Jiajia Yang1, Xu Zhang1, Yubo Ma1, Meng Wu1, Xingxing Hu1, Renfang Han1, Yaping Yuan1, Mengmeng Wang1, Mengya Chen1, Shanqun Jiang2, Jingjing Tong3, Shengqian Xu3, Jianhua Xu3, Zongwen Shuai3, Yanfeng Zou1, Faming Pan4. 1. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China. 2. School of Life Sciences, Anhui University, Hefei, China, 111 Jiulong Road, Hefei 230601, China. 3. Department of Rheumatism and Immunity, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China. 4. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China; The Key Laboratory of Major Autoimmune Diseases, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China. Electronic address: famingpan@ahmu.edu.cn.
Abstract
OBJECTIVES: Various studies have researched 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 systematically evaluate the correlations between serum levels of these adipokines and AS. METHODS: Electronic databases were retrieved to search relevant publications. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by the random-effect model. Cochrane Q test and I2 statistic were used to test heterogeneity. Subgroup analysis and meta-regression were applied to assess possible sources of heterogeneity. RESULTS: A total of sixteen articles were included. Meta-analysis results indicated no statistical differences between AS patients and normal controls in serum leptin and adiponectin levels (leptin, SMD=0.829, 95% CI=-0.116 to 1.774, p=0.085; adiponectin, SMD=0.460, 95% CI=-0.004 to 0.924, p=0.052). However, AS patients had higher serum resistin levels than controls (SMD=1.413, 95% CI=0.294 to 2.531, p=0.013). Subgroup analyses suggested that Asian and African AS patients as well as patients aged <40years 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.
OBJECTIVES: Various studies have researched 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 systematically evaluate the correlations between serum levels of these adipokines and AS. METHODS: Electronic databases were retrieved to search relevant publications. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by the random-effect model. Cochrane Q test and I2 statistic were used to test heterogeneity. Subgroup analysis and meta-regression were applied to assess possible sources of heterogeneity. RESULTS: A total of sixteen articles were included. Meta-analysis results indicated no statistical differences between AS patients and normal controls in serum leptin and adiponectin levels (leptin, SMD=0.829, 95% CI=-0.116 to 1.774, p=0.085; adiponectin, SMD=0.460, 95% CI=-0.004 to 0.924, p=0.052). However, AS patients had higher serum resistin levels than controls (SMD=1.413, 95% CI=0.294 to 2.531, p=0.013). Subgroup analyses suggested that Asian and African AS patients as well as patients aged <40years 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.