LAUSR

We thank Kucukseymen et al for their interest in our article. Although the etiology of coronary artery ectasia (CAE) is not well understood, atherosclerosis can be assumed as an important component of the process. Also, inflammation is a crucial stage in the atherosclerotic process. Several studies have reported a relationship between CAE and systemic inflammation. For example, Turhan et al reported a link between C-reactive protein and CAE. The aim of our study was to test the potential association of serum endocan level with CAE. We demonstrated that a higher endocan level reflects the presence and severity of isolated CAE. We certainly agree that inflammation may affect the endocan level independently. However, we had mentioned in the Limitation section that our study population was small and its design did not allow us to discuss in detail the pathological mechanisms of increased endocan levels in this population. Furthermore, we excluded patients with inflammatory and infectious diseases, and the neutrophil-to-lymphocyte ratio, a simple index of systemic inflammatory response, was similar in the 2 groups of our study. Our study was designed as a pilot study, with some inevitable confounding factors. Therefore, further larger studies are needed to detect a causal relation between endocan and isolated CAE. References