Related Experiment Video
Updated: Aug 18, 2025
Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
Published on: February 16, 2024
Prevalence and factors associated with atrophic gastritis and intestinal metaplasia: A multivariate, hospital-based,
Taned Chitapanarux1, Sarawut Kongkarnka2, Komson Wannasai2
1Gastrohepatology Unit, Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Northern Thai Research Group of Radiation Oncology (NTRG-RO), Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background:
Atrophic gastritis (AG) and intestinal metaplasia (IM) play an essential role in gastric carcinogenesis. This study aimed to determine the prevalence of AG and IM and their associated factors.
Methods:
Subjects who underwent upper endoscopy at Chiang Mai University Hospital from January 2018 to Dec 2021 were included. All participants were interviewed using a structured questionnaire to collect their personal histories. In addition, clinical and histological data and associated factors of AG and IM were analyzed.
Results:
A total of 947 subjects (mean age, 53.61 ± 9.73 years; 60% male) were included. The prevalence of AG and IM, diagnosed by histopathology, was 39% and 19%. Prevalence of AG and IM increased from 28% and 9% in those under 50 years to 43% and 30% in those above 60 (p < 0.05). In a multivariate analysis, Helicobacter pylori (H. pylori) infection, age 50-59 and over 60 years were significantly associated with higher odds of AG (odds ratio (OR), 2.07, 2.06, and 1.98) and IM (OR, 2.07, 2.18, and 4.46), respectively. Conversely, ingestion of spicy food was significantly associated with lower odds of AG and IM (OR, 0.75, and 0.62).
Conclusions:
This study confirms that age and H. pylori infection are risk factors, whereas spicy food intake is a protective factor against AG and IM, which are common in patients over 50. Therefore, upper endoscopy and gastric mapping sampling are recommended for patients with chronic dyspepsia older than 50 to reduce gastric cancer risk.
Related Concept Videos
01:27Gastritis-I: Introduction and Types
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...
01:17Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:23Gastritis III: Clinical Manifestations and Management
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...