According to statistical data, drug-induced adverse reactions in the gastrointestinal tract are more common, accounting for about 20% to 40% of the incidence of adverse reactions to all drugs. The incidence of drug-derived liver disease is second only to skin and mucous membrane damage and drug fever. Pharmacogenic liver disease accounts for 2% of inpatients with jaundice, while the incidence of pharmacogenic liver disease in outpatients is about 1 case per 100,000 people. There are currently more than 600 drugs that damage the liver, across almost all types of drugs. In addition, some drugs can cause pharmacogenic cholelithiasis, such as steroidal contraceptives, ceftriaxone, etc. Aluminum thioglycollate, aluminum hydroxide, and barium sulfate can also cause pharmacogenic fecal stones. Hydralazine and methyldopa can cause retroperitoneal fibrosis. Drugs can cause a variety of digestive symptoms, such as pharmacogenic nausea and vomiting, pharmacogenic diarrhea, pharmacogenic abdominal pain, pharmacogenic jaundice, etc. These drug-induced digestive symptoms have important diagnostic value for the diagnosis of pharmacogenic digestive organ damage. The pathogenesis of drug-induced digestive system damage is mainly the following. 1, the toxic side effects of drugs The toxic side effects of drugs are difficult to distinguish, and customarily vary according to the severity of the reaction. Side effects are mostly transient, the therapeutic effect of drugs disappears, the adverse reactions also subside, but sometimes also cause more serious consequences. For example, nausea and vomiting caused by oral administration of some drugs are mostly due to drug side effects; however, if nausea and vomiting are persistent and severe (vomiting caused by antineoplastic drugs), it can cause serious life-threatening complications such as esophageal rupture, upper gastrointestinal bleeding, electrolyte disturbance, malnutrition, etc. In general, drug toxic reactions are reactions that can cause certain functional or organic damage to cells, tissues and organs, such as congestion and erosion of the gastrointestinal mucosa due to long-term use of NSAID, and in severe cases, ulceration, bleeding and perforation, which are caused by drug toxic effects. The extent of NSAID damage to the gastrointestinal mucosa is related to the dose, duration of treatment and age of the drug. For example, carbon tetrachloride, paracetamol, adriamycin, isoniazid and other drugs in the liver by cytochrome P450 drug enzymes, metabolism into some toxic products, such as free radicals, electron-philic groups, oxygens and other covalent binding with macromolecules or cause lipid peroxidation, eventually leading to hepatocyte degeneration, necrosis, causing pharmacogenic liver disease. 2, drug metabolic reactions Certain drugs can cause metabolic reactions in the parenchymal organs of the digestive system (such as the liver and pancreas) in some patients, resulting in tissue damage or dysfunction of the parenchymal organs, causing jaundice, abdominal pain, liver dysfunction, elevated related enzymes, and acute hepatic necrosis and hemorrhagic necrotizing pancreatitis in severe cases, accompanied by fever, rash and other allergic symptoms. 3, secondary reaction Secondary reaction is not the effect of the drug itself, but the reaction induced by the action of the drug. For example, broad-spectrum antibiotics can cause dysbiosis and certain vitamin deficiencies and secondary infections, such as pseudomembranous enteritis and fungal enteritis, immunosuppressants, glucocorticoids can also cause the above reactions. 4, drug interactions When two or more drugs are used in combination, drug interactions are also one of the main pathogenic mechanisms leading to pharmacogenic digestive diseases. Aminoglycosides, tetracyclines, cephalosporins and other antibiotics, non-steroidal anti-inflammatory drugs, cimetidine and other drugs can cause the strengthening of the anticoagulant effect of coumarins and cause hemorrhagic reactions, such as bleeding in the gastrointestinal tract, intestinal wall, peritoneal cavity, substantive organs and rectus abdominis. 5. idiosyncratic reactions Normal people have different metabolizing ability to isoniazid and are divided into fast acetylators and slow acetylators. When taking the same dose of isoniazid, the former is more likely to cause liver damage due to the rapid metabolism of the drug in the body, generating more amount of hepatotoxic metabolite acetylhydrazine; the latter is more likely to cause peripheral neuritis due to the accumulation of isoniazid in the body. G6PD is directly related to the production of glutathione (GSH), a reducing substance in the body, and GSH is often insufficient in people with insufficient G6PD function. The use of primaquine, quinidine, certain sulfonamides, etc. can cause hemolytic anemia in those with G6PD deficiency and lead to pharmacogenic jaundice. 6. Carcinogenic effects Some drugs can cause damage to cell chromosomes and abnormal growth of cells and tissues (including carcinogenesis), such as long-term use of proton pump inhibitor omeprazole, which can lead to gastric pheochromocytoma hyperplasia and gastric polyp hyperplasia, while long-term application of cyproterone can lead to liver tumor production.