Duodenitis

　　(I) Etiology

　　1. The etiology of primary duodenitis has not been fully clarified, and may be related to the intake of irritant foods, alcohol, drugs (such as non-steroidal anti-inflammatory drugs), Helicobacter pylori infection, and so on. This disease can also be accompanied by other duodenal diseases or diseases of surrounding organs such as liver, gallbladder, and pancreas, often coexisting with chronic gastritis, peptic ulcer disease, and so on. Therefore, it is believed that it may have the same etiology. Some people believe that duodenitis can evolve into duodenal ulcer, and the evidence is as follows:

　　(1) At the beginning of inflammation, the acidity is normal, but later, due to the progression of inflammation, it interferes with the duodenum's inhibition of gastric juice secretion, leading to hyperacidity and the formation of ulcers.

　　(2) During duodenitis, the epidermal cells are lost due to inflammation, but the proliferation of acinar cells can compensate for this. When acinar cells fail to compensate for the loss due to exhaustion, erosion can occur, followed by the formation of ulcers.

　　2. Specific duodenitis is often caused by Crohn's disease, intestinal tuberculosis, parasites (such as hookworm, Giardia lamblia, etc.), fungi, and eosinophilic gastroenteritis, etc., which involve the duodenum and cause specific inflammation.

　　(II) Pathogenesis

　　The duodenal mucosa is congested, edematous, eroded, and bleeding, with a decrease in glands, and villi atrophy; inflammatory cells in the mucosa and submucosa, including lymphocytes, plasma cells, and monocytes infiltrate, and are divided into superficial, interstitial, and atrophic types according to the degree of inflammation and distribution.

　　1. Superficial - This type is the most common, accounting for about 50% to 80%, with inflammation limited to the villi, which become shorter, rounded or deformed, and the epithelial cells often show degenerative phenomena, becoming flatter, with vacuoles in the cytoplasm, sparse or condensed nuclear chromatin, the brush border becomes thin to disappear, and the inter-villus area is filled with inflammatory cells, while the muscularis mucosae and duodenal glands are basically normal.

　　2. Interstitial - Inflammatory cell infiltration is mainly seen in the crypts of the intestinal glands near the muscularis mucosae, sometimes involving the entire lamina propria, accompanied by lymphoid follicle proliferation.

　　3. Atrophic - The mucosa becomes thin, villi show varying degrees of atrophy, there are often severe epithelial cell degenerative changes, and there are large areas of shedding, leading to erosion, sometimes with gastric epithelial metaplasia; the number of intestinal glands decreases even disappears, goblet cells, mucous cells, and argentaffin fibers proliferate, the muscularis mucosae is broken, proliferates, and the muscle fibers have degenerative changes; there is extensive inflammatory cell infiltration in the lamina propria, mainly lymphocytes, plasma cells, and lymphoid follicle proliferation.

　　Gastrointestinal bleeding has an incidence rate of 3.4% to 35.5% reported in China, mostly presenting as melena or tarry stools, with some cases of hematemesis, and in some cases, bleeding is the initial symptom. Upper gastrointestinal bleeding refers to bleeding caused by esophageal, gastric, duodenal, and upper jejunum (about 50cm segment below the duodenal suspensory ligament), as well as pancreatic duct and bile duct lesions. Its clinical manifestations are mainly hematemesis and melena, which is a common surgical emergency.

　　1. Dyspeptic symptoms may include upper abdominal fullness, acid regurgitation, belching, nausea, and vomiting. Some patients may have no symptoms or signs.

　　2. Upper abdominal pain is similar to duodenal ampulla ulcer, mostly pain during hunger or at night, which is relieved after eating.

　　3. Upper gastrointestinal bleeding is a complication of erosive duodenitis, and can cause black stools or vomiting.

　　4. Common signs include mild upper abdominal tenderness, and some patients may have glossitis, anemia, and emaciation.

　　1. Primary duodenitis should eat less or not eat刺激性 foods, alcohol, and certain drugs (such as non-steroidal anti-inflammatory drugs).

　　2. Active treatment of the primary disease in specific duodenitis, such as Crohn's disease, intestinal tuberculosis, parasitic and fungal enteritis, etc.

