European Journal of Rheumatology
Original Article

Serum lipid changes and insulin resistance in familial Mediterranean fever

1.

Department of Rheumatology, Hacettepe University Faculty of Medicine, Ankara, Turkey

2.

Department of Infectious Diseases, Hacettepe University Faculty of Medicine, Ankara, Turkey

3.

Department of Radiology, Hacettepe University Faculty of Medicine, Ankara, Turkey

4.

Department of Internal Medicine, Hacettepe University Faculty of Medicine, Ankara, Turkey

5.

Department of Rheumatology, Hacettepe University Faculty of Medicine, Ankara, Turkey; Department of Internal Medicine, Hacettepe University Faculty of Medicine, Ankara, Turkey

6.

Division of Rheumatology, Department of Internal Medicine, Hacettepe University Faculty of Medicine, Ankara, Turkey

Eur J Rheumatol 2014; 1: 140-143
DOI: 10.5152/eurjrheumatol.2014.140045
Read: 2945 Downloads: 1390 Published: 03 September 2019

Abstract

Objective: Inflammation is known to alter lipid profiles and to induce insulin resistance. This study was planned to test the hypothesis that familial Mediterranean ferver (FMF) patients and their first-degree asymptomatic relatives may have lipid profile changes and/or insulin resistance, similar to other inflammatory diseases.

 

Material and Methods: We studied 72 FMF patients, 30 asymptomatic first-degree relatives, and 75 healthy controls. Fasting and 2-hour postprandial glucose, insulin, apolipoprotein (Apo) A1, Apo B, acute phase reactants, and lipid profiles of all subjects were studied. Insulin resistance was determined by the HOMA (Homeostasis Model Assessment) index.

 

Results: There was no difference between the groups with regard to sex, mean systolic and diastolic blood pressure, body mass index, smoking status, fasting and postprandial 2-hour glucose, insulin, acute phase reactants, and HOMA index levels. High-density lipoprotein cholesterol (HDL-C) levels were similar between FMF patients and FMF relatives (48.9±12.4 mg/dL vs 49.3±13.8 mg/dL; p=NS), and both were lower than controls (48.9±12.4 mg/dL vs 59.6±15.1 mg/dL; p<0.001 and 49.3±13.8 mg/dL vs 59.8±15.1 mg/dL; p=0.001, respectively). Apo A1 levels in FMF patients and asymptomatic first-degree FMF relatives were both lower than in controls, similar to the HDL-C levels (126.1±25.7 mg/dL vs 151.2±31.4 mg/dL; p<0.001 and 129.5±29.0 mg/dL vs 151.2±31.4 mg/dL; p=0.002, respectively). TG levels were significantly higher in FMF relatives as compared to controls (113.4±53.6 mg/dL vs 97.1± 54.9 mg/dL; p=0.025).

 

Conclusion: Low HDL-C and low Apo A1 levels are found in FMF patients and their first-degree asymptomatic relatives. Low-grade inflammation caused by MEFV mutations may be responsible for these lipid profile changes.

 

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EISSN 2148-4279