Abstract
Drugs represent the most common cause of platelet dysfunction in our overmedicated
society. While acetylsalicylic acid (aspirin), adenosine diphosphate receptor antagonists
(clopidogrel and prasugrel), and integrin αIIbβ3 (GPIIb-IIIa) receptor blockers (abciximab,
eptifibatide, and tirofiban) are well-known prototypes of antiplatelet drugs, other
widely used agents such as nonsteroidal anti-inflammatory drugs, antibiotics, cardiovascular
and lipid-lowering drugs, selective serotonin reuptake inhibitors, and volume expanders
can also impair platelet function and thus cause or aggravate hemorrhages in certain
clinical settings. Therefore, induction of a bleeding diathesis remains a significant
concern. This is especially relevant in patients with preexisting hemostatic defects
of any kind, which may remain compensated as long as platelet function (and/or coagulation)
is not inhibited pharmacologically. Identification of individual patients with preexisting
hemostatic defects remains crucial (1) to prevent otherwise unexpected bleeding complications,
(2) to manage hemorrhagic symptoms adequately, (3) to minimize the risk from invasive
procedures, and (4) to avoid unnecessary patient exposure to blood products. This
article provides a review of the large variety of agents that have not been designed
for antiplatelet therapy but nevertheless interfere with platelet reactivity or induce
platelet inhibition. In particular, drug interactions and mechanisms by which these
agents can trigger or cause platelet dysfunction are detailed.
Keywords nonsteroidal anti-inflammatory drugs (NSAIDs) - antibiotics - cardiovascular and lipid-lowering
drugs - psychotropic agents - drug interactions
