CRP, C-reactive protein; RRP, quick radiographic progression
CRP, C-reactive protein; RRP, quick radiographic progression. Open in a separate window Figure?3 Risk matrices showing the proportion of SWEFOT individuals who have developed radiographic progression (% and quantity with increase in SharpCvan der Hejde score 5 divided by total number in group) after 1?yr in all early rheumatoid arthritis individuals and stratified by sex. follow-up experienced radiographic progression. The following baseline parameters were self-employed predictors of radiographic progression at 1?12 months: baseline erosions (adjusted OR=2.29, 95% CI 1.24 to 4.24), erythrocyte sedimentation rate (adjusted OR per tertile increase=1.72, 95% CI 1.12 to 2.65) and C-reactive protein (adjusted OR per tertile increase=1.52, 95% CI 1.03 to 2.26). Current smoking was an independent predictor of radiographic progression (modified OR=2.17, 95% CI 1.06 to 4.45). These results remained after further adjustment for treatment strategy. Three-dimensional matrix including current smoking status, erosions and C-reactive protein tertiles showed a 12C63% risk gradient from individuals carrying none compared with all predictors. Rheumatoid element (RF)/anti-cyclic citrullinated peptide (anti-CCP) positivity did not significantly forecast radiographic progression using SHS increase 5 as cut-off. In a secondary exploratory analysis using cut-off 1, both RF and anti-CCP positivity were significant predictors in the unadjusted, but not the modified analyses. The additional guidelines also remained significant by using this lower cut-off. Conclusions In addition to previously explained predictors, we identified cigarette smoking as a strong independent risk element for radiographic progression in early RA. Trial sign up number “type”:”clinical-trial”,”attrs”:”text”:”NCT00764725″,”term_id”:”NCT00764725″NCT00764725. strong class=”kwd-title” Keywords: Early Rheumatoid Arthritis, Outcomes research, Smoking Introduction In rheumatoid arthritis (RA), broad evidence supports that treatment strategies focusing on early inflammatory control decrease radiographic progression.1 Nevertheless, a proportion of individuals progress, some despite having low disease activity.2 Since build up of joint damage over time correlates with decrease in both functional capacity and quality of life, it is important to identify those individuals at analysis who are likely to develop significant radiographic progression.3 4 Indeed, several studies have recently attempted to create clinically useful risk matrices to forecast so-called quick radiographic progression (RRP), related to an increase in Sharp-van der Hejde score (SHS) of 5 after 1?12 months, based on both early RA tests5 6 and cross-sectional cohorts7; their performance has been tested in both early8 and unselected9 RA populations. Among the baseline medical parameters that have been identified as predictors and included in those matrices RITA (NSC 652287) Rabbit polyclonal to NFKBIZ are inflammatory markers (erythrocyte sedimentation rate (ESR), C-reactive protein (CRP)), radiographic erosions at baseline, inflamed joint counts and auto-antibody status. However, none of them of these studies offers evaluated whether smoking practices associate with RRP after 1?yhearing, although several studies, especially earlier ones before the era of biological treatment, had indicated that RA individuals who smoke develop more radiographic damage.10C13 Furthermore, current smokers have been shown to respond worse clinically to both methotrexate and tumour necrosis element (TNF) inhibitors in early RA.14 15 Here, we examined baseline predictors of radiographic progression in the SWEFOT trial populace,16 17 including previously known ones as well as smoking practices. Methods Participants in the investigator-initiated, multicentre, randomised SWEFOT trial (n=487) served as our study base; it has been explained in detail elsewhere.16 17 Briefly, inclusion criteria were RA according to the 1987 revised American College of Rheumatology (ACR) criteria, age 18?years, sign duration 1?12 months, 28-joint disease activity score (DAS28) 3.2, no previous disease modifying antirheumatic drug (DMARD) treatment and stable prednisolone dose, if present, for 4?weeks before access and throughout the study of 10?mg/day. Individuals who accomplished DAS28 3.2 after 3C4?weeks continued on methotrexate (MTX, N=147), while the other individuals were randomised RITA (NSC 652287) to add either infliximab (N=128) or both sulfasalazine and hydroxychloroquine (N=130). Anti-cyclic citrullinated peptide (anti-CCP) antibodies were measured with the standard ELISA (Immunoscan-RA Mark2 ELISA test, Euro-Diagnostica, Malm?, Sweden) and rheumatoid element (RF) was determined by routine methods. Smoking status was defined as current, past or by no means cigarette smokers; individuals were also grouped as current smokers versus non-smokers, pooling past and never smokers in the second option group. X-rays of hands and ft were obtained at baseline and after 1?yhearing, and analysed from the modified SHS method. Radiographic progression was defined as an increase in total SHS of 5 after 1?12 months, as previously suggested, 6 8 which corresponds to the minimal clinically important progression, 18 and has also been referred to as RRP. In a secondary exploratory analyses, we RITA (NSC 652287) tested a lower cut-off of SHS 1.