Association of mitral annular calcification with fetuin-A levels

We read the article, entitled “Association of mitral annular calcification with endothelial dysfunction, carotid intima-media thickness, and serum fetuin-A: An observational study,” by Ziyrek et al. (1) in Anatolian J Cardiol 2013; 13: 752-8, in which they reported that their findings might reflect a close association between mitral annular calcification and cardiovascular risk factors in patients with coronary artery disease, based on fetuin-A and carotid intima-media thickness evaluation (1). We thank the authors for their valuable contribution to the medical literature. However, we want to point out an important issue about fetuin-A. Fetuin-A, an acute-phase glycoprotein that is synthesized and secreted by liver, plays a role in bone mineralization and insulin signaling regulation (2). Serum fetuin-A concentration is a good indicator of liver cell function, and it ranges from approximately 450-600 μg/mL in healthy individuals (3). The authors defined mean fetuin-A levels as 2.9±0.1 ng/mL and 3.0±0.2 ng/mL for the MAC group and control group, respectively. In this respect, though lots of previous studies, this study offered approximately 10,000-fold lower mean fetuin-A values, which could not be acceptable. It is already defined in the commercial ELISA kit that the authors used for the fetuin-A measurement that the measured concentration of samples calculated from the standard curve must be multiplied by their respective dilution factor, because the samples were diluted prior to the assay. Most likely, we think that the fetuin-A values of the study are derived from this post-analytical error. In conclusion, to prevent any misunderstanding, an explanation of this concern will certainly provide clearer information for the readers.