10.1136/annrheumdis-2017-eular.5858 Outcome in juvenile idiopathic arthritis Center for Diabetes Research, Gentofte Hospital, University of Copenhagen , Hellerup , Denmark Centre for Rheumatology, Royal Free Hospital , London , United Kingdom Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen Department of Medicine, University of Alabama at Birmingham , Birmingham, Alabama , United States Department of Medicine, University of Otago , Wellington , New Zealand Department of Rheumatology, University Hospital Zurich , Zurich , Switzerland Instituto de Salud Musculoesquelética , Madrid , Spain Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds NIHR Leeds Musculoskeletal Biomedical Research Centre, Chapel Allerton Hospital , Leeds , United Kingdom NNF Center for Basic Metabolic Research Paris Descartes University , Paris , France Rheumatology Department, Hôpital Ambroise Paré , Paris , France Rheumatology Division, Hospital de Cruces , Baracaldo, Vizcaya , Spain S.M. Nielsen Sanofi R&D , Alfortville , France Sanofi R&D , Chilly-Mazarin Sanofi-Aventis Deutschland GmbH , Frankfurt am Main , Germany Scleroderma program, University of Michigan , Ann Arbor , United States sanofi , Bridgewater , United States 2017 11 195 196 -

Background: Juvenile idiopathic arthritis (JIA) is a chronic inflammatory disease that often persists into adulthood. In addition to disability and poorer quality of life, JIA is associated with increased long-term morbidity and mortality. The long-term risk of comorbidities in JIA patients is uncertain and guidance on risk assessment is not currently available.

Objectives: To determine the frequency of comorbid conditions in adult JIA patients.

Methods: Patients with JIA transferred from the biologic registry BIKER to the follow-up (FU) registry JuMBO were included in this analysis. All comorbidities, except for serious infections, prospectively recorded by physicians to BiKeR or JuMBO were considered. Comorbidity rates among the various JIA categories were assessed. The Medical Dictionary for Regulatory Activities (MedDRA) was used for disorder coding. Differences in the occurence of comorbidities between JIA categories were analyzed by multinomial logistic regression.

Results: A total of 1,022 young adults (67% female) with JIA and a mean FU of 7.8 (SD=3.5) years (ys) were included in this analysis. The patients’ mean age was 22.5 ys (SD=3.7), and disease duration was 12.9 ys (SD=5.9) at the last FU.

The majority were classified as polyarticular JIA (36.4%) at BiKeR enrollment.

Patients had received a mean of 2.9 (SD=1.3) DMARDs, 77% were ever treated with biologics.

Comorbidities were reported for more than half of the patients (54%), 24.5% of the conditions were stated for the first time in adult age. Eye disorders were the most common comorbid condition group (15.1%), followed by skin and subcutaneous tissue disorders (9.3%), and psychiatric disorders (5.5%).

The most frequently reported single diseases were uveitis in 14.4%, chronic secondary pain syndrome in 4.4%, hypertension in 3.6%, and psoriasis in 3.3%. In addition, inflammatory bowel diseases were reported in 2.5% of cases, other immune-mediated disorders, namely autoimmune thyroiditis in 2.5%, type1 diabetes in 0.7% and celiac disease in 0.3%, depression in 2.3%, anxiety in 0.3%, osteoporosis in 1.6%, and amyloidosis in 0.4%. Among the reported comorbidities, there was one case with a cerebrovascular accident, but none with ischemic heart disease, heart failure or diverticulitis. The rate of comorbid condition accrued in the various JIA categories (table 1) differed significantly, with the highest rate in patients with extended oligoarthritis.

Conclusions: Young adults with JIA have a high rate of comorbidity overall, with extraarticular JIA manifestations being the most frequently reported comorbid conditions. Comorbidity rates vary among the various JIA categories. Patients with systemic JIA have the highest rate of cardiovascular risk factors and osteoporosis, while patients with extended OA have the highest rate of uveitis. An underreporting or unawareness of comorbidities by rheumatologists is possible, guidance on risk assessment in adults with JIA is needed.

Acknowledgements: The authors thank all rheumatologists for contributing patients to the JuMBO registry. BiKeR is funded by unconditional grants from Abbvie, Germany, Novartis, Germany, and Roche, Germany, JuMBO by unconditional grants from Abbvie, Pfizer, and Roche.

Disclosure of Interest: K. Minden Speakers bureau: Pfizer, Roche, PharmAllergan, N. Betenstehl: None declared, J. Klotsche: None declared, E. Seipelt: None declared, S. Tatsis: None declared, I. Foeldvari: None declared, G. Ganser: Background: To support internal compound development in systemic sclerosis, a study was performed to identify an mRSS signature in a longitudinal approach by analyzing skin biopsies.

Objectives: Identification of a gene signature that could be used as a quantitative surrogate marker for the mRSS independent of any treatment.

