Helicobacter pylori infection

　　Helicobacter pylori (Hp) can grow and reproduce in the low pH environment of the human stomach, causing tissue damage. Its pathogenic effect is mainly manifested as the colonization of bacteria on the gastric mucosa, invasion of the host's immune defense system, direct toxic action, and induced inflammatory and immune reactions. The toxins and toxic enzymes of Hp, as well as the mucosal inflammatory reactions induced by Hp, can cause damage to the gastric and duodenal mucosal barrier. The current research on the infection route of Helicobacter pylori mainly includes:

　　1. Factors that allow Helicobacter pylori to penetrate the mucus layer and settle on the surface of gastric epithelial cells.

　　2. Toxin factors that cause damage to gastric epithelial cells and others.

　　3. Various inflammatory cells and inflammatory mediators.

　　4. Immune response substances, etc.

　　These factors constitute the basic pathological changes of the pathogenesis of Helicobacter pylori infection, namely various types of acute and chronic gastritis. Among them, the functions and molecular biological studies of vacuolating cytotoxin vaca, cytotoxin-associated protein caga, and urease have received important attention in recent years.

　　The main diseases caused by Helicobacter pylori infection include gastric hemorrhage, anemia, gastric ulcer, and gastric cancer, as follows:

　　1. Gastric hemorrhage

　　Chronic gastritis with hemorrhage is not uncommon, with symptoms such as mucosal atrophy and thinning, exposed blood vessels, abrasion of rough food, and erosion and hemorrhage of the mucosa, mainly manifested as melena. If the hemorrhage is large, it can suddenly cause hematemesis. Severe cases may present with dizziness, palpitations, blackening of the vision, profuse sweating, and even shock.

　　2. Anemia

　　After a large amount of bleeding in chronic gastritis, megaloblastic anemia and iron deficiency anemia may occur. Megaloblastic anemia, also known as pernicious anemia, presents with anemia, dizziness, fatigue, palpitations, and pale complexion. Iron deficiency anemia is caused by chronic bleeding; by insufficient nutrition due to eating less in chronic gastritis patients; and by lack of gastric acid.

　　3. Gastric ulcer

　　Gastric ulcer coexists with superficial gastritis and erosive gastritis, with obvious inflammatory stimulation. The gastric mucosa atrophy becomes thin, and complications such as erosion and ulceration occur. Gastroscopy should be performed in a timely manner to avoid delays in diagnosis and treatment.

　　4. Gastric cancer

　　The canceration of early chronic gastritis is closely related to gastritis hyperplasia. There are two situations where chronic gastritis is prone to canceration: one is chronic gastritis accompanied by pernicious anemia, with a canceration rate 20 times higher than that of other gastrointestinal diseases, which should be paid attention to by gastrointestinal disease patients. The other is atrophic gastritis accompanied by intestinal metaplasia and severe atypical hyperplasia.

　　The symptoms of Helicobacter pylori (Hp) infection mainly include acid regurgitation, heartburn, and stomach pain, as well as halitosis. Helicobacter pylori infection can cause chronic gastritis, with main clinical manifestations of upper abdominal discomfort, dull pain, and sometimes belching, acid regurgitation, nausea, and vomiting. The course is relatively slow, but it is prone to recurrence. After infection with Helicobacter pylori, patients produce various pathogenic factors, leading to damage to the gastric mucosa, and the occurrence of clinical diseases shows diversity, with most patients presenting with acid regurgitation, belching, and a feeling of fullness. The toxins and enzymes with toxic effects of Hp, as well as the mucosal inflammatory reactions induced by Hp, can cause damage to the gastric and duodenal mucosal barrier.

　　Due to the unclear source of transmission and route of Helicobacter pylori (Hp) infection, it has brought difficulties to the prevention of Hp infection. Since the 1990s, significant progress has been made in the research of Hp vaccines, and it is expected that in the near future, the prevention and treatment of Hp infection through vaccination will become a reality and may also be an important measure for the prevention and treatment of Hp-related diseases in the future. Oral hygiene should be maintained, dental problems eliminated, and cups, water bottles, and stainless steel thermal bottles should not be mixed. It is also necessary to frequently steam sterilize, especially during the period of drug treatment, and to disinfect dishes and chopsticks separately.

　　The main clinical examination methods for Helicobacter pylori (Hp) infection include gastroscopy sampling detection, direct bacterial examination, urease test, immunological detection, and polymerase chain reaction technology examination, as follows:

　　1. Gastroscopy sampling detection

　　To detect the presence of Helicobacter pylori. If positive, it can be diagnosed as a positive infection with Helicobacter pylori.

　　2. Direct bacterial examination

　　Through gastroscopy, the gastric mucosa (mostly antrum mucosa) is sampled for direct smear, staining, tissue section staining, and bacterial culture to detect Helicobacter pylori (Hp). Gastric mucosal bacterial culture is the most reliable method for diagnosing Hp and can serve as the 'gold standard' for verifying other diagnostic tests, while also allowing for drug sensitivity testing to guide clinical drug selection.

