Serum lipid changes and insulin resistance in familial Mediterranean fever

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

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Inflammation is known to alter lipid profiles and to induce insulin resistance.

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Key Findings & Data: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.

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Conclusion & Impact: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

🔬Design:Modeling & Simulation

📍Scope:Comprehensive Sample

⚙️Variables:Domain Parameters

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

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Cite This Article

CANDAN, Z., KALYONCU, U., KİRAZ, S., KARADAĞ, Ö., ÇALGÜNERİ, M., BİLGEN, Ş., ERTENLİ, A., AKDOĞAN, A., ŞAHİN, A. (2022). Serum lipid changes and insulin resistance in familial Mediterranean fever. European Journal of Rheumatology, Cilt: 1 - Sayı: 4, 140–143. https://ajindex.com/articles/511849

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References (2)

Touitou I. The spectrum of Familial Mediterra- nean Fever (FMF) mutations. Eur J Hum Genet 2001; 97: 473-83. [CrossRef] Livneh A, Aksentijevich I, Langevitz P, Torosyan Y, G-Shoham N, Shinar Y, et al. A single mutated MEFV allele in Israeli patients suffering from famil- ial Mediterranean fever and Behcet's disease (FM- F-BD). Eur J Hum Genet 2001; 9: 191-6. [CrossRef] Tunca M, Kirkali G, Soyturk M, Akar S, Pepys MB, Hawkins PN. Acute phase response and evo- lution of familial Mediterranean fever. Lancet 1999; 353: 1415. [CrossRef] Haskard DO. Accelerated atherosclerosis in in- flammatory rheumatic diseases. Scand J Rheu- matol 2004; 33: 281-92. [CrossRef] Livneh A, Langevitz P, Zemer D, Zaks N, Kees S, Lidar T, et al. Criteria for the diagnosis of familial Mediterranean fever. Arthritis Rheum 1997; 40: 1879-85. [CrossRef] Lidar M, Scherrmann JM, Shinar Y, Chetrit A, Niel E, Gershoni-Baruch R, et al. Colchicine nonre- sponsiveness in familial Mediterranean fever: clinical, genetic, pharmacokinetic, and socio- economic characterization. Semin Arthritis Rheum 2004; 33: 273-82. [CrossRef] Ikeda Y, Suehiro T, Nakamura T, Kumon Y, Hashi- moto K. Clinical significance of the insülin resis- tance index as assessed by Homeostasis Model Ass- esment. Endocrine Journal 2001; 48: 81-6. [CrossRef] Borba EF, Bonfa E. Dyslipoproteinemias in sys- temic lupus erythematosus:influence of dis- ease, activity, and anticardiolipin antibodies. Lupus 1997; 6: 533-9. [CrossRef] van Halm VP, Nielen MM, Nurmohamed MT, van Schaardenburg D, Reesink HW, Voskuyl AE, et al. Lipids and inflammation: serial measurements of the lipid profile of blood donors who later developed rheumatoid arthritis. Ann Rheum Dis 2007; 66: 184-8. [CrossRef] Van Halm VP, Van Denderen JC, Peters MJ, Twisk JW, van der Paardt M, van der Horst-Bruinsma IE, et al. Increased disease activity is associated with a deteriorated lipid profile in patients with ankylosing spondylitis Ann Rheum Dis 2006; 65: 1473-7. [CrossRef] Sattar N, McCarey DW, Capell H, McInnes IB. Ex- plaining how "high-grade" systemic inflamma- tion accelerates vascular risk in rheumatoid ar- thritis. Circulation 2003; 108: 2957-63. [CrossRef] Spanakis E, Sidiropoulos P, Papadakis J, Gano- takis E, Katsikas G, Karvounaris S, et al. Modest but sustained increase of serum high density li- poprotein cholesterol levels in patients with in- flammatory arthritides treated with infliximab. J Rheumatol 2006; 33: 2440-6.
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