Short-term effect of low-dose colchicine on inflammatory biomarkers, lipids, blood count and renal function in chronic coronary artery disease and elevated high-sensitivity C-reactive protein.

Inflammation plays a pivotal role in atherothrombosis. Colchicine is an anti-inflammatory drug that may attenuate this process. Cardiovascular protective effects of anti-inflammatory drugs, however, seem to be limited to patients with a biochemical response. We therefore investigated whether short-term exposure to colchicine reduced inflammatory markers and whether additional laboratory changes occur in patients with chronic coronary artery disease. In 138 consecutive patients with chronic coronary artery disease and a high sensitivity C-reactive Protein (hs-CRP) ≥ 2 mg/L, inflammatory markers, lipids, haematologic parameters and renal function were measured at baseline and after 30 days exposure to colchicine 0.5mg once daily. Hs-CRP decreased from baseline 4.40 mg/L (interquartile range [IQR] 2.83-6.99 mg/L) to 2.33 mg/L (IQR 1.41-4.17, median of the differences -1.66 mg/L, 95% confidence interval [CI] -2.17 - -1.22 mg/L, p-value <0.01), corresponding to a median change from baseline of -40%. Interleukin-6 decreased from 2.51 ng/L (IQR 1.59-4.32 ng/L) to 2.22 ng/L (median of the differences -0.36 ng/L, 95%CI -0.70 - -0.01 ng/L, p-value 0.04), corresponding to a median change from baseline of -16%. No clinically relevant changes in lipid fractions were observed. Both leukocyte and thrombocyte count decreased (median change from baseline -7% and -4% respectively). Estimated glomerular filtration rate decreased with a mean change from baseline of -2%. In patients with chronic coronary artery disease and elevated hs-CRP, one-month exposure to colchicine 0.5 mg once daily was associated with a reduction of inflammatory markers. A small effect was seen on white blood cell count and platelet count, as well as a small decrease in estimated glomerular filtration rate.

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None of the authors has any financial or non-financial competing interest in relation to the research currently provided. The authors are all employed by local and academic hospitals. Additional funding for the research was provided by means of a governmental grant (The Netherlands Organisation for Health Research and Development [grant number 848015014]) and in-kind contributions from the research personnel from the participating sites. The authors received the drugs free-of-charge by TioPharma (Oud-Beijerland, the Netherlands). This commercial funder had no role in design of the study, accruement of the data, analysis of the data, drafting or reviewing of the manuscript or submission of the manuscript. There were no restrictions in interpretation or publication of the data instituted by the supplier of the drug or the governmental grant. None of the authors has financial ties with the supplier of the drugs. None of the authors has paid endorsements with the funder of the drug for consultative or marketing purposes. There are no authors with (pending) patents, stocks or shares related to the mechanisms or compounds described in the manuscript. No reimbursements for travel or educational purposes were provided by the funder of the drug. None of the authors serves or has served on the Editorial Board of PLOS ONE. None of the authors have acted as an expert witness in relevant legal proceedings. None of the authors sits or sat on a committee for an organization that may benefit from publication of the paper. None of the authors is employed as lobbyist or within advocacy companies.