The Effect of Human Prostate Tissue on Platelet CD40 Ligand, Toll-like Receptor 4, P-selectin and Platelet-Leukocyte Aggregation: an In Vitro Study

Transurethral resection of the prostate (TURP) is a common and standard urological surgical procedure for managing benign prostatic hyperplasia (BPH). Although surgical technology improved in recent decades, severe complications such as TURP syndrome, hematuria, and postoperative hemorrhage were still considerable. Coagulopathy is one of rare but devastating complication which may contribute to bleeding during and after TURP. Although the exact pathophysiological condition of coagulopathy is not clear, there are several possible mechanisms of TURP associated coagulopathy including: urokinase- (u-PA) and tissue-type plasminogen activator (t-PA)-related fibrinolysis; absorption of irrigating fluid associated dilutional coagulopathy; release of prostatic particles rich in tissue thromboplastins into the circulation causing secondary fibrinolysis and disseminated intravascular coagulopathy (DIC); sepsis with DIC associated with bacteria entering the circulation due to prostatic venous sinuses opening and the using of high pressure irrigation. On the other hand, platelet are essential to hemostasis and thrombosis and its activation also contributes to leukocyte recruitment and DIC. Furthermore, previous studies demonstrated that activated platelets could express TLR4, CD40L, P-selectin and induce platelet-leukocyte aggregation (PLA), which were considered important for systemic inflammatory responses and DIC development. Currently, no study investigating the association of prostate particle and platelet activation. Here, we tested the hypothesis that prostate tissue may induce inflammatory responses through platelet activation by measuring the expression of TLR4, CD40L, P-selectin and PLA on platelets.