OVERVIEW
Non-steroidal anti-inflammatory drug (NSAID) (such as antipyretic and analgesic drugs, antiplatelet aggregating drugs, etc., represented by aspirin) related gastropathy refers to acute and chronic gastric mucous membrane damage due to the application of non-steroidal anti-inflammatory drugs (NSAIDs), including erosions, peptic ulcers and concomitant hemorrhage, perforation and stenosis. The incidence of ulcers caused by NSAIDs ranges from 15% to 30%, and the incidence of gastric ulcers is higher than that of duodenal ulcers.
Etiology
1. Prolonged or high-dose use of NSAIDs, or in combination with glucocorticoids and anticoagulants.
2. Helicobacter pylori infection.
3. Comorbidities with other underlying diseases, history of peptic ulcer, and age greater than 60 years are also risk factors.
Symptoms
1. Clinical manifestations of dyspepsia such as fullness, belching, nausea and vomiting are non-specific.
2. Peptic ulcers caused by non-steroidal anti-inflammatory drugs often do not have obvious epigastric pain, only a small number of patients can have epigastric pain, without obvious regularity and rhythm.
3. If the patient is complicated with bleeding, it can be manifested as vomiting blood, black feces; if the bleeding is large, it can be manifested as dizziness, palpitation, blackness and fainting, or even shock, which can cause death if not rescued in time.
4. Patients with gastrointestinal perforation may suddenly experience severe abdominal pain.
Examination
Gastroscopy reveals diffuse hemorrhagic spots, bleeding spots and erosion of the mucosa, most of which are distributed in the proximal pylorus, gastric sinus and gastric fundus, and can be manifested as superficial ulcers of varying sizes, multiple, and varied morphology. Endoscopy is the main means of diagnosing this disease.
Diagnosis
1. Medical history
There is a history of long-term or high-dose use of non-steroidal anti-inflammatory drugs.
2. Clinical manifestations
Clinical manifestations associated with acute and chronic gastric mucosal injury.
2.Auxiliary examination
Endoscopy is the main means of diagnosing this disease. Gastroscopy shows superficial ulcers of various sizes and forms near the pylorus, gastric sinus and fundus, with or without active bleeding.
Treatment
1. Treatment of etiology
The risk of gastrointestinal side effects needs to be thoroughly assessed before applying NSAIDs, and NSAID-associated gastropathy should be avoided as much as possible.
Once it occurs, NSAIDs should be discontinued or used with caution. If they must be used, they should be chosen to minimize damage to the gastric mucosa and to reduce the duration and dosage of the medication. Avoid using multiple NSAIDs at the same time, and avoid combining glucocorticoids, anticoagulants and NSAIDs.
2. Drug therapy
The main inhibitors of gastric acid secretion and gastric mucosa protection drugs. Although misoprostol can prevent the occurrence of gastric ulcers and promote the healing of ulcers, it is seldom used in the clinic because of its side effects of abdominal pain and diarrhea. Inhibitors of gastric acid secretion include proton pump inhibitors and H2 receptor antagonists, which play an important role in inhibiting gastric acid secretion and promoting ulcer healing.
Prevention
1. Before using NSAIDs, testing for Helicobacter pylori is needed, and if there is any Helicobacter pylori eradication treatment is needed to reduce the incidence of NSAID-associated gastropathy.
2. Proton pump inhibitors (PPI) can effectively prevent the occurrence of NSAID-induced ulcers, and should be combined with PPIs in the application of NSAIDs for those with risk factors to minimize the damage to the gastric mucosa.