Gout is the most prevalent inflammatory arthritis and affects 2.5% of the general population in the UK. It is also the only arthritis that has the potential to be cured with safe, inexpensive and well tolerated urate-lowering treatments, which reduce serum uric acid by either inhibiting xanthine oxidase – eg allopurinol, febuxostat – or by increasing the renal excretion of uric acid. Of these, xanthine oxidase inhibitors are used first line and are effective in ‘curing’ gout in the vast majority of patients. Gout can be diagnosed on clinical grounds in those with typical podagra. However, in those with involvement of other joints, joint aspiration is recommended to demonstrate monosodium urate crystals and exclude other causes of acute arthritis, such as septic arthritis. However, a clinical diagnosis of gout can be made if joint aspiration is not feasible. This review summarises the current understanding of the pathophysiology, clinical presentation, investigations and treatment of gout.

Objective: Calcium pyrophosphate deposition (CPPD) disease is prevalent and has diverse presentations, but there are no validated classification criteria for this symptomatic arthritis. The American College of Rheumatology (ACR) and EULAR have developed the first‐ever validated classification criteria for symptomatic CPPD disease.Methods: Supported by the ACR and EULAR, a multinational group of investigators followed established methodology to develop these disease classification criteria. The group generated lists of candidate items and refined their definitions, collected de‐identified patient profiles, evaluated strengths of associations between candidate items and CPPD disease, developed a classification criteria framework, and used multi‐criterion decision analysis to define criteria weights and a classification threshold score. The criteria were validated in an independent cohort.Results: Among patients with joint pain, swelling, or tenderness (entry criterion) whose symptoms are not fully explained by an alternative disease (exclusion criterion), the presence of crowned dens syndrome or calcium pyrophosphate crystals in synovial fluid are sufficient to classify a patient as having CPPD disease. In the absence of these findings, a score >56 points using weighted criteria, comprising clinical features, associated metabolic disorders, and results of laboratory and imaging investigations, can be used to classify as CPPD disease. These criteria had a sensitivity of 92.2% and specificity of 87.9% in the derivation cohort (190 CPPD cases, 148 mimickers), whereas sensitivity was 99.2% and specificity was 92.5% in the validation cohort (251 CPPD cases, 162 mimickers).Conclusion: The 2023 ACR/EULAR CPPD disease classification criteria have excellent performance characteristics and will facilitate research in this field.

Immunosuppressive treatments inhibit vaccine-induced immunity against SARS-CoV-2. We evaluated whether a 2-week interruption of methotrexate treatment immediately after the COVID-19 vaccine booster improved antibody responses against the S1 receptor-binding domain (S1-RBD) of the SARS-CoV-2 spike protein compared with uninterrupted treatment in patients with immune-mediated inflammatory diseases. We did an open-label, prospective, two-arm, parallel-group, multicentre, randomised, controlled, superiority trial in 26 hospitals in the UK. We recruited adults from rheumatology and dermatology clinics who had been diagnosed with an immune-mediated inflammatory disease (eg, rheumatoid arthritis, psoriasis with or without arthritis, axial spondyloarthritis, atopic dermatitis, polymyalgia rheumatica, and systemic lupus erythematosus) and who were taking low-dose weekly methotrexate (≤25 mg per week) for at least 3 months. Participants also had to have received two primary vaccine doses from the UK COVID-19 vaccination programme. We randomly assigned the participants (1:1), using a centralised validated computer randomisation program, to suspend methotrexate treatment for 2 weeks immediately after their COVID-19 booster (suspend methotrexate group) or to continue treatment as usual (continue methotrexate group). Participants, investigators, clinical research staff, and data analysts were unmasked, while researchers doing the laboratory analyses were masked to group assignment. The primary outcome was S1-RBD antibody titres 4 weeks after receiving the COVID-19 booster vaccine dose, assessed in the intention-to-treat population. This trial is registered with ISRCT, ISRCTN11442263; following the pre-planned interim analysis, recruitment was stopped early. Between Sept 30, 2021 and March 3, 2022, we recruited 340 participants, of whom 254 were included in the interim analysis and had been randomly assigned to one of the two groups: 127 in the continue methotrexate group and 127 in the suspend methotrexate group. Their mean age was 59·1 years, 155 (61%) were female, 130 (51%) had rheumatoid arthritis, and 86 (34%) had psoriasis with or without arthritis. After 4 weeks, the geometric mean S1-RBD antibody titre was 22 750 U/mL (95% CI 19 314–26 796) in the suspend methotrexate group and 10 798 U/mL (8970–12 997) in the continue methotrexate group, with a geometric mean ratio (GMR) of 2·19 (95% CI 1·57–3·04; p<0·0001; mixed-effects model). The increased antibody response in the suspend methotrexate group was consistent across methotrexate dose, administration route, type of immune-mediated inflammatory disease, age, primary vaccination platform, and history of SARS-CoV-2 infection. There were no intervention-related serious adverse events. A 2-week interruption of methotrexate treatment for people with immune-mediated inflammatory diseases resulted in enhanced boosting of antibody responses after COVID-19 vaccination. This intervention is simple, low-cost, and easy to implement, and could potentially translate to increased vaccine efficacy and duration of protection for susceptible groups. National Institute for Health and Care Research.

