidence of 1.18%. The progression from chronic atrophic gastritis to gastric cancer is as follows: superficial gastritis → atrophic gastritis → intestinal metaplasia and atypical hyperplasia (dysplasia) → gastric cancer. Atrophic gastritis is often accompanied by intestinal metaplasia (where normal gastric mucosa disappears and small intestinal epithelial cells appear). Previously, intestinal metaplasia and pyloric gland metaplasia were considered precancerous lesions, but current domestic and international expert research suggests that neither is directly related to cancer. Only atypical hyperplasia of gastric mucosal cells, especially severe atypical hyperplasia, qualifies as a precancerous lesion.

(2) Gastric polyps: There are two types of gastric polyps—hyperplastic and adenomatous—and only adenomatous polyps can become malignant. Multiple polyps or polyps larger than 2 cm have a higher risk of malignancy.

(3) Residual stomach: After major gastrectomy for gastric or duodenal ulcers or other gastric diseases, the remaining portion of the stomach is called the residual stomach, and cancer arising in the residual stomach is termed residual stomach cancer. The malignancy rate of residual stomach cancer is twice that of the general population, with an incidence of 0.5%–1%. The main reasons for malignant transformation in the residual stomach are postoperative bile reflux causing atrophic gastritis in the residual stomach, combined with the proliferation of nitrate-reducing bacteria due to lack of gastric acid, which further promotes the formation of carcinogenic nitrosamines. In addition, bile acids themselves have carcinogenic effects.

(4) Gastric ulcers: Duodenal ulcers do not become malignant, but gastric ulcers can, albeit at a low rate, estimated at less than 1%.

Section 2: Diagnosis