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Objectives To determine the frequency, accrual, attribution and outcome of neuropsychiatric (NP) events and impact on quality of life over 3 years in a large inception cohort of patients with systemic lupus erythematosus (SLE). Methods The study was conducted by the Systemic Lupus International Collaborating Clinics. Patients were enrolled within 15 months of SLE diagnosis. NP events were identified using the American College of Rheumatology case definitions, and decision rules were derived to determine the proportion of NP disease attributable to SLE. The outcome of NP events was recorded and patient-perceived impact determined by the SF-36. Results 1206 patients (89.6% female) with a mean (±SD) age of 34.5±13.2 years were included in the study. The mean disease duration at enrolment was 5.4±4.2 months. Over a mean follow-up of 1.9±1.2 years, 486/1206 (40.3%) patients had ≥1 NP events, which were attributed to SLE in 13.0–23.6% of patients using two a priori decision rules. The frequency of individual NP events varied from 47.1% (headache) to 0% (myasthenia gravis). The outcome was significantly better for those NP events attributed to SLE, especially if they occurred within 1.5 years of the diagnosis of SLE. Patients with NP events, regardless of attribution, had significantly lower summary scores for both mental and physical health over the study. Conclusions NP events in patients with SLE are of variable frequency, most commonly present early in the disease course and adversely impact patients' quality of life over time. Events attributed to non-SLE causes are more common than those due to SLE, although the latter have a more favourable outcome.

Objective:To identify potential risk factors for the onset of inflammatory arthritis (IA) in a large cohort of patients with psoriatic arthritis (PsA) of recent onset.Methods:We recruited cases with psoriasis and an onset of IA within the past 5 years. Controls were patients who had psoriasis but no arthritis. We assessed potential factors associated with the development of IA using a detailed postal questionnaire. An unmatched analysis adjusted for age and gender was performed. Exposure was censored in the controls at a “dummy-date” assigned randomly in proportion to the percentage of cases developing IA in any given year.Results:We studied 98 cases and 163 controls. Exposures showing a positive association before the onset of IA in patients with psoriasis were: rubella vaccination (OR (95% CI) = 12.4 (1.2 to 122)), injury sufficient to require a medical consultation (2.53 (1.1 to 6.0)), recurrent oral ulcers (4.2 (2.0 to 9.0)) and moving house (2.3 (1.2 to 4.4)). Cases were also more likely to have experienced a fractured bone requiring hospital admission (50% vs 9%, p = 0.040).Conclusions:We found a number of environmental exposures associated with the onset of IA in subjects with psoriasis. The strongest associations were with trauma thereby adding to the hypothesis of a “deep Koebner phenomenon” in PsA. Our data also suggest that exposure of the immune system to certain infection-related triggers may also be of relevance. Further studies are needed to verify these observations and to examine potential immunological mechanisms that underlie them.

Aims To compare the British Isles Lupus Assessment Group (BILAG) 2004, the Safety of Estrogens in Lupus Erythematosus National Assessment (SELENA) flare index (SFI) and physician's global assessment (PGA) in assessing flares of disease activity in patients with systemic lupus erythematosus (SLE). Methods Sixteen patients with active SLE were assessed by a panel of 16 rheumatologists. The order in which the patients were seen was randomised using a 4×4 Latin square design. Each patient's flare status was determined at each assessment using the BILAG 2004 activity index; the SFI and a PGA. A group of five specialists designated each patient into severe, moderate, mild or no flare categories. Results The rate of complete agreement (95% CI) of the four individual examining physicians for any flare versus no flare was 81% (55% to 94%), 75% (49% to 90%) and 75% (49% to 90%) for the BILAG 2004 index, SELENA flare instrument and PGA, respectively. The overall agreement between flare defined by BILAG 2004 and the SFI was 81% and when type of flare was considered was 52%. Intraclass correlation coefficients (95% CI), as a measure of internal reliability, were 0.54 (0.32 to 0.78) for BILAG 2004 flare compared with 0.21 (0.08 to 0.48) for SELENA flare and 0.18 (0.06 to 0.45) for PGA. Severe flare was associated with good agreement between the indices but mild/moderate flare was much less consistent. Conclusions The assessment of flare in patients with SLE is challenging. No flare and severe flare are identifiable but further work is needed to optimise the accurate ‘capture’ of mild and moderate flares.

