Related Experiment Video
Updated: Apr 10, 2026

Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
Published on: February 16, 2024
The optimal serum pepsinogen cut-off value for predicting histologically confirmed atrophic gastritis
Eun Hye Kim1, Huapyong Kang1, Chan Hyuk Park2
1Division of Gastroenterology, Department of Internal Medicine, Severance Hospital, Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Republic of Korea.
Background:
Although serum pepsinogen tests are useful for predicting the presence of atrophic gastritis, the optimal cut-off values have not been fully evaluated.
Aim:
To determine the optimal serum pepsinogen cut-off value for predicting atrophic gastritis.
Methods:
Patients scheduled for upper endoscopy at Severance Hospital, Korea, between August 2012 and October 2013, were recruited prospectively. Endoscopic biopsies for atrophic gastritis were obtained and histologically graded, based on the updated Sydney system.
Results:
Ninety-five patients were enrolled in the study. The mean age was 57.7±12.1 years, and 44.2% of the patients were male. Serum pepsinogen I/II ratios were lower in patients with atrophic gastritis than in those without it (antrum, 4.2±1.7 vs. 5.2±2.1, P=0.040; corpus, 3.3±1.9 vs. 5.4±1.9, P<0.001). Serum pepsinogen I/II ratios were significantly correlated with histologic atrophic gastritis (antrum, P=0.030; corpus, P<0.001). Using a cut-off value of 4.9, the sensitivity and specificity of the serum pepsinogen I/II ratio for predicting atrophic gastritis in the antrum were 68.2% and 60.3%, respectively.
Conclusion:
The optimal serum pepsinogen I/II ratio cut-off values for atrophic gastritis of the antrum and for the corpus were 4.9 and 3.5, respectively. Serum pepsinogen I/II ratios, with these cut-off values, are useful for screening patients for the presence of atrophic gastritis.
Related Concept Videos
Pathophysiology 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...
Peptic 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.
Gastritis 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...
Peptic 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...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Gastritis-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...
