Prostate Tissue-Induced Platelet Activation and Platelet–Neutrophil Aggregation Following Transurethral Resection of the Prostate Surgery: An In Vitro Study

Background: This study aimed to investigate the effects of prostate tissue on platelet activation markers, primarily assessed through P-selectin expression, and to assess the formation of platelet–leukocyte aggregations in response to prostate tissue exposure. Furthermore, we compared platelet activation induced by prostate tissue homogenates with that induced by thrombin stimulation. These processes may play a role in the development of disseminated intravascular coagulation (DIC) following transurethral resection of the prostate (TURP). Methods: We collected prostate tissue samples from 12 patients undergoing TURP. The samples were homogenized and used to stimulate platelet-rich plasma in vitro. Flow cytometry was used to measure platelet P-selectin expression and platelet–leukocyte aggregation. Additionally, four experimental groups were established: (A) saline control, (B) thrombin stimulation, (C) phosphate-buffered saline (PBS) control, and (D) prostate tissue homogenate. Data were analyzed to assess the impact of prostate tissue and thrombin on platelet activation and platelet–leukocyte interactions. Results: Prostate tissue homogenates significantly increased platelet P-selectin expression and platelet–neutrophil aggregation compared with the control groups (p < 0.05). Overall, platelet–leukocyte aggregation was not significantly different between the thrombin and prostate tissue groups. However, prostate tissue exposure did not significantly affect platelet–monocyte and platelet–lymphocyte aggregations. Conclusions: Prostate tissue exposure during TURP induces platelet activation, particularly platelet P-selectin expression and platelet–neutrophil aggregation, suggesting a potential mechanism for DIC development. These findings highlight the importance of monitoring platelet activity in patients undergoing TURP and indicate that interventions targeting platelet P-selectin expression and platelet–neutrophil interactions may help mitigate DIC risk.