Prospective analysis shows differences in platelet aggregation in response to NSAIDs in nephrolithiasis, suggesting nuanced COX impact.
Objective: to reveal the dependence of the efficiency of platelet (PL) aggregation on crosstalk between signaling pathways associated with stimulation of the thromboxane receptor (TxR) and purine P2 receptors at different activity of cyclooxygenase (COX) during the administration of non-steroidal anti-inflammatory drugs (NSAIDs) in patients with nephrolithiasis (NLT). Materials and Methods. Our study was prospective in its nature. It included 60 patients with NLT who were prescribed non-selective NSAIDs as part of medical expulsive therapy (MET) for analgesia. The cohort of patients was distributed among two groups: with effective (Group 1, n=30) and ineffective (Group 2, n=30) COX inhibition. The activity of the TxR and purine P2 receptors (P2X1 and P2Y receptors) of PL was assessed on a Chrono-Log Hematology Analyzer (USA). Agonists (adenosine triphosphate, adenosine diphosphate and arachidonic acid) were used at EC50 and EC10 concentrations. Results. In Group 1, after 72 hours of MET, the activity of the TxR and P2 receptors of PL decreased to the level of hyporeactivity. Regulation of the compensatory response of PL to hematuria was ensured through the synergism of P2X1 and P2Y receptors, TxR, and P2X1 receptors. In Group 2, after 72 hours of MET, the hyperreactivity of the TxR and P2 receptors persisted. The maximum increase in PL aggregation was achieved with synergism between the TxR and P2Y receptors. Conclusion. The effectiveness of PL aggregation in hematuria of patients with NLT during the administration of NSAIDs is determined by intracellular signaling associated with the TxR and P2 receptors.
No takes yet. Share an insight, caveat, or question.
Баринов et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: