Barinov Edward, Sulaieva Oksana, Lyakch Yuriy, Guryanov Vitaliy, Kondratenko Petr, Radenko Yevgeniy
Department of Histology, Cytology, and Embryology, Donetsk, Ukraine.
Clin Exp Gastroenterol. 2013 Aug 5;6:139-48. doi: 10.2147/CEG.S45685. eCollection 2013.
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.
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.
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).
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.
本研究旨在通过使用人工神经网络对血小板反应性进行体外评估，确定与胃十二指肠溃疡出血患者止血不可持续风险相关的因素。
对合并出血的胃十二指肠溃疡患者进行研究。使用比浊法测量血小板聚集，以5 μM二磷酸腺苷、2.5 μM肾上腺素、10 μM 5-羟色胺、1 μM胶原蛋白和0.06 NIH单位/mL凝血酶作为激动剂。采用多因素逻辑回归评估人口统计学、临床、内镜和实验室数据与溃疡出血患者血小板反应性体外评估及局部止血参数之间的独立关系。
对胃十二指肠溃疡出血患者的血小板聚集分析确定了血小板对有效浓度诱导50%血小板聚集（EC50）的不同激动剂反应的变异性。证明了血小板聚集与合并出血的溃疡的时空特征之间的关系。血小板的肾上腺素反应性与溃疡出血开始后的时间及出血程度相关。在活动性出血患者（P < 0.001）和近期止血不可持续患者（P < 0.01）中检测到对胶原蛋白和凝血酶的血小板反应最低。溃疡出血患者中二磷酸腺苷诱导的血小板聚集降低与血小板对凝血酶（r = 0.714，P < 0.001）和胶原蛋白（r = 0.584，P < 0.01）的反应相关。
体外评估血小板反应性表明溃疡出血患者止血失败的关键机制。除性别外，止血不可持续的一个重要决定因素是血小板对凝血酶和二磷酸腺苷的反应降低。
