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Plasma Saturated and Monounsaturated Fatty Acids in Behçet's Disease
Meriam Messedi1, Manel Naifar2, Sahar Grayaa1
1Unit of Research Molecular Bases of Human Diseases, 12ES17, Faculty of Medicine of Sfax, University of Sfax, 3029 Sfax, Sfax, Tunisia.
Background:
Fatty Acid (FA) composition of serum has been associated with many markers of inflammation. In this study, we tried to examine plasma Saturated Fatty Acid (SFA) and Monounsaturated Fatty Acid (MUFA) composition in Behçet's Disease (BD) patients. The associations between the circulating FA levels and some markers of inflammation have also been investigated.
Methods:
This study is a cross-sectional one. In fact, a total of 101 BD patients and healthy controls group of 99 subjects are enrolled. Gas Chromatograph equipped with a Capillary Split/Splitless Injector and flame ionization detector was used to analyze the plasma SFA and MUFA compositions. The high sensitivity C-Reactive Protein (hsCRP) and fibrinogen levels were measured using standard techniques.
Results:
BD patients had significantly higher proportions of Mystiric Acid (MA), Palmitic Acid (PAM), Palmitoleic Acid (POA) and Stearoyl-CoA Desaturase (SCD)-16, compared to controls.The results revealed that patients with severe involvements had high levels of POA and total MUFA associated with higher SCD-16 activity compared to those with minor ones. The receiver operator characteristic curve analysis revealed that POA could well discriminate BD patients with severe clinical manifestations. In the bivariate analysis, hsCRP was found to be positively correlated with total SAFA and POA elongase activity index but negatively correlated with SCD-18 activity index. The STA, POA, elongase and SCD-16 activity index are correlated with fibrinogen. On the other hand, the multivariate analysis showed that POA remained associated with higher levels of hsCRP.
Conclusion:
Unfavourable plasma SFA and MUFA profile were reported in BD patients. POA, which is associated with higher plasma hsCRP level, may play a role in the pathogenesis of BD.
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