Selective serotonin reuptake inhibitors reduce P2Y12 receptor-mediated amplification of platelet aggregation

Prescription drugs associated with false-positive results when using faecal immunochemical tests for colorectal cancer screening

“…Consistent with our previous study of FP results with the guaiac test [6], the risk of FP results with the FIT increased with successive screening, while women showed a two-fold greater likelihood of a FP compared with men. We wanted to gather information regarding prescription drug use because our initial hypothesis was that SSRI use, due to its effect on platelet aggregation [12], could explain the difference between the sexes because they are prescribed more often to women. Also, there is evidence that SSRIs may be associated with upper gastrointestinal bleeding, especially when used concurrently with NSAIDs, APAs or OACs [33][34][35].…”

“…For instance, drugs with potential haemorrhagic risk may increase the FP rate, and some studies have already shown that antiplatelet agents (APAs) [7][8][9], oral anticoagulants (OACs) [8][9][10][11] and/or non-steroidal anti-inflammatory drugs (NSAIDs) [5] can affect FIT results. Therefore, other drugs associated with gastrointestinal bleeding, such as selective serotonin reuptake inhibitors (SSRIs) which affect platelet aggregation [12] and proton pump inhibitors (PPIs) which may cause haemorrhage in the lower gastrointestinal tract [13][14][15][16][17], could affect the FP rate. In this study, we aimed to identify factors associated with FP results in a FIT-based CRC screening programme, with special attention given to prescription drugs.…”

Blood cells: an historical account of the roles of purinergic signalling

“…It was suggested that cAMP regulates ADPstimulated platelet activation due to inhibition of heat shock protein (HSP) 27 phosphorylation via p38 mitogen-activated protein MAP kinase [262]. 5-HT reuptake inhibitors reduce P2Y 12 receptor-mediated amplification of platelet aggregation [263]. Inhibition of P2Y 12 receptors potentiated the antiplatelet effect of prostacyclin [264].…”

Characterization of a Novel Function-Blocking Antibody Targeted Against the Platelet P2Y 1 Receptor

“…Two G-protein coupled receptors, P2Y 1 and P2Y 12 are required for full ADP-induced platelet aggregation, but each of these receptors plays a different role in this process 2,3 . P2Y 1 receptor (P2Y 1 R) triggers a rapid and transient intracellular calcium increase which causes platelet shape change and initiates the process of platelet activation 4,5,6 . P2Y 12 receptor (P2Y 12 R) mediates a slower and more sustained decrease in cyclic adenosine monophosphate (cAMP), which amplifies and consolidates ADP-driven platelet activation 4,5,7 .…”

“…P2Y 1 receptor (P2Y 1 R) triggers a rapid and transient intracellular calcium increase which causes platelet shape change and initiates the process of platelet activation 4,5,6 . P2Y 12 receptor (P2Y 12 R) mediates a slower and more sustained decrease in cyclic adenosine monophosphate (cAMP), which amplifies and consolidates ADP-driven platelet activation 4,5,7 . Co-activation of both P2Y 1 R and P2Y 12 R is required for a complete platelet response; however, blockade of either receptor significantly decreases ADP-induced platelet aggregation and thrombosis 8,9 .…”