Familial Mediterranean fever (FMF) is a self-limiting autoinflammatory disease with well-defined genetic and clinical features. Recurrent episodes of fever and serositis accompanied by increased acute phase reactants and good response to colchicine are the core components of the disease. The frequency of this disease, which is common in Eastern Mediterranean countries, is variable according to regions, but it is reported as 1/1000. In the pathogenesis of the disease, the mutation of the MEFV (Mediterranean Fever) gene, which is located on the 16th chromosome and encodes the pyrin protein, is known as the basic mechanism.In rheumatic diseases, inflammatory mediators cause CS by first creating changes in the regulation of pain in peripheral neurons and then in spinal and supraspinal pathways. Stimulation of peripheral nerves by mediators released during inflammation results in neurogenic inflammation, which is among the peripheral sensitization (PS) mechanisms. PS is defined as the increased sensitivity of nociceptive neurons to normal or below-threshold stimuli and constitutes the first step in the development of CS.Similar to other autoimmune diseases, it is possible that the neuroinflammatory process triggers peripheral and central sensitization mechanisms in FMF patients and affects pain pathways.
Familial Mediterranean Fever (FMF) is an autosomal recessive inherited disease with a course of autoinflammation, which is characterized by the episodes of fever and serositis. Central sensitization (CS) is defined as increased response to normal or sub-threshold stimuli of central nervous system and its close relationship with many rheumatological diseases has been demonstrated in several studies. However, there are no data on the frequency of CS in FMF patients.