Subgroup analyses suggested that Asian and African AS patients as well as patients aged < 40 years had higher serum leptin and resistin levels when compared to controls .
Serum adiponectin levels were higher in AS patients compared to controls in subgroup of age ≥ 40 , and serum resistin levels in subgroup of BMI ≥ 25 .
Measurement method was a source of heterogeneity for resistin .
Publication bias was not observed and the robustness of study results was confirmed by sensitivity analysis .
Conclusion : Serum resistin , but not leptin or adiponectin levels may be closely associated with the development of AS .
HighlightsSerum levels of resistin are associated with the pathogenesis of AS.In specific subgroups , leptin and adiponectin may be related to AS.Measuring type is one of sources of heterogeneity for the studies about resistin
Objectives : Various studies have research ed the serum levels of leptin , adiponectin and resistin in patients with ankylosing spondylitis ( AS ) , but the results were inconclusive .
The purpose of this study was to systematic ally evaluate the correlations between serum levels of these adipokines and AS .
Leptin and adiponectin levels in patients with ankylosing spondylitis. The effect of infliximab treatment.
BACKGROUND Adipose tissue-derived leptin and adiponectin control hunger , energy expenditure , insulin sensitivity , endothelial function , reproduction and immunity and are thought to play a role in autoimmune diseases . However , their role in ankylosing spondylitis ( AS ) is not clearly defined . Tumour necrosis factor ΤNF-α is a potential modulator of adipocytokines . The effect of longterm anti-TNF-α treatment on plasma levels of leptin and adiponectin has not been assessed so far . OBJECTIVES To assess the effect of a 6-month anti-TNF-α treatment on serum leptin and adiponectin levels in AS patients . METHODS Thirty men with AS were included in the study . Thirty age- and weight-matched men served as controls . Clinical and biochemical parameters were assessed and serum levels of leptin and adiponectin were measured with enzyme immunoassay methods prior to and after the 6-month treatment with infliximab . RESULTS Mean age and disease duration of AS patients were 40.6±13.7 and 13.4±8.4 years , respectively . At baseline , AS patients exhibited significantly higher adiponectin ( 15.4±8.3 vs. 8.6±4.2 μg/ml , p<0.05 ) , but no difference in leptin levels ( 7.2±2.9 vs. 8.9±6.4 ng/ml , p = NS ) . Adipocytokines did not correlate with any disease parameter . Body weight of the patients did not change significantly over the 6-month period . Serum levels of leptin and adiponectin did not change significantly after the 6-month treatment . CONCLUSIONS Adiponectin levels were significantly higher in AS patients compared with  controls . Infliximab treatment did not change serum levels of leptin and adiponectin suggesting that the anti-TNF-α treatment may not modulate significantly their levels
Subgroup analyses suggested that Asian and African AS patients as well as patients aged < 40 years had higher serum leptin and resistin levels when compared to controls .
Serum adiponectin levels were higher in AS patients compared to controls in subgroup of age ≥ 40 , and serum resistin levels in subgroup of BMI ≥ 25 .
Measurement method was a source of heterogeneity for resistin .
Publication bias was not observed and the robustness of study results was confirmed by sensitivity analysis .
Conclusion : Serum resistin , but not leptin or adiponectin levels may be closely associated with the development of AS .
HighlightsSerum levels of resistin are associated with the pathogenesis of AS.In specific subgroups , leptin and adiponectin may be related to AS.Measuring type is one of sources of heterogeneity for the studies about resistin
Objectives : Various studies have research ed the serum levels of leptin , adiponectin and resistin in patients with ankylosing spondylitis ( AS ) , but the results were inconclusive .
The purpose of this study was to systematic ally evaluate the correlations between serum levels of these adipokines and AS .