Response to ‘Serum level of adiponectin is a surrogate independent biomarker of radiographic disease progression in early rheumatoid arthritis: results from the ESPOIR cohort’ – authors’ reply

We read with great interest the recent article in Arthritis Research & Therapy in which Meyer and colleagues evaluated different circulating adipokines in patients with recent-onset rheumatoid arthritis (RA) [1]. The authors found that total adiponectin was independently associated with baseline radiographic score and with a change in this score over time. The authors concluded that total adiponectin at the time of diagnosis is a surrogate marker for radiographic progression in early RA. However, there are some compelling reasons why the role of adiponectin in RA requires further elucidation. The conclusion by Meyer and colleagues should thus be tempered. First, several studies have investigated circulating concentrations of leptin, adiponectin, visfatin and resistin in RA, showing, in general, elevated levels. However, the link between these adipose products and disease activity remains controversial. Second, both proinflammatory and anti-inflammatory effects of adiponectin have been reported. Third, adiponectin exists in various isoforms, monomers and multimers. These different isoforms perform distinct and sometimes counteracting biological functions: low molecular weight adiponectin has been shown to inhibit lipopolysaccharide-mediated IL-6 release and to stimulate IL-10 secretion [2]. Conversely, high molecular weight (HMW) adiponectin induces secretion of IL-6 by monocytes, and increases production of monocyte chemoattractant protein-1 and IL-8 by peripheral