PUB - Publikationen an der Universität Bielefeld

Treatment failure due to variability in the pharmacologic response to drugs has more commonly been attributed to non-genetic factors than to prototypic pharmacogenetic mechanisms.1 Treatment failure on low-dose aspirin taken to prevent arterial thrombotic events, including myocardial infarction and stroke, is no exception. A closer look at aspirin’s human pharmacology reveals many potential sources of variability that are rooted in platelet biology, from aspirin insensitive mechanisms of activation to accelerated turnover.