Background Ankylosing spondylitis (AS) is chronic inflammatory disease of spine and sacroiliac joints. It clinically presents with extraarticular involvement and entesitis along with axial and peripheral involvement. Recent studies demonstrated that adipocytokines released from white adipose tissue contribute to inflammation and tissue damage. Apelin is produced in a variety of tissues, and is also shown to be a new adipokine secreted from the adipocytes and is present in plasma.
Objectives Although there are studies assessing the relation between AS and serum adipocytokines, there is almost no study investigating this relation in terms of apelin. Thus, in our study we aimed to investigate serum apelin level, association with clinical and laboratory parameters, disease activity and radiographical damage in AS patients.
Methods Eighty-five AS patients (M/F=63/22) (mean age 36.70±10.99 years) followed up in Ondokuz Mayıs University Medicine Faculty Physical Medicine and Rehabilitation (Rheumatology) Department, 79 RA patients (M/F =11/68) (mean age 47.97±13.69 years) and 76 healthy controls (M/F =41/35) (mean age 37.40±13.40 years) were enrolled in the study. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) was used for disease activity, Bath Ankylosing Spondylitis Functional Index (BASFI) for functionality, Bath Ankylosing Spondylitis Metrology Index (BASMI) for spinal movement, Modified Stoke Ankylosing Spondylitis Score System (mSASSS) for radiological damage, and Short Form-36 (SF-36) for quality of life assessment. Apelin and TNF-α levels were determined by ELISA method.
Results Apelin levels of AS (2.94±0.81) and RA (3.25±0.90) patients were statistically higher than healthy controls (2.38±0.77) (p<0.05) and apelin levels of AS patients were statistically lower than RA patients (p=0.049). Statistically significant difference was found between three groups in terms of TNF- α level. While TNF-α levels of RA and AS patients were significantly higher than healthy controls (p<0.05), there was no statistically difference between AS and RA patients (p>0.05). Quality of life scores of AS patients except social function were lower than healthy controls. A positive correlation was found between apelin and TNF- α levels (p=0.002, r=0.33). While there was a negative correlation between apelin and BASDAI, BASFI, ESR and CRP, there was no correlation with m-SASSS and BASMI. There was positive correlation between apelin and physical function, physical role and pain parameters of quality of life.
Conclusions We found serum apelin levels higher in AS and RA patients comparing to healthy controls. We couldn't find any correlation between apelin and radiological progression in AS patients. Nevertheless, there was a negative correlation between apelin and clinical and laboratory measurements that show disease activity. By these findings, we concluded that serum apelin level increases at disease course of AS, it may be a marker of clinical activity rather than new bone formation.
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Disclosure of Interest None declared