Acetylcholinesterase and butyrylcholinesterase as markers of low-grade systemic inflammation.

Low-grade systemic inflammation plays a significant role in the pathogenesis of insulin resistance, type 2 diabetes mellitus, hypertension, hyperlipidemias, Alzheimer’s disease, proliferative diabetic retinopathy; age-related macular degeneration, minimal change nephropathy and various rheumatological conditions.1,2 Hence, development of reliable, unique and robust markers is essential. In this context, I noted that plasma and/or tissue levels of acetylcholinesterase and butyrylcholinesterase activities could form reliable indices to detect and diagnose the existence of low-grade systemic inflammation in all the above-mentioned conditions.3,4 The work of Lampón, et al.5 published in the present issue wherein they observed a significant positive correlation between butyrylcholinesterase (BChE) and hs-CRP though, for hsCRP concentrations > 3 mg/L the correlation between these variables (BChE and hsCRP) was found to be significantly negative (p < 0.001), as in patients with acute inflammation (hsCRP > 10 mg/L) is in support of this contention. It is interesting that BChE activity was negatively correlated with hsCRP when the latter levels are more than 3 mg/L. The close positive correlation seen between BChE and plasma albumin concentrations not only suggests that hepatic tissue produces these two molecules in a coupled fashion but also implies that when the albumin synthesis is interfered with BChE may not a reliable marker of inflammation. CHOLINESTERASE AND BUTYRYLCHOLINESTERASE