Familial Mediterranean Fever as an Emerging Clinical Model of Atherogenesis Associated with Low-Grade Inflammation

Şahru Yüksel1, *, Lilit Ayvazyan2, Armen Yuri Gasparyan3
1 Boğaziçi University, Department of Molecular Biology and Genetics, Istanbul, Turkey
2 Yerevan State Medical University, Yerevan, Armenia
3 Dudley Group of Hospitals NHS Foundation Trust, West Midlands, UK

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© Yüksel et al.; LicenseeBentham Open.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

* Address correspondence to this author at the Boğaziçi University, Department of Molecular Biology and Genetics, 34342 Bebek/Istanbul, Turkey; Tel: +90(212) 359-77-84; Fax: +90 (212) 287-2468; E-mail:


Numerous inflammatory and innate immune pathways are involved in atherogenesis. Elaboration of clinical models of inflammation-induced atherogenesis may further advance our knowledge of multiple inflammatory pathways implicated in atherogenesis and provide a useful tool for cardiovascular prevention. Familial Mediterranean fever (FMF) is a chronic inflammatory disorder with profiles of inflammatory markers close to that seen in the general population. In a few recent studies, it has been shown that endothelial dysfunction, increased atherosclerotic burden and activation of platelets accompany attack-free periods of FMF. Colchicine is proved to be useful in suppression of inflammation in FMF. Preliminary basic and clinical studies suggest that this relatively safe drug may be useful for cardiovascular protection in patients with FMF and in the general population. Multinational prospective studies are warranted to further elaborate clinical model of inflammation-induced atherosclerosis associated with FMF.

Keywords: Familial mediterranean fever, atherosclerosis, endothelial dysfunction, neutrophils, platelets, colchicine..