| Hi all. Usually when a med is prescribed to me by any other doc except my hem I always ask if it affect platelets or not. I was taking Effexor for a month and I asked my pain doc if it'll affect my platelets or can trigger TTP. He said no, so I took it. When it came time to refill it, my insurance will no long pay for it. So. he calls the pharmacy A WEEK LATER and orders Paroxetine HCL aka Paxil GSK. I never had the chance to remind him if it's ok on platelets. I have been taking it since Monday and it is now I find myself wondering about this drug. Here is what I found... Paroxetine decreases platelet serotonin storage and platelet function
in human beings.Clinical pharmacology and therapeutics 2000;68(4):435-42.
BACKGROUND:
Serotonin is a platelet agonist and potent vasoconstrictor that has
recently received attention concerning its potential role in acute
coronary artery thrombosis. Selective serotonin-reuptake inhibitors,
such as paroxetine, are widely used antidepressant agents. We sought to
characterize the potential inhibitory effect of paroxetine on platelet
function. METHODS: Healthy male volunteers received 20 mg/d paroxetine
for 2 weeks in a randomized, double-blind, placebo-controlled, two-way
cross-over trial. RESULTS: Paroxetine decreased intraplatelet serotonin
concentrations by -83% (P < ..01). This inhibited platelet plug
formation as reflected by a 31% prolongation of closure time measured
with the platelet function analyzer-100 (P < .05). Furthermore,
paroxetine lowered expression of the platelet activation marker CD63 in
response to two different concentrations of thrombin
receptor-activating peptide (P < .01). Plasma concentrations of
prothrombin fragment, von Willebrand factor antigen, and circulating
P-selectin remained unchanged in either period, indicating that
paroxetine does not increase activation of coagulation, endothelium, or
platelets in vivo, underlining a favorable safety profile. CONCLUSIONS:
Paroxetine substantially decreases intraplatelet serotonin content and
thereby reduces platelet plug formation under shear stress, and
responsiveness to thrombin receptor activating peptide-induced platelet
activation. Further studies will reveal whether these pharmacodynamic
effects can be exploited for treatment of thrombotic artery disease. AS AN OBSERVATION IT IS ALWAYS GOOD TO CHECK ON THESE THINGS I USE PAROXETINE AND PLATELETS AS KEY WORDS. I WILL CALL MY HEMA TO FIND IF THIS IS A MED I SHOULD KEEP USING BECAUSE THIS INTRAPLATELET SEROTONIN THING HAS ME WONDERING. HP TO ALL ![]() |