Objectives. The objectives of this study were to examine changes in the incidence and prevalence of RA between 1990 and 2014 and to explore if there is any geographic variation in the incidence and prevalence of RA in the UK. Methods. This was a primary care–based prospective cohort study. People contributing acceptable data to Clinical Practice Research Datalink between 1 January 1990 and 31 December 2014 were included. Read codes were used to identify RA cases ⩾18 years of age. The prevalence and incidence rates for each year were standardized to the 2014 population and the regional incidence and prevalence of RA for the year 2014 were standardized to the overall population. Results. The incidence and prevalence of RA was 3.81/10 000 person-years and 0.67%, respectively, in 2014. The annual incidence of RA decreased by 1.6% (95% CI 0.8, 2.5) between 1990 and 2014, with significant joinpoints at 1994 and 2002. The prevalence of RA increased by 3.7%/year (95% CI 3.2, 4.1) from 1990 to 2005 and decreased by 1.1%/year (95% CI 2.0, 0.2) between 2005 and 2014. There were significant differences in the occurrence of RA throughout different regions of the UK, with the highest incidence in East Midlands, Yorkshire and Humber and the highest prevalence in North East, Yorkshire and Humber. Conclusion. The incidence of RA is decreasing, with a reduction in prevalence in recent years. There is significant geographic variation in the occurrence of RA in the UK. Further research is required to identify the reasons underlying this phenomenon so that public health interventions can be designed to further reduce the incidence of RA.

To examine temporal trends in all-cause and cause-specific mortality in RA. Data from the Clinical Practice Research Datalink were used. Incident RA cases and four age-, sex- and general practice–matched controls were identified from at-risk cohorts for each calendar year and followed-up for up to 5 years. Mortality rates and 95% CIs were computed. Cox proportional hazard ratios (HRs) were calculated to estimate associations and adjusted for covariates. The temporal trend in mortality was examined using the Joinpoint regression program. Data management and analysis were performed using Stata version 14. A total of 21 622 cases with incident RA and 86 488 controls were included. The mortality rate of RA cases and controls was 26.90 (95% CI 25.87, 27.97) and 18.92 (18.48, 19.36)/1000 person-years, respectively. The mortality rate in RA cases did not change significantly between 1990 and 2004 but decreased by 7.7%/year between 2005 and 2009. However, the mortality rate in controls improved steadily by 2.2%/year between 1990 and 2009. RA was associated with a 32% excess risk of mortality in the entire cohort [adjusted HR 1.32 (95% CI 1.26, 1.38)], but this was only 15% in cases incident after 2006 [adjusted HR 1.15 (95% CI 1.03, 1.29)]. Similarly, the HR of death due to cardiovascular diseases decreased in cases incident in recent years. The mortality rate in RA cases incident after the year 2006 has declined significantly, with a trend towards a decline in death from cardiovascular diseases. This could be due to improved management of RA. However, even in cohorts from recent years, RA still associates with higher mortality rates.

Objective Calcium pyrophosphate deposition (CPPD) disease is prevalent and has diverse presentations, but there are no validated classification criteria for this symptomatic arthritis. The American College of Rheumatology (ACR) and EULAR have developed the first-ever validated classification criteria for symptomatic CPPD disease. Methods Supported by the ACR and EULAR, a multinational group of investigators followed established methodology to develop these disease classification criteria. The group generated lists of candidate items and refined their definitions, collected de-identified patient profiles, evaluated strengths of associations between candidate items and CPPD disease, developed a classification criteria framework, and used multi-criterion decision analysis to define criteria weights and a classification threshold score. The criteria were validated in an independent cohort. Results Among patients with joint pain, swelling, or tenderness (entry criterion) whose symptoms are not fully explained by an alternative disease (exclusion criterion), the presence of crowned dens syndrome or calcium pyrophosphate crystals in synovial fluid are sufficient to classify a patient as having CPPD disease. In the absence of these findings, a score>56 points using weighted criteria, comprising clinical features, associated metabolic disorders, and results of laboratory and imaging investigations, can be used to classify as CPPD disease. These criteria had a sensitivity of 92.2% and specificity of 87.9% in the derivation cohort (190 CPPD cases, 148 mimickers), whereas sensitivity was 99.2% and specificity was 92.5% in the validation cohort (251 CPPD cases, 162 mimickers). Conclusion The 2023 ACR/EULAR CPPD disease classification criteria have excellent performance characteristics and will facilitate research in this field.