Background: Inflammation plays an important role in the development of atherosclerotic vascular disease which is the leading cause of morbidity and mortality in the adult population. Several adhesion molecules, cytokines and growth factors secreted from the endothelium aggravate inflammation and increase subendothelial lipid accumulation. With continuing inflammation, plaque rupture occurs resulting in acute coronary syndromes. Several clinical trials have shown that suppression of the inflammatory response can delay or decrease the atherosclerotic process.

Objectives: The aim of this study is to compare carotid intima-media thickness (CIMT) between the patients with chronic disease history and gout using colchicine and the patients with cardiovascular risk factors.

Methods: 102 patients (85 female, 17 male) were included. There was two groups in the study: Group 1: the patients with gout using colchicine (0,5 mg twice a day for at least 6 months) and having any chronic disease (followed by Physical Therapy and Rehabilitation); Group 2: the patients with cardiovascular risk factors followed for at least 1 year (followed by Cardiology). All patients underwent B-mode ultrasonography via high resolution linear probe for the measurements of CIMT. Additionally, the serum concentrations of C-reactive protein (CRP) and the levels of lipids such as cholesterol, triglycerid, low-density lipoprotein (LDL), high-density lipoprotein (HDL) were measured.

Results: The mean age of patients was 62.35±6.68 years and 64.27±5.32 years in Group 1 and in Group 2, respectively. There was also no statistically significant difference in the levels of lipids between groups (p>0.05). The value of CIMT (mm) and CRP (mg/dL) in Group 1 and Group 2 were 0.99±0.20 and 0.26±0.14, 1.18±0.15 and 0.58±0.42, respectively. There was statistically significant difference between groups (p<0.05).

Conclusion: Colchicine has anti-inflammatory properties, including both the inhibition of key inflammatory signaling networks, known as the inflammasome (NLRP3) and proinflammatory cytokines (such as IL-1β and IL-18), and an anti-tubulin effect that inhibits neutrophil function and chemotaxis. Thus, it could have a role in preventing the transformation of a stable plaque to an unstable plaque by inhibiting a neutrophil-mediated inflammatory pathway. It is seemed to colchicine in addition to statins and other standard therapies is an effective treatment for the prevention cardiovascular and serebrovascular events in the patients with cardiovascular risk factors. Further studies are needed to detect the dosage and using duration of colchicine in the treatment of atherosclerosis.

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[3] Martínez GJ, Robertson S, Barraclough J, Xia Q, Mallat Z, Bursill C, Celermajer DS, Patel S. Colchicine Acutely Suppresses Local Cardiac Production of Inflammatory Cytokines in Patients With an Acute Coronary Syndrome. J Am Heart Assoc. 2015; 4(8): e002128. doi: 10.1161/JAHA.115.002128.

[4] Vaidya K, Arnott C, Martínez GJ, Ng B, McCormack S, Sullivan DR, Celermajer DS, Patel S. Colchicine Therapy and Plaque Stabilization in Patients With Acute Coronary Syndrome: A CT Coronary Angiography Study. JACC Cardiovasc Imaging. 2018; 11(2 Pt 2): 305-316. doi: 10.1016/j.jcmg.2017.08.013.

Figure 1.

Ultrasonographic examination of carotid intima media thickness.

Acknowledgements: NIL.

Disclosure of Interests: None declared.

© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.