Abstract
Although the genetic etiology of familial Mediterranean fever (FMF) is known, limited information is available regarding the regulation of inflammation during attack-free periods. The aim of this study was to determine the alterations in serum copper (Cu), zinc (Zn) and selenium (Se) levels that may be associated with inflammation during attack-free periods in FMF patients. This study included 33 patients with FMF and 30 healthy volunteers. Erythrocyte sedimentation rate (ESR), the serum C-reactive protein (CRP) level and serum levels of Cu, Zn and Se in FMF patients and healthy volunteers were assessed by the atomic absorption spectrophotometry method. ESR and serum CRP levels and serum Cu and Zn levels were similar between patients with FMF during an attack-free period and healthy controls (p>0.05). Serum Se levels in the patient group were significantly higher than in the control group (p<0.05). Our study shows that levels of trace elements in serum are variable in patients with FMF during attack-free periods. Serum Se concentrations may at least in part contribute to the subclinical inflammation in FMF patients during attack-free periods. However, further studies are necessary to confirm this result.
Highlights
Familial Mediterranean fever (FMF), known as hereditary polyserositis, is an autosomal recessively-transmitted disease that is principally recognized in certain Mediterranean populations [1]
Erythrocyte sedimentation rate (ESR) and serum C-reactive protein (CRP) levels and serum Cu and Zn levels were similar between patients with FMF during an attack-free period and healthy controls (p>0.05)
Our study shows that levels of trace elements in serum are variable in patients with FMF during attack-free periods
Summary
Familial Mediterranean fever (FMF), known as hereditary polyserositis, is an autosomal recessively-transmitted disease that is principally recognized in certain Mediterranean populations [1]. FMF is manifested clinically by periodic episodes of fever with peritonitic abdominal pain, pleuritis, rashes and arthritis and is associated with a severe acute phase response [2]. FMF is a chronic inflammatory characterized by a mutation in the FMF gene (MEFV), which maps to chromosome 16p and encodes the pyrin/Marenostrin protein [3, 4]. MEFV is highly expressed neutrophils [4, 5]. Pyrin participates in various intracellular signaling pathways to cause overexpression of IL-1beta in neutrophils. Excessive neutrophil activation increases the level of oxygen free radicals, such as the superoxide anion radical and hydroxyl radical, and induces systemic inflammation, which is implicated in the pathogenesis of several diseases, such as rheumatoid arthritis, ankylosing spondylitis and Behcet’s disease [6, 7]
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