These data suggest that in patients receiving a-TNF treatment, lower serum levels of RANKL and RANKL/OPG ratio may serve to predict remission.

The objective of the study was to develop evidence-based and practical recommendations for the detection and management of comorbidity in patients with rheumatoid arthritis (RA) in daily practice. We used a modified RAND/UCLA methodology and systematic review (SR). The process map and specific recommendations, based on the SR, were established in discussion groups. A two round Delphi survey permitted (1) to prioritize the recommendations, (2) to refine them, and (3) to evaluate their agreement by a large group of users. The recommendations cover: (1) which comorbidities should be investigated in clinical practice at the first and following visits (including treatments, risk factors and patient's features that might interfere with RA management); (2) how and when should comorbidities and risk factors be investigated; (3) how to manage specific comorbidities, related or non-related to RA, including major adverse events of RA treatment, and to promote health (general and musculoskeletal health); and (4) specific recommendations to assure an integral care approach for RA patients with any comorbidity, such as health care models for chronic inflammatory patients, early arthritis units, relationships with primary care, specialized nursing care, and self-management. These recommendations are intended to guide rheumatologists, patients, and other stakeholders, on the early diagnosis and management of comorbidity in RA, in order to improve disease outcomes.

Objective. The presence of serum rheumatoid factor (RF) and spontaneous RF‐secreting B cells is a common feature in most patients with rheumatoid arthritis (RA). This study analyzed the cytokine(s) that controls the final maturation of B cells capable of spontaneous IgM‐RF secretion in vitro. Methods. RA patients' peripheral blood mononuclear cells (PBMC), as well as adherent and nonadherent cell fractions, were cultured, and spontaneous IgM‐RF and interleukin‐1 0 (IL‐1 0) secretion were determined by enzyme‐linked immunosorbent assay. Results. The RF+ RA PBMC, but not PBMC from RF– RA patients or healthy controls, actively produced IgM‐RF in a linear manner for 14 days. This activity depended on the presence of fetal calf serum and did not require cellular DNA synthesis. Spontaneous IgM‐RF secretion depended on IL‐1 0, as deduced from the following findings: 1) IL‐1 0, but not a variety of cytokines including IL‐6, restored missing IgM‐RF secretion by PBMC in serum‐free supplemented cultures; 2) the addition of anti–IL‐1 0, but not anti–IL‐6, blocking antibodies inhibited PBMC IgM‐RF secretion, and this effect could be reversed by exogenous IL‐1 0; and 3) RA PBMC actively produced IL‐1 0 in vitro. The cells responsible for endogenous IL‐1 0 production were found in the adherent cell fraction. Finally, IL‐1 0 induced IgM‐RF, but not total IgM, secretion by RA PBMC. Conclusion. In patients with RA, circulating B cells capable of spontaneous IgM‐RF secretion require IL‐1 0 production by adherent cells to reach terminal maturation.

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