Response to ‘Adipokines, inflammation, insulin resistance, and carotid atherosclerosis in patients with rheumatoid arthritis’

In a recent report in Arthritis Research & Therapy, Kang and colleagues [1] assessed a series of patients with rheumatoid arthritis (RA) to establish whether adipokines could be a link between inflammation, insulin resistance, and atherosclerosis in RA. We have noticed that Kang and colleagues did not pay attention to our former studies on the same issue. In this regard, in the last decade, we conducted a series of studies on insulin resistance and adipokines in a cohort of Spanish patients with long-standing RA, undergoing anti-tumor necrosis factor-alpha (anti-TNF-α) infliximab therapy because of severe disease, refractory to conventional disease-modifying anti-rheumatic drugs [2-6]. Kang and colleagues described that resistin was associated with erythrocyte sedimentation rate (ESR) (r = 0.322, P <0.001), C-reactive protein (CRP) (r = 0.209, P = 0.004), and increased disease duration (r = 0.176, P = 0.014) [1]. These data are not new. We previously reported a close association between laboratory markers of inflammation, particularly CRP and resistin levels [3]. In our series, we found a significant association between the mean ESR (r = 0.405, P = 0.03) and CRP (r = 0.571, P = 0.0005) from disease diagnosis and ESR (r = 0.486, P = 0.004), CRP (r = 0.599, P = 0.0005), and platelet count (r = 0.559, P = 0.0007) at the time of the study and resistin levels [3]. These findings, along with these new data described by Kang and colleagues, highlight the potential role of resistin in the inflammatory cascade in RA. Kang and colleagues also found a positive correlation between adiponectin and ESR (r = 0.162, P = 0.025) [1]. Prior to these results, in our series of patients with