　　Imaging diagnosis:

　　1. Barium meal X-ray examination: There are no clear X-ray characteristics for this disease, generally showing irritation, spasm, accelerated emptying of the duodenal bulb, thickening and irregular mucosal folds, but without ulcers and fixed deformities, so the positive rate of X-ray diagnosis for this disease is not high.

　　2. Endoscopic examination: Duodenal inflammation often occurs in the bulb, and the endoscopic examination shows rough, congested, edematous, erosive, and bleeding mucosa at the lesion site, or the mucosa has a granular sensation and nodular hyperplasia, or the mucosal folds are thick and large, or blood vessels are exposed beneath the mucosa. Different manifestations can be seen due to the varying degrees of lesions.

　　Laboratory diagnosis

　　(One) Gastric juice analysis: Gastric acid or gastric juice secretion is normal or high, and the gastric acid level in some cases is similar to that of duodenal ulcer.

　　(Two) Analysis of duodenal juice: Duodenal juice may be turbid, with mucus, and the microscope examination shows a large number of epithelial cells. In patients with low gastric acid, there may be more bacteria.

　　Eat easily digestible foods such as congee, noodles, steamed buns, flower rolls, dumplings, soft pancakes, and soft rice, chew slowly, and it is easy to digest and absorb fully.

　　Eat less legumes, onions, potatoes, sweet potatoes, and other foods that are easy to produce acid and gas. Avoid cold, greasy, spicy, and alcohol to prevent adverse factors from stimulating ulcers.

　　Especially recommended for nourishing the stomach and spleen: yam lotus and lily congee, peanuts, red dates, and millet congee. Eggs, minced meat, chicken puree, fish puree, minced vegetables, fruit granules, and milk can be added for seasoning to increase nutrition.

　　If you feel like vomiting when eating eggs, it is best not to eat them to avoid damaging the food.

　　(1) Antacid: Aluminum magnesium hydroxide suspension can be used, 15-30ml each time, 3 times a day, taken 1-2 hours after meals. Antacids can neutralize stomach acid, reduce pepsin activity, alleviate the damage to the digestive tract mucosa, and relieve pain.

　　(2) Anti-secretory drugs: They can be selected according to the patient's economic bearing capacity and other factors. Proton pump inhibitors can be used, such as omeprazole 20mg, 1-2 times a day, or rabeprazole 10-20mg, 1-2 times a day; H2-receptor antagonists can be used, such as famotidine 20mg, 2 times a day, or ranitidine 150mg, 2 times a day. Anti-secretory drugs can inhibit the secretion of gastric acid by gastric cells, reduce the irritation of gastric acid to the existing inflamed mucosa, and effectively improve the symptoms, but cannot reverse pathological abnormalities.

　　(3) M-receptor antagonists: Pirenzepine 50mg, 2 times a day, or scopine (654-2) tablets 5mg, 3 times a day, taken orally, can inhibit the secretion of gastric acid. In addition, it also has inhibitory effects on the secretion of pepsin.

　　(4) Mucosal protective agents: Colloidal bismuth preparations can form a protective film by combining with the glycoproteins of ulcers and inflamed tissues in an acidic environment, preventing the attack of gastric acid and pepsin, and having the effect of killing Helicobacter pylori. Colloidal bismuth, 50mg, 4 times a day, can be used. Prostaglandins can reduce the secretion of gastric acid, enhance the mucosal anti-damage ability, and have the effects of maintaining mucosal blood flow and promoting mucus secretion, etc. Misoprostol 200μg, 4 times a day, or enprostil 70μg, 2 times a day, can be used.

　　(5) Gastrointestinal motility drugs: Domperidone 10-20mg, 3 times a day, or mosapride 5-10mg, 3 times a day, taken orally 15-30 minutes before meals, can adjust the movement of the gastric antrum and duodenal ampulla, and reduce the acid secretion caused by the gastrin secretion of the gastric antrum G cells due to bile reflux.

　　(6) Helicobacter pylori (Hp) eradication treatment: Common anti-Hp drugs include amoxicillin, metronidazole (or tinidazole), furazolidone, tetracycline, clarithromycin, and bismuth preparations, etc. The eradication rate of monotherapy is less than 20%, so it is usually combined with 2 or more antibiotics and anti-secretory drugs (PPI or H2RA) to form triple therapy and quadruple therapy. The course of treatment is generally 1-2 weeks. The triple therapy containing PPI is the most researched treatment plan for H. pylori infection in recent years.