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The authors propose a solution to reporting response in rheumatoid arthritis (RA) clinical trials. They consider the success of the American College of Rheumatology (ACR) criteria for 20% improvement in RA disease activity (ACR20) in organizing trial reports and paving interpretation of trial data to direct patient experience. Problems with the classic type of data presentation are discussed. A discussion on the components of the proposed solution is detailed.

The author highlights growing interest of patient reported outcome's use in rheumatoid arthritis (RA) clinical trials and in clinical practice. He discusses several studies that determine differences between patient's and physician's assessments of disease activity, and factors that influence the two measures. It also highlights that a patient's global assessment of ≤1 on a scale of 0-10 is needed as per Boolean remission criteria of the new The American College of Rheumatology (ACR/EULAR).

A letter to the editor is presented in response to the article in the previous issue on the cost-utility analysis of the BeSt (behandelstrategietrialën voor reumatoide artritis) trial.

A letter to the editor is presented in response to the article "How antirheumatic drugs protect joints from damage in rheumatoid arthritis," by Schett and colleagues.

The author reflects on the pathophysiogical aspects of rheumatoid arthritis (RA). He challenges the traditional view of the disease and argues on the unnecessary view of J. R. Kirwan on split and on the intriguing details of the study by A. K. Brown. He views that subclinical joint information shown by ultrasound and magnetic resonance imaging (MRI) best explains the structural deterioration of RA patients.

The author talks about the study conducted to evaluate the effectiveness of spleen tyrosine kinase (Syk) in the suppression of rheumatoid arthritis (RA). The data collected from a 3-month methotrexate (MTX) failure trial suggested the ineffectiveness of fostamatinib in patients with relatively treatment-resistant disease. According to the author, the findings suggest that Syk kinase inhibition with fostamatinib is unreliable.

A letter to the editor in response to the article "Infliximab and Methotrexate As Induction Therapy in Patients With Early Rheumatoid Arthritis" in a 2007 issue and a response by A. E. van der Bijl et al. to the letter are presented.

Objective To compare rates of sustained low and minimal disease activity and remission according to the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) criteria during 3-year followup in rheumatoid arthritis (RA) patients treated with etanercept and adalimumab in routine care. Methods Four hundred seven RA patients previously unexposed to tumor necrosis factor antagonists were treated with etanercept (n = 203) or adalimumab (n = 204) and assessed at 3- and later 6-month intervals. Treatment allocation was at the discretion of the treating rheumatologist. Clinical parameters were measured at each time point, as were anti-adalimumab antibodies in adalimumab-treated patients. Achievement of clinical outcome was defined as the occurrence of sustained (at least 12 consecutive months) low disease activity (28-joint Disease Activity Score [DAS28] <3.2), minimal disease activity (DAS28 <2.6), or ACR/EULAR remission based on the Simplified Disease Activity Index (SDAI). Non-overlapping response rates were calculated. Results Among the adalimumab group, 13% reached sustained low disease activity but not sustained minimal disease activity, 15% reached sustained minimal disease activity but not sustained remission according to the SDAI, and 16% reached sustained ACR/EULAR remission. In the etanercept group the corresponding rates were 16%, 11%, and 12%, respectively ( P = 0.42, overall test for linear trend). Adalimumab-treated patients without anti-adalimumab antibodies (n = 150 [74%]) had the best outcomes, and adalimumab-treated patients with anti-adalimumab antibodies the worst, with outcomes in etanercept-treated patients in between ( P < 0.0001). Differences were most apparent in the sustained SDAI remission and sustained minimal disease activity categories. For example, 40% of anti-adalimumab antibody-negative patients, 23% of etanercept-treated patients, and 4% of anti-adalimumab antibody-positive patients achieved at least sustained minimal disease activity. Conclusion Overall, etanercept and adalimumab treatment appear similar in inducing a good long-term clinical outcome. However, in the case of adalimumab this is strongly dependent on the presence or absence of anti-adalimumab antibodies. [ABSTRACT FROM AUTHOR]

Objective To evaluate the effects of oral nonsteroidal antiinflammatory drugs (NSAIDs) on C-reactive protein (CRP) levels in rheumatoid arthritis (RA) patients, with a prespecified focus on the different NSAIDs. Methods We performed a systematic search in Medline via PubMed, the Cochrane Central Register of Controlled Trials, EMBase via OVID, the Institute for Scientific Information Web of Science, and other sources. Eligible trials were parallel-group, randomized, placebo-controlled trials of oral NSAID therapy in RA patients for which there were extractable CRP data. Standardized mean differences (SMDs) with 95% confidence intervals (95% CIs) were calculated from the differences in means of CRP levels between groups (active treatment minus placebo) divided by the pooled SDs. For the meta-analysis, a random-effects model was used to estimate the overall change in CRP level, and stratified analysis was used to examine differences among NSAIDs. Results We included 19 trials of 10 different NSAIDs. Overall, NSAIDs showed no effect on the CRP level (SMD 0.01 [95% CI −0.03, 0.06], P = 0.62). However, the prespecified stratified analysis indicated varying effects on the CRP level according to the different NSAIDs; lumiracoxib caused a statistically significant and consistent (I2 = 0%) increase in the CRP level (SMD 0.13 [95% CI 0.01, 0.25], P = 0.037), whereas naproxen caused a statistically significant and consistent (I2 = 0%) decrease in the CRP level (SMD −0.11 [95% CI −0.20, −0.02], P = 0.022). Conclusion Overall, NSAIDs have no effect on the CRP level. However, the nonselective NSAID naproxen was associated with a significant decrease in the CRP level, whereas the cyclooxygenase 2-selective NSAID lumiracoxib was associated with a significant increase in the CRP level. This finding is interesting considering the suspected influence of NSAIDs on cardiovascular complications. [ABSTRACT FROM AUTHOR]

The article presents a study which examines the effects and safety of selective estrogen receptor α (ERα) agonist Org 37663 in rheumatoid arthritis (RA) patients. It states that a 10-week, randomized, and proof-of-concept trial was initiated in RA postmenopausal female patients who receive background treatment with methotrexate or sulfasalazine. The results showed that Org 37663 was safe and well tolerated, but was not effective in influencing the disease activity in RA patients.

The article discusses the study on the association of rheumatoid arthritis (RA) with an increased risk of cardiovascular disease (CVD). It reveals that the incidence of CVD in patients with RA was nine percent and 4.3 percent in the general population. It is concluded that there is an increased risk of CVD in RA that is equivalent to the risk for CVD in type 2 diabetes mellitus (DM).