Methods: 77 forearm skin biopsies from 32 patients at baseline, and from the same patients after 8 weeks of treatment with SAR100842 (a LPA1 antagonist) or placebo (N=30) and after an additional 16 weeks of treatment with SAR100842 (N=15) in a phase 2 trial, were collected. Total RNA was extracted with the RNeasy® Fibrous Tissue Mini kit according to the manufacturer’s instructions. Total RNA was quantified by spectrofluormetry and qualified by capillary electrophoresis using Agilent Bioanalyzer 2100. Whole transcriptome analysis was performed using Affymetrix chips. Genes highly correlated (Pearson’s correlation) with the mRSS were identified at each treatment visit. A signature was identified as a set of genes whose expression levels correlated consistently either positively or negatively with the mRSS at all study visits regardless of treatment group.

The correlation value between the genes and the mRSS at baseline had to be >0.5 or < -0.5.The association between mRSS and the single composite marker obtained was investigated. A multivariate analysis of the correlation between the identified genes was performed using the median polish algorithm and PCA. The gene signature underwent pathway analysis using QIAGEN’s Ingenuity Pathway Analysis (IPA).

Results: This methodology led to the identification of 64 genes considered for the signature and viewed as a single composite marker that was highly correlated to the mRSS. A principal component analysis was computed and the first component explaining the maximum variance in the signature was highly correlated to the mRSS at baseline and week 8. This correlation was confirmed with the median polish algorithm (Pearson’s correlation coefficient of -0.75 and -0.73 respectively).

The most significant disease and disorder biological functions associated with the mRSS signature genes were related to immunological diseases. A significant enrichment was also detected for genes associated with inflammatory response and connective tissue disorders with p-values from 2.98E-05 to 2.47E-02.

Conclusions: An mRSS signature was identified using skin biopsies in SSc patients. Some of these genes (i.e. IRF7, THBS1, COMP or BANK1) have been published using similar approaches in other sets of SSc patients (1), which supports our results. The functional categories of this signature are characteristic How diet influences musculoskeletal diseases OP0340

WEIGHT LOSS FOR OVERWEIGHT AND OBESE INDIVIDUALS WITH GOUT: A SYSTEMATIC REVIEW OF LONGITUDINAL

OBSERVATIONAL STUDIES Background: Weight loss is a commonly recommended treatment for gout, but the magnitude of effect to expect has to our knowledge not previously been evaluated in a systematic review.

Objectives: The aim of this systematic review was to determine the benefits and harms associated with weight loss in overweight patients with gout.

Methods: Based on a pre-defined protocol (CRD42016037937), we searched six databases for longitudinal studies, quantitatively reporting the effect of weight loss in overweight gout patients. Risk of bias was assessed using the ROBINS-I tool. The quality of the evidence was assessed using GRADE.

Results: From 3,991 potentially eligible studies, 10 were included (incl. one RCT). Interventions included diet with/without physical activity, bariatric surgery, diuretics, metformin, or no intervention. Due to clinical heterogeneity of the included studies, data are presented for each study and synthesised separately.

The effect on serum uric acid (sUA) ranged from -168 to 30 µmol/L, and 0% to 60% patients achieved sUA normalisation (i.e. sUA <360 µmol/L). Six out of eight studies (75%) showed beneficial effects on gout attacks. A dose-response relationship was indicated in two studies for sUA, sUA normalisation and gout attacks. At short term (<3 months) after bariatric surgery, one study showed temporary increase in sUA, and another showed temporary increased number of gout attacks. Other possible harmful effects, measured by proxies such as withdrawals due to adverse events and serious adverse events, were poorly reported.

Conclusions: The available evidence is in favour of weight loss for overweight Fluid Capsulitis/synovitis Extracapsular oedema CL thickening CL oedema CL degeneration Proximal joint bone oedema Distal joint bone oedema Proximal joint bone cyst Distal joint bone cyst 30 (3) – (0) – (0) 50 (5) 40 (4) 40 (4) – (0) – (0) – (0) 10 (1) gout patients, with low, moderate and low quality of evidence for an effect on sUA, sUA normalisation, and gout attacks, respectively. At short term, temporary increased sUA and gout attacks may occur after bariatric surgery. There is an urgent need to initiate rigorous prospective studies (preferably RCTs) to provide more trustworthy estimates of benefits and harms of weight loss in overweight gout patients.

References: [1] Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis 2016:1–14, doi: 10.1136/annrheumdis-2016-209707.

Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2017-eular.2651 Can targeting disease activity in hand osteoarthritis improve our treatment in the 21st century

CAN PAIN IN HAND OSTEOARTHRITIS BE ASSOCIATED WITH

MRI COLLATERAL LIGAMENT ABNORMALITIES? Background: Many patients with hand osteoarthritis (OA) have little symptoms.

Bone oedema and synovitis have been associated to pain in OA, but inflammation involving ligaments has not been studied, likely limited by inadequate MRI resolution. We have previously found significant ligament pathology in early and established hand OA (HOA) [1].

Objectives: We hypothesise that the well innervated ligaments are key to a better understanding of the relationship between joint structure and pain in HOA. This

Median score (IQR) HC (n=10)

OA no pain (n=11)

OA pain (n=15)

OA no pain (n=11)

OA pain (n=15) *Accounting for clustering of joints within patients. CI = confidence interval; HC = healthy controls; IQR = inter-quartile range; CL = collateral ligaments.

Joints % (n)