Gastric cyto-secretory correlations in peptic ulcer
Related Experiment Video
Updated: Oct 18, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia
Published on: February 16, 2024
G Testino1, M Cornaggia, M Valentini
1Department of Gastroenterology and Digestive Endoscopy, S. Martino Hospital, Genova, Italy.
Background/Aims:
Maximal acid output, parietal cell mass, serum pepsinogen A (PGA) and total peptic activity (TPA) in gastric juice were studied and compared in duodenal ulcer and in different gastric ulcer sites.
Methodology:
152 peptic ulcer patients were studied. 64 cases of gastric ulcer (GU) were subdivided according to Johnsons's classification and compared with 88 duodenal ulcer (DU) patients diagnosed for the first time. 40 normal subjects were studied as controls.
Results:
Duodenal ulcer is characterized by normo-hyperparietalism, normo-hyperchloridria and an increase in peptic activity. In cases of GU, such correlation is not only conditioned by the topographic seat of the ulcer, but by the histological condition of the gastric mucosa too. Body GU is characterized by hypoparietalism, hypochloridria, hyper-PGA and hyper-TPA. Pre-pyloric GU is characterized by normo-hyperparietalism, normo-hyperchloridria, hyper-PGA and hyper-TPA. In GU the cyto-secretory behavior is characterized by the histology of the body mucosa with prevalence of preatrophic-atrophic gastritis in case of body GU and prevalence of superficial gastritis in case of GU type II and III.
Conclusions:
The results confirm the anatomic-functional analogy between DU and type II and III GU. If considered from the functional point of view, these conditions differ considerably from those that are characteristic of type I GU (as they closely follow the chronic gastritis pattern).
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 to M3...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease II: Pathophysiology
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.
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
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...
