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The Relationship Among the Level of Serum Amyloid A, High-Density Lipoprotein and Microalbuminuria in Patients With Familial Mediterranean Fever

Date

2016

Author

Uslu, Ali Ugur
Aydin, Bahattin
Icagasioglu, Ibrahim Serhat
Balta, Sevket
Deveci, Koksal
Alkan, Filiz
Yildiz, Gursel
Sahin, Ali

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Abstract

BackgroundSerum amyloid A (SAA), which is produced in the liver, acts as an apoprotein of high-density lipoprotein (HDL) accumulation in extracellular matrix of tissues and organs. SAA elevations play a significant role in the development of amyloidosis. Microalbuminuria (MAU) is the early period of amyloidosis in patients with familial Mediterranean fever (FMF). We assessed the association between SAA as an important factor for the development of amyloidosis in patients with FMF and cytokines, HDL, and MAU. MethodsA total of 40 FMF patients diagnosed with Tel-Hashomer criteria and making regular follow-up visits at the tertiary referral center from 2012 to 2013 were included in this study, besides 40 age- and sex-matched individuals as controls. ResultsCompared with controls, FMF patients had higher SAA (25.20 45.78 vs. 1.68 +/- 0.63 ng/ml; P = 0.002). Also, FMF patients had higher MAU than controls (23.20 +/- 39.86 vs. 9.40 +/- 5.32 mg/day; P = 0.036). HDL was significantly lower in the patient group than in controls (39.35 +/- 10.45 vs. 47.82 +/- 15.31 mg/dl; P = 0.023). Interleukin-1 beta (IL-1), IL-6, and tumor necrosis factor alpha (TNF-) levels were higher in the FMF group than in controls (P < 0.0001, P = 0.009, P = 0.003, respectively). ConclusionsOur results suggest that IL-1, IL-6, TNF-, SAA, and HDL may serve as markers of subclinical inflammation in FMF patients. Due to increased plasma HDL levels, antiinflammatory and antioxidant effects may elevate in FMF patients.

Source

JOURNAL OF CLINICAL LABORATORY ANALYSIS

Volume

30

Issue

6

URI

https://dx.doi.org/10.1002/jcla.21971
https://hdl.handle.net/20.500.12418/7121

Collections

  • Makale Koleksiyonu [5200]
  • Makale Koleksiyonu [5745]
  • Öksüz Yayınlar Koleksiyonu - WoS [6162]



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