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THU0489 Enho Gene Expression and Serum Adropin Level in Rheumatoid Arthritis and Systemic Lupus Erythematosus
  1. S. Yolbas1,
  2. M. Kara2,
  3. A. Yildirim1,
  4. B. Gundogdu1,
  5. M. Kalayci3,
  6. S. Aydin3,
  7. S.S. Koca1
  1. 1Department Of Rheumatology, Faculty Of Medicine, Firat University, Elazig
  2. 2Department of Medical Genetics, Faculty of Medicine, Mugla Sitki Kocman University, Mugla
  3. 3Department of Biochemistry, Faculty Of Medicine, Firat University, Elazig, Turkey


Background Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are chronic inflammatory diseases. Adipokines, including leptin, adiponectin, resistin, and visfatin have been studied widely in chronic inflammatory diseases due to the metabolic, cardiovascular and inflammatory actions of adipokines. Adropin, a secreted protein, is encoded by the Energy Homeostasis Associated (ENHO) gene. It is expressed by a variety of tissues and cells. It has been implicated in the several physiological and pathological processes such as angiogenesis and apoptosis.

Objectives The aim of the present study was to investigate the ENHO gene expressions and serum adropin levels and in patients with RA and SLE.

Methods The study included 36 patients with RA, 22 patients with SLE, and 20 healthy controls (HC). The patients were fulfilling the established classification criteria. Disease activity statuses were determined by the disease activity score (DAS)28-erythrocyte sedimentation rate in the RA group (patients with >2.6 score were accepted as active) and SLE disease activity index (SLEDAI) in the SLE group (patients with >6 score were accepted as active). Serum adropin levels were analyzed by ELISA method using an appropriate commercial kit. ENHO and GAPDH gene expressions by peripheral blood mononuclear cells were analyzed by real-time PCR.

Results ENHO gene mRNA expression was significantly higher in the RA group than in HC group (p=0.024, Table), although it was similar in the SLE and HC groups (p=0.920). On the other hand, there was no significant differences among the study groups in terms of serum adropin levels (p>0.05, for all). Moreover, there was no significant difference in terms of ENHO expression and serum adropin level between active (n=17) and inactive (n=19) RA patients, and between active (n=13) and inactive (n=9) SLE patients.

Table 1.

The demographics and laboratory parameters

Conclusions Although ENHO gene expression is increase, serum adropin level is not altered in RA. Similarly, adropin seems not to be associated with SLE. However, the potential link between adropin and inflammatory diseases may be tested by a further study.


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Disclosure of Interest : None declared

DOI 10.1136/annrheumdis-2014-eular.5252

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