http://www.TurkJBiochem.com ISSN 1303–829X (electronic) 0250–4685 (printed) 43 C-Reactive protein vs. high - sensitivity C - reactive protein: What is the difference? [C-Reaktif protein ve yüksek duyarlıklı CRP: Fark nerede?] Editorial [Editörden] Yayın tarihi 30 Mart, 2014 © TurkJBiochem.com [Published online 30 March, 2014] doi: 10.5505/tjb.2014.92408 Türk Biyokimya Dergisi [Turkish Journal of Biochemistry–Turk J Biochem] 2014; 39 (1) ; 43–44 Doğan Yücel Dept. of Medical Biochemistry, Ankara Training and Research Hospital, Cebeci, Ankara Yazışma Adresi [Correspondence Address] ??? ????? Registered: 22 April 2013; Accepted: 13 November 2013 [Kayıt Tarihi: 22 Nisan 2013; Kabul Tarihi: 13 Kasım 2013] C-reactive protein (CRP) is an acute phase reactant produced by liver under the control of cytokines, especially by interleukin-6. CRP is commonly measured as a non-specific acute phase protein in inflammatory, infectious and neoplastic cases and in tissue damage for a long time. CRP is present in plasma at a concentration <5 mg/L and concentrations >5 to 10 mg/L show the presence of overt infection or inflammation [1,2]. In healthy young adult volunteers the median CRP concentration is 0.8 mg/L, the 90 th percentile is 3.0 mg/L, and the 99 th percentile is 10 mg/L, and following an acute phase case, CRP concentrations may increase 10 000-fold [3]. CRP is measured by immunoassays, mostly by immunoturbidimetric and nephelometric techniques for routine monitoring of infectious or inflammatory processes, and detection limits of these assays are 3 to 5 mg/L [4]. In the mid-1990s, more sensitive CRP immunoassays than those previously used were developed by use of ultrasensitive ELISA or particle - enhanced techniques and these assays were named as “high-sensitivity” or “highly sensitive” CRP (hs-CRP). In general, detection limits of these assays are <0.3 mg/L and limits of quantification are in a concentration range of 0.11 to 0.31 mg/L [5]. Currently, within - laboratory analytical imprecision of hs-CRP assays are less than 10% [2]. It has been well established that inflammation is essential for cardiovascular disease pathogenesis [3]. In this connection, in the last 15 - 20 years, several prospective epidemiologic studies have demonstrated that hs-CRP is an indicator of upcoming vascular events such as acute myocardial infarction, stroke or peripheral vascular disease [6-10]. Hs-CRP is also associated with diabetes mellitus, metabolic syndrome, hypertension, and obesity [11- 13]. Based on this information, hs-CRP is accepted as a biomarker for the assessment of cardiovascular risk and proposed as a component of Reynolds Risk Score for calculation of 10 years risk in addition to age, blood pressure, cholesterol concentration, smoking, and genetic susceptability [14]. In summary, hs-CRP is a cardiovascular risk biomarker rather than an overt inflammatory biomarker. However, currently, use of hs-CRP for this aim is highly critisized because of high individual biological variability of CRP and relatively high assay imprecision [15-17]. Fortunately, the assay calibrators are traceable to WHO Reference Material 85-506, so there is not a harmonisation problem presently. In this issue of Turkish Journal of Biochemistry, Günal et al. [18] present a study on some inflammatory markers and acute phase reactants such as neopterin, procalcitonin, erythrocyte sedimentation rate, and hs-CRP during