In rheumatoid arthritis (RA), chronic inflammation is thought to drive increased cardiovascular risk through accelerated atherosclerosis. It may also lead to a more high-risk plaque phenotype. We sought to investigate carotid plaque phenotype in RA patients using Dynamic Contrast-Enhanced MRI (DCE-MRI) and Fludeoxyglucose Positron Emission Tomography(FDG-PET). In this pilot study, RA patients and age/sex-matched controls were evaluated for cardiovascular risk factors and carotid plaque on ultrasound. Subjects with plaque >2 mm thick underwent DCE-MRI, and a subgroup of patients had FDG-PET. Comparison of MRI findings between groups and correlation between clinical, serological markers and imaging findings was undertaken. 130 patients and 62 controls were recruited. Plaque was more prevalent in the RA group (53.1% vs 37.0%, p = 0.038) and was independently associated with IL6 levels (HR[95%CI]: 2.03 [1.26, 3.26] per quartile). DCE-MRI data were available in 15 patients and 5 controls. Higher prevalence of plaque calcification was noted in RA, despite similar plaque size (73.3% vs 20%, p = 0.04). FDG-PET detected plaque inflammation in 12/13 patients scanned and degree of inflammation correlated with hs-CRP (r = 0.58, p = 0.04). This study confirms increased prevalence of atherosclerosis in RA and provides data to support the hypothesis that patients have a high-risk plaque phenotype.

Cognitive dysfunction is a common aspect of systemic lupus erythematosus (SLE) and is increasingly reported as a problem by patients. In many cases the exact cause is unclear. Limited correlations between specific autoantibodies or structural brain abnormalities and cognitive dysfunction in SLE have been reported. It may be that the most appropriate biomarkers have yet to be found. Functional magnetic resonance imaging (fMRI) is a technique used in many other conditions and provides sensitive measures of brain functionality during cognitive tasks. It is now beginning to be employed in SLE studies. These studies have shown that patients with SLE often perform similarly to healthy controls in terms of behavioural measures on cognitive tasks. However, SLE patients appear to employ compensatory brain mechanisms, such as increased response in fronto-parietal regions, to maintain adequate cognitive performance. As there have been only a few studies using fMRI in SLE to investigate cognitive dysfunction, many questions remain unanswered. Further research could, however, help to identify biomarkers for cognitive dysfunction in SLE.

Objectives The aim of the current study was to compare levels of vascular cell adhesion molecule-1 (VCAM-1) and E-selectin in lupus patients and controls and to investigate their association with clinical phenotype, disease activity and damage. Methods We compared levels of serum VCAM-1 and E-selectin in 178 female lupus patients and 69 age-and sex-matched controls. Using linear regression we also examined the association between these markers and disease activity, damage, renal and skin involvement as well as clinical and subclinical cardiovascular disease. Results E-selectin was increased in patients compared to controls (median (IQR) 10.5 (6.85, 13.9) vs 7.86 (5.39, 10.4) ng/ml; p < 0.001). E-selectin was also associated with overall damage and carotid plaque (β (95% confidence interval): 0.27 (0.029, 0.511) and 0.26 (0.148, 0.507)). Whilst there was no significant difference in VCAM-1 levels between groups overall, we found a significant association between VCAM-1 and with active renal disease (β (95% confidence interval): 1.10 (0.69, 1.51)). Conclusions E-selectin may act as a marker of cardiovascular risk in SLE, whilst VCAM-1 may have a role as a non-invasive biomarker for lupus nephritis activity.

Objective: Psoriasis of early onset (type I; age of onset ⩽40 years) is associated with HLA-Cw*06 while the shared epitope (SE) is associated with rheumatoid arthritis susceptibility. Our aim was to investigate the role of HLA-Cw*06 and HLA-DRB1 genes (including SE) with psoriatic arthritis (PsA) susceptibility.Methods:In a case–control association study, HLA-Cw*06 phenotype frequencies were compared between patients with PsA (n = 480), psoriasis alone (n = 611) and healthy controls (n = 166). Similarly, at the HLA-DRB1 locus, phenotype and SE frequencies were compared in patients with PsA (n = 480), early undifferentiated inflammatory arthritis alone (n = 1621) and healthy controls (n = 537).Results:The HLA-Cw*06 phenotype was associated with type I psoriasis (OR 6.9, 95% CI 4.4, 11.1, p = 2.2×10−21) and with patients with PsA having type I psoriasis (OR 5.0, 95% CI 3.2, 7.9, p = 4.39×10−13), but not with patients with PsA having type II psoriasis (age of onset >40 years). HLA-DRB1*07, in linkage disequilibrium with HLA-Cw*06, was also associated with patients with PsA having type I psoriasis (OR 2.7, 95% CI 2.1, 3.7, p<0.00001). HLA-DRB1*04 alleles and the SE were associated with undifferentiated inflammatory arthritis but not with PsA.Conclusions:The SE is not a PsA susceptibility locus. HLA-Cw*06 and HLA-DRB1*07 are associated with patients with PsA having type I psoriasis, suggesting that the primary association is with age of onset of psoriasis. Patients with PsA having type I psoriasis, therefore, have a genetic background different to those with type II psoriasis, and adjustment for this is necessary in future studies that investigate the genetic susceptibility of PsA.

