Related Experiment Video
Updated: Apr 5, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
Published on: April 9, 2018
Relationship between leukocytes recruitment and risk of rebleeding in patients with peptic ulcers
Oksana Sulaieva1, Victoriia Deliy1, Stanislav Zharikov2
1Department of Histology, Cytology and Embryology, Zaporozhye State Medical University, Ukraine.
Aim:
The aim of this study was to assess the impact of leukocytes reaction on rebleeding development among patients with peptic ulcers.
Methods:
This was a single-center cohort study enrolling 232 patients with a diagnosis of gastroduodenal ulcer bleeding. The end point was the in-hospital rebleeding rate during the three days after admission. The impact of clinical, demographic, endoscopic and laboratory data at the time of admission, as well as macrophages (CD68) and neutrophils count in ulcer margin, on bleeding outcome was assessed. In addition, impact of the leukocytes on the platelets aggregation induced with ADP (5μM) and collagen (1μM) was measured in vitro.
Results:
Acute ulcer bleeding was accompanied with an acute inflammatory response to damage and hemorrhage. Despite the increase of neutrophil count (P=0.031) in peripheral blood of bleeders, there were not significant influence of this parameter on the outcome. It was shown that the most significant predicting factors were an increased neutrophils (OR 1.4; 95% CI 1.1-1.8) and macrophages count in the ulcer margin (OR 3.5; 95% CI 1.9-4.87); an endoscopically diagnosed active bleeding (OR 3.0; 95% CI 1.4-6.3); an enhanced level of plasma fibrinogen (OR 1.04; 95% CI 1.0-1.08). Co-incubation of platelets with leukocytes significantly decreased the collagen induced aggregation (P=0.008) that could indicate either alteration of mechanisms of platelets adhesion, or inhibition of stabilization phase of thrombogenesis.
Conclusion:
The severity of the local acute inflammatory reaction promotes progressive tissue damage of ulcer margin, and increases the risk of rebleeding.
Related Concept Videos
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...
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.
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
Peptic Ulcer Disease IV: Management
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

