Association between leptin, adiponectin and resistin and long-term progression of hand osteoarthritis
Association between leptin, adiponectin and resistin and long-term progression of hand osteoarthritis
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DOI：
10.1136/ard.2010.146282
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发表时间：
2011-07-01
影响因子：
27.4
通讯作者：
Kloppenburg, Margreet
中科院分区：
文献类型：
--
作者：
Yusuf, Erlangga;Ioan-Facsinay, Andreea;Kloppenburg, Margreet
目的探讨血清瘦素、脂联素和抵抗素水平与手骨关节炎（HOA）长期进展的关系（平均年龄60岁，81%的妇女）（定义为至少两个手关节的Kellgren和Lawrence评分>= 2）评估关节间隙狭窄（JSN）使用国际骨关节炎研究学会图谱，进展定义为JSN评分总和的变化高于最小可检测变化2，反映了高于测量误差的变化。在基线时测量血清脂肪因子，并将患者按脂肪因子三分位数分类。使用广义估计方程，相对于第一个三分位数，计算第二个和第三个三分位数患者的HOA进展RR（和95% CI）。调整了年龄，性别和身体质量index.Results患者在两个最高的三分位数的脂联素有一个HOA进展的风险降低了70%（RR = 0.3（0.2至0.7））相比，患者在最低的三分位数。结论脂联素水平与HOA的进展有关，提示脂联素可能参与了OA的病理生理过程。
Objective To investigate the association between baseline serum adipokines levels-leptin, adiponectin and resistin-and long-term progression of hand osteoarthritis (HOA).Methods Baseline and 6-year radiographs of 164 patients (mean age 60 years, 81% women) with HOA (defined as a Kellgren and Lawrence score >= 2 in at least two hand joints) were assessed for joint space narrowing (JSN) in 32 hand joints using the Osteoarthritis Research Society International atlas. Progression was defined as a change in the sum of the JSN score above the smallest detectable change of 2, reflecting change above measurement error. Serum adipokines were measured at baseline and patients were categorised by adipokine tertiles. RRs (and 95% CI) of HOA progression for patients in the second and third tertiles were calculated relative to the first tertile, using generalised estimating equations. Adjustments were made for age, sex and body mass index.Results Patients in the two highest tertiles of adiponectin had a decreased risk of 70% (RR = 0.3 (0.2 to 0.7)) for HOA progression in comparison with patients in the lowest tertile. Leptin and resistin levels were not associated with progression.Conclusion Adiponectin levels are associated with progression of HOA, suggesting that adiponectin may be involved in the pathophysiology of OA.