Aspirin Induced Gastric Ulcer: Review Article

Gastric diseases range from mild, temporary upsets to life-threatening emergencies that require immediate intervention. Gastric ulcers in animals arise from a breakdown in the stomach's protective mucosal barrier, caused by an imbalance between corrosive stomach acids and natural defense mechanisms. These ulcers are broadly categorized into non-infectious (the majority of cases) and infectious origins across various species. The excessive use of (NSAIDs), The Non-Steroidal Anti-inflammatory Drugs such as (aspirin, flunixin meglumine, or carprofen) and corticosteroids significantly reduces the production of protective stomach prostaglandins (PGs), directly damaging the mucosa.

NSAIDS like aspirin hinders the cyclooxygenase (COX) activities which causes a decrease in prostaglandins leading to several key associations: -

Bicarbonate secretion and reduced mucus.

Weakened platelet aggregation.

Damage of epithelia due to microvascular structures being altered.

An increase in adhesion of leukocytes, lipid peroxidation and neutrophil infiltration.

A decrease in the antioxidant enzymes like Catalase, Superoxide Dismutase, Glutathione Peroxidase, Glutathione S- Transferase and Glutathione (GSH).

Uncoupling of oxidative phosphorylation.

Drug being trapped inside epithelial cells.

Gastric injury pathogenesis due to lipid peroxidation and superoxide generation.

Gastric Injury is to be diagnosed by the endoscopy procedure and most of the time, treatment will require medication administration to reduce the secretion of gastric acid and facilitate mucosal protection. H2 receptor blockers that has ranitidine, cimetidine, and famotidine are the most typical used drugs to decrease the secretion of acid. Omeprazole, a widely used proton pump inhibitors (PPI) are also used to decrease stomach acid.