Understanding Drug-Induced Gastritis: from Molecular Mechanisms to Therapeutic Management

Abstract

Drug-induced gastritis (DIG) represents an underrecognized yet clinically important cause of gastric mucosal injury with significant morbidity and mortality. It arises from the widespread use of medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, bisphosphonates, iron supplements, selective serotonin reuptake inhibitors (SSRIs), antibiotics, and chemotherapeutic agents. These drugs disrupt gastric defense mechanisms through diverse pathways, including direct mucosal irritation, inhibition of prostaglandin synthesis, immune-mediated injury, and gut microbiota dysbiosis. Clinically, DIG may present with nonspecific symptoms like epigastric pain, nausea, and dyspepsia, but can progress to complications such as ulceration, bleeding, or perforation. Diagnosis relies on careful history-taking, supported by endoscopic evaluation, biopsy, and laboratory investigations. Management primarily involves withdrawal or substitution of the offending drug, along with acid suppression therapy using proton pump inhibitors, complemented by mucosal protective agents like misoprostol or sucralfate when appropriate. Preventive strategies, including co-prescription of PPIs, use of gastroprotective formulations, risk stratification in high-risk populations, and patient education, remain essential. Future perspectives emphasize personalized approaches through pharmacogenomics, gut microbiome modulation, and biomarker discovery for early detection. Overall, improved awareness and integration of preventive and precision medicine strategies are crucial to mitigate the global burden of drug-induced gastritis.