The pharmacological armamentarium for the treatment of SLE is expanding and a number of novel therapies are currently under investigation. In spite of this, steroid therapy remains the cornerstone of treatment and intravenous methylprednisolone (IVMP) is still widely used in clinical practice. There is however surprisingly little evidence on which to define its precise role. The objective of this review was to consider the published evidence relating to the use of IVMP in SLE patients and also to identify open questions that still need to be answered with regard to its use. In acute flares, IVMP induces rapid suppression of acute inflammation. There is not however a strong evidence base to support the use of high doses compared to low IVMP doses or oral prednisolone. In maintenance regimes, secondary analyses suggest that IVMP may confer additional long-term renal survival over oral steroids as part of a cyclophosphamide regime. Therefore, in addition to the evaluation of novel therapies for SLE, better evidence to define the precise role of IVMP in SLE is still required. (Lupus (2007) 16, 387—393)

A phase 3 trial of anifrolumab, a monoclonal antibody to type I interferon receptor subunit 1, showed benefit in a composite primary end point of lupus scores. A previous phase 3 trial failed to meet its primary objective but showed an effect in secondary end points.

BackgroundSystemic Lupus Erythematosus (SLE) is a complex autoimmune disease and its heterogeneity means that many cohorts and clinical trials do not collect the same data, making comparative studies difficult.ObjectivesWe aimed to ascertain what data is commonly collected in SLE registries/trials. Our ultimate goal is to generate a core minimal dataset for future SLE studies.#8232;MethodsWe designed and distributed a questionnaire to members of the Systemic Lupus Erythematosus International Collaborating Clinics (SLICC) as well as additional research active centres in China. Our survey included 26 questions about the types of data that are routinely collected for research. Data collected by ≥ 75% of participating centres was used as a threshold for concordance.#8232;ResultsEighteen centres; eight from USA/Canada, five from China and five from Europe responded. Table 1 shows the data that ≥ 75% centres collected. Notably, the EULAR/ACR 2019 criteria was collected by 33.3% and even the most commonly collected patient reported outcome (PRO) - the SF36, was only collected by 53.3%. The SLICC/ACR SLE damage index did not reach our threshold (68.4%). Current treatment data collected did include drug name, dose, frequency and start date. Previous treatment reason for cessation was collected only pertaining to antimalarials. Baseline anti-dsDNA (ELISA) and Crithidia were collected by 70.6% and 52.9% respectively and baseline immunoglobulins were measured by 70.6%. Follow-up blood counts and complement C3/4 were collected by ≥ 75% of centres.Table 1.Data that ≥ 75% centres collectedSociodemographicRacial background,Educational attainment,Occupation,Smoking status,Alcohol consumption,Contraception use,Pregnancy history (number of pregnancies, miscarriage, stillbirth and neonatal death)SLE specificDate at and age of diagnosis,Disease duration,Family history of SLE,ACR 1997 classification criteria,SLEDAI-2000 disease activity measureComorbidityDiabetes,Hypertension,Bone disease/osteoporosis,Cerebrovascular disease,Ischaemic heart disease,Renal disease,Infection,Malignancy, Cardiovascular risk factors: smoking status, diabetes, hypertension and obesity, Renal data: renal biopsy, BP, serum creatinine, Urine Protein-Creatinine Ratio and estimated GFRBaseline bloodsFBC,Complement C3/4,ESR,LFTSBaseline immunologyAnti-cardiolipin antibody,ANA (IIF),ENA,Lupus anticoagulant,Anti-Beta2 glycoproteinTreatment dataCurrent:Biologic (Name, Dose, Frequency, Start date),Immunosuppressant (Name, Dose, Frequency, Start date),Antimalarial (Name, Dose, Frequency, Start date),IV/PO Glucocorticoid (Name, Dose, Frequency, Start date),NSAID (Name only)Previous:Biologic (Name only),Immunosuppressant (Name only),PO Glucocorticoid (Name, Dose, Start date, End date),Antimalarial (Name, Start date, End Date, Reason for cessation)ConclusionAn initial set of commonly collected data was identified. This forms the basis to start to consider a core minimum dataset for SLE. Development and further refinement of this dataset is needed, as will common definitions of each data field to allow widespread use.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsStephen McDonald: None declared, Jialin Teng: None declared, Michelle Barraclough: None declared, Ian N. Bruce Speakers bureau: Speaker for AstraZeneca, GSK and UCB., Consultant of: Consultancies; Eli Lilly, GSK, Merck Serono, UCB and ILTOO., Grant/research support from: Grants/research support; Genzyme/Sanofi, GSK, Roche and UCB.