Insulin resistance and metabolic syndrome frequency in familial mediterranean fever patients

Familial Mediterranean Fever (FMF) is an autosomal recessive genetic disorder characterized by localized or systemic inflammation and characterized by serous membrane involvement such as recurrent peritonitis, arthritis and pleuritis. Although the disease progresses clinically with episodes, there are many studies showing that the level of acute phase reactants, cytokines and other inflammatory proteins increases during the episode-free period and the underlying subclinical inflammation in FMF. Metabolic syndrome (MetS) is a condition with high risks for the development of atherosclerosis and cardiovascular diseases characterized by glucose tolerance disorder, abdominal obesity, hypertension, atherogenic dyslipidemia, prothrombotic and proinflammatory conditions. (ID) has been supported by many studies to date to the view that it is the cornerstone of the pathogenesis of MetS. Many of the pro-inflammatory cytokines involved in chronic inflammation play a role in the etiopathogenesis of insulin resistance. In many rheumatologic diseases with chronic inflammation, it is thought that the inflammatory component is the cause of the association of metabolic syndrome and insulin resistance. However, studies investigating the frequency of increased metabolic syndrome and insulin resistance in FMF are limited and this relationship is not clear. In this study, we aimed to show whether the frequency of metabolic syndrome and insulin resistance in FMF patients differed from healthy individuals. In our study 50 fmf patients and 50 healthy control groups with similar demographic characteristics who applied to Gaziosmanpasa University Faculty of Medicine Internal Medicine outpatient clinic were compared. BMI, waist circumference, lipid parameters, fasting blood glucose, insulin level and insulin resistance, peripheral arterial blood pressure levels, disease duration, colchicine use and smoking were evaluated in both groups. MetS was evaluated using NCEP-ATP III diagnostic criteria and ID was evaluated using HOMA-IR formula. Although the incidence of metabolic syndrome and insulin resistance was higher in FMF patients, there was no statistically significant difference. In the comparison between the patient and healthy control group, no significant difference was observed except that the LDL level was statistically high (p = 0.046) in the control group. No significant effect of smoking, duration of disease and colchicine v dose on the incidence of metabolic syndrome and insulin resistance was observed in FMF patients. When AAA patients were divided into two groups with and without metabolic syndrome and insulin resistance, as expected, significant differences were observed between the two groups in terms of metabolic parameters, but no significant differences were observed in terms of colchicine dose and disease duration. In conclusion, although it is a chronic autoinflammatory and subclinical inflammation, the prevalence of metabolic syndrome and insulin resistance in FMF is not different from healthy individuals, unlike many other chronic inflammatory diseases. More comprehensive studies are needed to determine the effect of pathogenesis, continuous colchicine use or different underlying MEFV gene mutations on this condition.