Platelet aggregation measurement for assessment of hemostasis failure mechanisms in patients with gastroduodenal ulcer bleeding

Edward Barinov,¹ Oksana Sulaieva,¹ Yuriy Lyakch,² Vitaliy Guryanov,² Petr Kondratenko,³ Yevgeniy Radenko<sup>3

1</sup>Department of Histology, Cytology, and Embryology, ²Department of Medical, Biological Physics, Medical Informatics, and Biostatistics, ³Department of Surgery and Endoscopy, M Gorky Donetsk National Medical University, Donetsk, Ukraine

Background: The purpose of this study was to identify factors associated with the risk of unsustainable hemostasis in patients with gastric and duodenal ulcer bleeding by in vitro assessment of platelet reactivity using artificial neural networks.
Methods: Patients with gastroduodenal ulcers complicated by bleeding were studied. Platelet aggregation was measured using aggregometry with adenosine diphosphate 5 µM, epinephrine 2.5 µM, 5-hydroxytryptophan 10 µM, collagen 1 µM, and thrombin 0.06 NIH Unit/mL as agonists. Multiple logistic regression was used to evaluate the independent relationship between demographic, clinical, endoscopic, and laboratory data and in vitro assessment of platelet reactivity and local parameters of hemostasis in patients with ulcer bleeding.
Results: Analysis of platelet aggregation in patients with gastroduodenal ulcer bleeding allowed the variability of platelet response to different agonists used in effective concentration which induces 50% platelet aggregation (EC₅₀) to be established. The relationship between platelet aggregation and the spatial-temporal characteristics of ulcers complicated by bleeding was demonstrated. Adrenoreactivity of platelets was associated with time elapsed since the start of ulcer bleeding and degree of hemorrhage. The lowest platelet response to collagen and thrombin was detected in patients with active bleeding (P< 0.001) and unsustainable recent bleeding (P < 0.01). Decreased adenosine diphosphate-induced platelet aggregation in patients with ulcer bleeding was correlated with the platelet response to thrombin (r = 0.714, P < 0.001) and collagen (r = 0.584, P < 0.01).
Conclusion: Estimation of platelet reactivity in vitro indicates the key mechanisms of failure of hemostasis in patients with ulcer bleeding. In addition to gender, an important determinant of unsustainable hemostasis was a decreased platelet response to thrombin and adenosine diphosphate.

Keywords: ulcer, hemostasis, blood platelets