Department of Endocrinology, Yuzuncu Yil University, Van, TurkeyYalcinkaya and Celik comment on the issue of theimpact of aspirin esterase on aspirin resistance (1). Itis probable that previous observations regardinghydrolysis of aspirin could be an underlying alterna-tive explanation, which supports the relationshipbetween high total cholesterol levels and aspirin resis-tance in our study.The authors raise concerns about the relationshipbetween inflammation and aspirin resistance. Incontrast to what is claimed, in our study diabeticand non-diabetic subjects were comparable in termsof inflammatory conditions mentioned by Yalcinkayaand Celik such as hypertension (79.6% versus 70.3%,respectively, p = 0.26, data not shown in article),coronary heart disease (34.4% versus 32.4%, respec-tively, p = 0.83), and American Heart Association/American College of Cardiology stage C or D chronicheart failure (15.1% versus 16.2%, respectively,p = 0.87, data not shown) (2). Since these conditionsshow collinearity and most previous studies exploringaspirin resistance were performed in patients withischemic heart disease, we just included the presenceof coronary heart disease as a potential predictor ofaspirin resistance (3). Among other suggested inflam-matoryconditionssuggested,noneofourpatientshada previous history of stroke; only one diabetic malesufferedfromaprimaryReynaudphenomenon,whichwas not associated with any connective tissue disease.Serum levels of more sensitive and certain experi-mentalinflammatorymarkers,suchasinterleukin-6orhigh-sensitivity C-reactive protein, and markers ofoxidative stress may have a relationship with aspirinresistance. However, we presume that the clinicallysignificant effect size of the aforementioned factors onaspirin resistance would be small, if any, due to thepresence of low numbers of patients with so-calledinflammation(i.e.coronaryheartdisease)inourstudy.Yet,YalcinkayaandCelikarerightabouttheimpactofinflammation on aspirin resistance, since the inflam-mation is closely related with platelet activation.Finally, we conducted this study to explore theeffects of overt diabetes mellitus (DM) instead ofinsulin resistance on aspirin resistance. Perhaps thecomparable frequency of insulin resistance resulted ina comparable frequency of aspirin resistance in bothgroups. No matter what, our primary interest was therelationship, not the causality. Demonstration ofsuch an effect of insulin resistance instead of DM onaspirin resistance nevertheless would not change ourconclusion.Declaration of interest: The authors report noconflictsofinterest.Theauthorsaloneareresponsiblefor the content and writing of the paper.References