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Abstract
Background Fat tissue synthesizes and releases a series of biologically active substances (adipokines), which are involved in bone metabolism through effects on bone formation and resorption. There are gender-specific differences in the expression of adipokines and there are also gender specific-differences in the development of structural damage in the spine in patients with ankylosing spondylitis - AS. The reason for less structural damage in the spine in female AS patients is not well understood until now.
Objectives The aim of this study was to investigate the gender-specific role of adipokines as predictors of radiographic spinal progression in patients with AS.
Methods Altogether 120 patients (82 men and 38 women) from the ENRADAS trial who completed the study per protocol were included into the analysis. Spinal radiographs (lumbar and cervical spine, lateral views) were scored independently by two trained readers according to the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) scoring system. Radiographic spinal progression was defined as 1) mSASSS worsening by ≥2 units after 2 years, and 2) development of at least one new syndesmophyte or progression of existing syndesmophytes (i.e., formation of a bridging syndesmophyte) after 2 years. Serum levels of adipokines (leptin, adiponectin, lipocalin-2, omentin, visfatin, resistin, and chemerin) were measured at baseline.
Results A significant association with radiographic spinal progression was found for leptin only. Mean baseline leptin levels were significantly lower in patients with mSASSS worsening by ≥2 units after 2 years (n=29) as compared to those without progression (n=91): 10.3±8.8 vs. 15.9±13.7 ng/ml, respectively, p=0.002, and in patients with syndesmophyte formation (n=25) as compared to those without syndesmophyte formation (n=95): 10.1±9.6 vs. 15.7±13.4 ng/ml, respectively, p=0.002. This difference was especially evident in males, but not in females. However, in females the serum level of leptin at baseline was in general significantly higher than in males: 24.0±17.4 vs. 10.2±6.8 ng/ml, p<0.001 that was independent of body mass index.
In the ROC analysis leptin had an area under the curve (AUC) of 0.69 (95% CI 0.57–0.81) for no mSASSS worsening by ≥2 units and 0.70 (95% CI 0.57–0.82) for no syndesmophyte formation. Leptin level of 7.5 ng/ml was identified in the ROC analysis as an optimal threshold for the prediction of protection from radiographic spinal progression after two years – table.
In the logistic regression analysis, a protective value of higher leptin serum level regarding radiographic spinal progression could be confirmed: odds ratio (OR) =1.15 (95% CI 1.02–1.3) for no mSASSS worsening by ≥2 units, and OR =1.28 (95% CI 1.1–1.5) for no syndesmophyte formation (meaning a 15%/28% increase of the odds for no radiographic spinal progression after 2 years with each baseline leptin serum level increase by 1 ng/ml), both adjusted for baseline syndemophytes, elevated C-reactive protein (CRP), smoking, body mass index, sex, and NSAIDS intake score.
Conclusions Higher serum levels of leptin seem to protect patients with AS from radiographic spinal progression. Female patients with AS have significantly higher leptin levels that might explain lesser extent of structural damage in the spine in female AS patients in general.
Disclosure of Interest None declared