Aspirin mechanism of gastric ulcer

Use of nonsteroidal anti-inflammatory drugs, including Aspirin, is a common cause of peptic ulcer disease. About 30% of patients using long-term non-steroidal anti-inflammatory drugs will develop undesirable effects on the gastrointestinal tract. The following article provides you with information on the mechanism of aspirin causing stomach ulcers and the prevention of complications of the drug on the gastrointestinal tract.

Aspirin has analgesic, antipyretic and anti-inflammatory effects. Aspirin's mechanism of action is similar to that of other nonsteroidal anti-inflammatory drugs. Aspirin inhibits the enzyme cyclooxygenase (COX), leading to inhibition of the synthesis of thromboxane, prostaglandins and other products such as prostacyclin of cyclooxygenase.
There are two types of COX enzymes in the body: the COX-1 enzyme is found in normal tissues (COX-1 maintains normal gastric mucosa; kidney and platelet function); COX-2 enzymes are found mainly at inflammatory sites, stimulated to increase prostaglandin production by cytokines and chemical mediators of the inflammatory process.
Aspirin covalently binds to both COX enzymes resulting in irreversible inhibition of the activity of these enzymes, so the duration of action of Aspirin is related to the cyclooxygenase cycle rate. Meanwhile, with other non-steroidal anti-inflammatory drugs, because they only competitively inhibit the COX site of action, the duration of action of these drugs will be directly related to the time the drug remains in the body. In addition, aspirin also inhibits platelet aggregation, through the mechanism by inhibiting platelet COX leading to inhibition of thromboxane A2 synthesis - the substance that causes platelet aggregation. In addition, aspirin also inhibits the production of prostaglandins in the kidneys.

2.1. Indications Aspirin is used to relieve mild to moderate pain, reduce fever. However, because aspirin has a high rate of gastrointestinal side effects, it is often replaced by paracetamol. Aspirin is used in the treatment of acute and chronic inflammation: juvenile rheumatoid arthritis, rheumatoid arthritis, osteoarthritis. Aspirin is used in a number of cardiovascular conditions such as myocardial infarction, angina pectoris, and for the prevention of cardiovascular complications in high-risk patients. The drug is also used in the treatment and prevention of some cerebrovascular diseases such as stroke; in the treatment of Kawasaki syndrome. 2.2.Contraindications Due to the risk of cross-allergic reactions, aspirin should not be used in patients who have had symptoms of asthma, rhinitis, or urticaria when taking aspirin or non-steroidal anti-inflammatory drugs in the past. Aspirin should not be used in patients with medical conditions such as: hemophilia, thrombocytopenia, bronchial asthma, active gastric or duodenal ulcer, moderate and severe heart failure, renal failure especially at high speed. glomerular filtration rate less than 30ml/min, liver failure and cirrhosis.

The mechanism of gastric ulceration of aspirin is similar to that of other non-steroidal anti-inflammatory drugs, including:
The COX-1 enzyme, found in most normal tissues, has a catalytic effect. the formation of structural prostaglandins, which maintain a variety of normal physiological effects, including protection of the gastric mucosa, renal and platelet function. Non-steroidal anti-inflammatory drugs have a local irritating effect on the upper gastrointestinal epithelium, causing a decrease in the mucosal barrier. Nonsteroidal anti-inflammatory drugs inhibit the enzyme COX-1, reduce the synthesis of prostaglandins that protect mucous membranes and reduce blood flow to the gastric mucosa. This allows gastric acid to diffuse back into the mucosa, damaging cells and blood vessels causing inflammation and stomach ulcers. The group of NSAIDs together interfere with the repair of superficial lesions in the gastric mucosa. The acidic nature of NSAIDs also contributes to the pathogenesis of gastric ulcers caused by these drugs, by interfering with hemostasis, impairing healing, and inactivating some growth factor important in mucosal protection and repair.

Risk factors for gastrointestinal complications include:
History of gastrointestinal events, especially complicated events. Age > 65. Concomitant use of anticoagulants, other NSAID drugs including high dose NSAID and low dose aspirin. The disorder causes chronic weakness in the body, especially cardiovascular disease. Low-dose aspirin is also a risk factor for gastrointestinal complications. Most current evidence supports that H. pylori infection increases the risk of peptic ulcers with the use of NSAIDs. Patients with a history of peptic ulcer, before using the NSAID group, should be given priority to test for H.pylori and apply antibiotic therapy to kill H.pylori if positive for H.pylori. Classification of the risk of peptic ulcers when using NSAIDs:

Low-dose aspirin is commonly used to reduce cardiovascular and cerebrovascular thrombotic events. Patients using low-dose aspirin are often elderly, taking concomitant antiplatelet agents or anticoagulants. Thus, increasing the risk of gastrointestinal complications, the relative risk being 4 times higher in high-risk patients. In patients with a history of ulcerative gastrointestinal bleeding, consideration of secondary ulcer prophylaxis with a proton pump inhibitor and replacement of aspirin with other antiplatelet therapy is not recommended.

Before using non-steroidal anti-inflammatory drugs, the patient's history should be considered to assess the risk of gastrointestinal toxicity. Accordingly, patients should be informed of the potential undesirable effects of the drug.
Proton pump inhibitors (PPIs) significantly reduce peptic ulcer and its complications, and prevent recurrence of gastrointestinal injury in patients taking NSAIDs or COX-2 inhibitors. Misoprostol is a prostagladin E1 analogue, using the maximum dose (800 mcg/day) has the effect of protecting the stomach by inhibiting gastric acid secretion and pepsin, enhancing the resistance of the mucosa, and preventing ulcers. and its complications in patients taking non-steroidal anti-inflammatory drugs. However, its clinical efficacy is limited by gastrointestinal side effects such as abdominal pain, muscle cramps, and diarrhea. H2-receptor antagonists: Use of H2-receptor antagonists is significantly less effective than proton pump inhibitors. Studies have shown that taking a single daily dose of H2-receptor antagonists does not prevent the complications of peptic ulcers associated with the use of non-steroidal anti-inflammatory drugs; Prophylactic efficacy when compared with placebo was only observed with double dose H2 receptor antagonists. The mechanism of gastric ulceration of the group of non-steroidal anti-inflammatory drugs, including aspirin, is due to the inhibition of protective factors and the NSAID itself is also an attack factor to damage the stomach. Before using Aspirin, patients need to identify risk factors, perform H.Pylori test and treat bacteria to limit the impact of the drug on the gastrointestinal tract. In addition, an appropriate non-steroidal anti-inflammatory drug regimen should be selected to prevent peptic ulcer and its complications.
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