Abstract :
Familial Mediterranean fever (FMF) is an autosomal recessive disorder resulting in improper leukocyte clearance during
inflammation. The disease often presents in early childhood and
is characterized by recurrent attacks. Current treatment includes
suppression of inflammation by colchicine. Typical to other rheumatological diseases, FMF is characterized by elevated white
blood cell (WBC) count, erythrocyte sedimentation rate (ESR),
and serum pro-inflammation markers, such as C-reactive protein
and fibrinogen (1). These factors are responsible for increased
leukocyte trafficking, vascular permeability, and endothelial dysfunction. These cellular consequences can fundamentally alter
the elastic properties of blood vessels. Indeed, rheumatological
diseases with recurrent inflammatory attacks, such as FMF, are
associated with increased arterial stiffness (2)