Diakonhjemmet Hospital and University of Oslo, Oslo, Norway.
Boston University School of Medicine, Boston, Massachusetts.
Arthritis Rheumatol. 2022 May;74(5):810-817. doi: 10.1002/art.42056. Epub 2022 Mar 23.
To examine the association of body mass index (BMI) with pain in people with hand osteoarthritis (OA), and explore whether this association, if causal, is mediated by systemic inflammatory biomarkers.
In 281 Nor-Hand study participants, we estimated associations between BMI and hand pain, as measured by the Australian/Canadian Osteoarthritis Hand Index (AUSCAN; range 0-20) and Numerical Rating Scale (NRS; range 0-10); foot pain, as measured by NRS (range 0-10); knee/hip pain, as measured by the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC; range 0-20); painful total body joint count; and pain sensitization. We fit natural-effects models to estimate natural direct and natural indirect effects of BMI on pain through inflammatory biomarkers.
Each 5-unit increase in BMI was associated with more severe hand pain (on average increased AUSCAN by 0.64 [95% confidence interval (95% CI) 0.23, 1.08]), foot pain (on average increased NRS by 0.65 [95% CI 0.36, 0.92]), knee/hip pain (on average increased WOMAC by 1.31 [95% CI 0.87, 1.73]), generalized pain, and pain sensitization. Mediation analyses suggested that the effects of BMI on hand pain and painful total body joint count were partially mediated by leptin and high-sensitivity C-reactive protein (hsCRP), respectively. Effect sizes for mediation by leptin were larger for the hands than for the lower extremities, and were statistically significant for the hands only.
In people with hand OA, higher BMI is associated with greater pain severity in the hands, feet, and knees/hips. Systemic effects of obesity, measured by leptin, may play a larger mediating role for pain in the hands than in the lower extremities. Low-grade inflammation, measured by hsCRP, may contribute to generalized pain in overweight/obese individuals.
探讨身体质量指数（BMI）与手部骨关节炎（OA）患者疼痛之间的关系，并探讨如果这种关系是因果关系，是否由系统性炎症生物标志物介导。
在 281 名 Nor-Hand 研究参与者中，我们通过澳大利亚/加拿大骨关节炎手部指数（AUSCAN；范围 0-20）和数字评分量表（NRS；范围 0-10）评估 BMI 与手部疼痛之间的关系；通过 NRS（范围 0-10）评估足部疼痛；通过 Western Ontario 和 McMaster 大学骨关节炎指数（WOMAC；范围 0-20）评估膝关节/髋关节疼痛；评估全身疼痛关节计数；以及疼痛敏化。我们拟合自然效应模型，以通过炎症生物标志物估计 BMI 对疼痛的直接和间接自然效应。
BMI 每增加 5 个单位，手部疼痛就会更严重（平均 AUSCAN 增加 0.64[95%置信区间（95%CI）0.23，1.08]），足部疼痛（NRS 平均增加 0.65[95%CI 0.36，0.92]），膝关节/髋关节疼痛（WOMAC 平均增加 1.31[95%CI 0.87，1.73]），全身性疼痛和疼痛敏化。中介分析表明，BMI 对手部疼痛和全身疼痛关节计数的影响分别部分由瘦素和高敏 C 反应蛋白（hsCRP）介导。瘦素介导的效应大小在手部比在下肢更大，并且仅在手部具有统计学意义。
在手部 OA 患者中，较高的 BMI 与手部、足部和膝关节/髋关节疼痛严重程度增加相关。肥胖的系统性影响，由瘦素测量，在手部疼痛中可能比在下肢疼痛中起更大的中介作用。hsCRP 测量的低度炎症可能导致超重/肥胖个体的全身性疼痛。
