Desmoid Tumors and Celecoxib with Sorafenib

Abstract

To the Editor: In the Study of Platelet Inhibi-tion and Patient Outcomes (PLATO), Wallentin et al. (Sept. 10 issue) 1 found that in patients with acute coronary syndromes, the use of ticagrelor, as compared with clopidogrel, significantly re-duced the rate of death, myocardial infarction, or stroke without increasing the rate of bleeding. Ticagrelor, a direct-acting oral antagonist of the adenosine diphosphate receptor, was associated with adverse events, including dyspnea, ventricu-lar pauses, and increased levels of creatinine and uric acid. Although the mechanism of these ef-fects is unknown, components of the molecular structure of ticagrelor are almost identical to those of adenosine, which can be degraded to uric acid, and it is conceivable that metabolites of ti-cagrelor activate adenosine receptors. It is well known that adenosine induces dyspnea by broncho-con striction, 2 depresses the atrioventricular node, 3 and causes deterioration in renal function by ar-teriolar constriction. 4 These adverse events were generally self-limiting, but discontinuation of the study drug because of adverse events occurred more frequently in the ticagrelor group than in the clopidogrel group. Since only 4.1 to 5.9% of the study patients had chronic renal disease, con-gestive heart failure, or obstructive pulmonary disease, the adverse effects of ticagrelor require further evaluation.