　　3. Urease test

　　Hp infection can be diagnosed by detecting urease. Urease decomposes urea in the stomach to produce ammonia and carbon dioxide, which lowers the urea concentration and increases the ammonia concentration. Hp has a high urease activity and can decompose urea to produce NH+4. By measuring the presence or absence of NH+4, it is indirectly determined whether there is Hp infection. Methods include pH indicator method, analytical chemistry method, and isotope-labeled urea test.

　　4. Immunological detection

　　Hp infection can be detected by measuring the Hp antibodies in the serum, including complement fixation tests, agglutination tests, passive hemagglutination assays, immunoblotting techniques, and enzyme-linked immunosorbent assays (ELISA).

　　5. Polymerase Chain Reaction Technique

　　The detection rate of Hp in patients with chronic gastritis is very high, ranging from 50% to 80%, and the detection rate of Hp in patients with chronic active gastritis is even higher, reaching over 90%.

　　Helicobacter pylori infection often has a family clustering phenomenon. To eradicate it completely and avoid reinfection, it is best for other family members to also receive treatment at the same time, and implement separate meals to avoid reinfection. The following aspects should be paid attention to in the diet and lifestyle of patients with Helicobacter pylori infection:

　　1. Patients should pay attention to regular and quantitative meals, a nutrition-rich diet, small and frequent meals, and chew slowly. Food should be soft and easy to digest, avoid overeating, eating raw, cold, sour, spicy, and fried stimulating foods, and avoid smoked and preserved foods. Foods containing nitrosamines, such as preserved foods, also have a carcinogenic effect. Combined with the effect of Helicobacter pylori, it will increase the chance of cancer.

　　2. Prevent disease from entering through the mouth, do not eat unclean food.

　　3. Develop good hygiene habits, wash hands before and after meals.

　　5. Promote the use of communal chopsticks and separate meals at home, and disinfect tableware to avoid contact with infection. The traditional Chinese practice is to have a family share a table of food together, especially some parents like to chew food and feed it to their babies, which will increase the opportunities for the spread of Helicobacter pylori. This habit should be strictly prohibited.

　　4. Vomit and feces should be cleaned up in time, and hands and utensils should be disinfected.

　　With the unified understanding of the diseases related to Helicobacter pylori (Hp) infection, the treatment for eradicating Hp has been widely used in clinical practice. Eradication refers to the absence of Hp in the stomach after one month of treatment. In vitro drug sensitivity tests show that many antibiotics have good antibacterial activity against Hp, but in the low pH environment of the body, most antibiotics have reduced activity and cannot penetrate the mucus layer to reach effective杀菌 concentrations locally, therefore, Hp infection is often difficult to eradicate in clinical practice. To date, there is no single antibiotic that can effectively eradicate Hp. Therefore, various treatment plans that combine antibiotics, bismuth agents, and anti-secretory drugs have been developed. Currently, the general approach is to use triple or quadruple therapy, with low dose and short course being preferred.

　　Currently, the treatment of Helicobacter pylori infection mainly relies on anti-Helicobacter pylori drugs. Although Helicobacter pylori is sensitive to many antibacterial drugs in vitro, it is not as effective in vivo. It is not recommended to use a single antibacterial drug because its cure rate is low and it is prone to develop drug resistance. The main principles for selecting treatment plans for Helicobacter pylori (Hp) infection are as follows:

　　1. Adopt a combined medication method;

　　2. The eradication rate of Helicobacter pylori is >80%, preferably above 90%;

　　3. No significant side effects, good tolerance by the patient;

　　4. Economic affordability of the patient. The effectiveness of the treatment for Helicobacter pylori infection should be judged according to the eradication rate of Helicobacter pylori, which means that at least one month after the end of treatment, the absence of bacterial growth is confirmed through bacteriology, pathological histology, or isotope tracing methods.

　　Before eradicating Helicobacter pylori, attention should be paid to oral hygiene, use mouthwashes and antibacterial toothpaste for a period of time to repair oral problems such as tooth decay, dental plaque, calculus, etc., and you can change your toothbrush first. Do not use cups, water cups, and stainless steel thermal cups together, and they should be frequently steamed and disinfected, especially during medication.

　　The commonly used anti-Helicobacter pylori drugs in China outside are Gaifuchun tablets, amoxicillin, metronidazole, clarithromycin, doxycycline, furazolidone, organically colloidal bismuth preparations, Gaodele, Ledewei, and others. Patients with ulcers can appropriately combine the application of proton pump inhibitors or H2 receptor antagonists with two antibiotics, or proton pump inhibitors (such as omeprazole) with one antibiotic, and the course of treatment is generally two weeks. Due to the widespread use of antibacterial regimens for Helicobacter pylori infection, there is a possibility of expanding the problem of drug resistance. Therefore, alternative treatment or preventive strategies such as vaccine prevention or immunotherapy research are worthy of attention.