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Background: Distal interphalangeal (DIP) joint involvement is a feature of both psoriatic arthritis (PsA) and hand osteoarthritis (OA), and nail-changes are features seen both in PsA and nail psoriasis patients without joint involvement (PsO). In both PsA and OA, ultrasonography (US) is used to quantify DIP joint inflammation.Objectives: To explore disease-specific US-detected characteristics in the DIP-joints and extensor tendon entheses in patients with DIP-joint OA, PsA, PsO with nail involvement, and healthy controls (HC).Methods: In PsA, PsO, OA and HC US examination of DIP joints 2-5 and the extensor tendon were performed. The US images were scored for DIP joint grey-scale synovitis, DIP joint Doppler, osteophytes and erosions (grade 0-3) and presence/absence of enthesitis and peritendonitis of the extensor tendon according to OMERACT standards. Prevalences were calculated on all included fingers (i.e. four fingers per participant), and differences in prevalences were tested using Chi-square statistics.Results: Fifty PsA patients (44% females; mean age: 55y), 13 PsO patients (38% females; mean age 54y), 12 OA patients (100% females, mean age 71y), and 29 HC (52% females, mean age 48y) participated. The prevalences across the diagnosis groups are shown in figure 1, and the distribution of US outcomes was significantly different (highest Chi-square P-value: 0.0127). The PsA group had the largest prevalence of extensor tendon enthesitis (45.5%), peritendonitis (15%), and DIP joint erosions (11%), but also exhibited a considerable prevalence of osteophytes (46%). In the PsO group, the most marked findings were synovitis (33%) and enthesitis (35%). The OA group had the largest prevalence of DIP joint synovitis (67%) and osteophytes (88%) but also 25% prevalence of enthesitis. 24% of the HC group had a grade 1 synovitis.Conclusion: This cross-sectional study found significant patterns of US findings distributed dependent on the underlying condition. PsA patients were mainly differentiated by the presence of extensor tendon enthesitis and peritendonitis. A high prevalence of enthesitis and synovitis was seen in patients with DIP joint OA. The high prevalence of enthesitis in PsO is consistent with a preclinical phase of PsA in this group.Disclosure of Interests: Jørgen Guldberg-Møller Speakers bureau: Novartis, Ely Lilly, AbbVie, BK Ultrasound, Marius Henriksen: None declared, Mikael Boesen Speakers bureau: Image Analysis Group, AbbVie, AstraZeneca, Eli Lilly, Esaote, Glenmark, Novartis, Pfizer, UCB, Lene Dreyer: None declared, Karen Ellegaard: None declared, Marie Skougaard: None declared, Christine Ballegaard: None declared, Ai Lyn Tan: None declared, Richard Wakefield Speakers bureau: Novartis, Janssen, GE, Lars Erik Kristensen Consultant of: UCB Pharma (Advisory Board), Sannofi (Advisory Board), Abbvie (Advisory Board), Biogen (Advisory Board), Speakers bureau: AbbVie, Amgen, Biogen, Bristol-Myers Squibb,Celgene, Eli Lilly, Gilead, Forward Pharma, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, and UCB Pharma

Background: There is a strong association between gout and obesity. Lowering urate is the cornerstone of gout management [1] and urate levels correlate strongly with central obesity. Previous studies suggest that weight loss has a positive effect on serum urate, however, the studies are sparse and small [2].Objectives: To assess the impact of an initial low-calorie diet-induced weight loss and subsequent randomisation to the body weight-lowering drug liraglutide (a glucagon-like peptide 1 receptor agonist) or placebo on serum urate levels.Methods: In the LOSE-IT trial (NCT02905864), a randomised, double-blinded, placebo-controlled, parallel group, single-centre trial [3], 156 obese individuals with knee osteoarthritis, but without gout, were offered an initial 8-week intensive diet intervention (week -8 to 0) on Cambridge Weight Plan (800-1000 kcal/day) followed by a weight loss maintenance period in which participants were randomised to either liraglutide 3 mg/day or placebo for 52 weeks. We conducted a secondary analysis of blood samples collected at week -8, 0 and 52. The primary outcome measure was change in serum urate. We used paired t-test for the change from week -8 to 0, and for change from week 0 to 52 we used an ANCOVA model adjusted for stratification factors (sex, age category and obesity class), and the level of the outcome at baseline. Data were analysed as observed (i.e. no imputation of missing data).Results: 156 individuals were randomised and 155 had blood samples taken at baseline. In the initial intensive diet intervention period (week -8 to 0) they lost a mean of 12.5 kg (9513.1 to -11.9, n 156). In the following 52 weeks, the liraglutide group lost an additional 4.1 kg (SE 1.2, n 71) whereas the control group was almost unchanged with a weight loss of 0.2 kg (SE 1.2, n 66). Looking at the main outcome of serum urate levels change, the initial intensive diet resulted in a mean decrease of 0.21 mg/dL (95.35 to 0.07, n 155) for the entire cohort. In the following year (week 0 to 52) the liraglutide group exhibited a further mean decrease in serum urate of 0.48 mg/dL (SE 0.11, n 69), whereas the placebo group exhibited a slight decrease in mean serum urate of 0.07 mg/dL (SE 0.12, n 65) resulting in a significant between-group difference of -0.40 mg/dL (950.69 to -0.12, n 134) textendash see Figure 1. Four participants in each group experienced serious adverse events; no deaths were observed.Conclusion: This secondary analysis of the LOSE-IT trial suggests that liraglutide provides a potential novel serum urate lowering drug mechanism in obese patient populations, with potential implication for gout treatment.References: [1]Richette P et al. 2016. Ann Rheum Dis 2017;76:29textendash42.[2]Nielsen SM et al. Ann Rheum Dis 2017 76(11):1870-1882.[3]Gudbergsen H et al. BMJ 2019. 71textendash2.Disclosure of Interests: Kristian Zobbe: None declared, Sabrina Mai Nielsen: None declared, Robin Christensen: None declared, Anders Overgaard: None declared, henrik gudbergsen Speakers bureau: Pfizer 2016, Marius Henriksen: None declared, Henning Bliddal Grant/research support from: received research grant fra NOVO Nordic, Consultant of: consultant fee fra NOVO Nordic, Lene Dreyer: None declared, Lisa Stamp: None declared, Filip Krag Knop Shareholder of: Minority shareholder in Antag Therapeutics Aps, Grant/research support from: AstraZeneca, Gubra, Novo Nordisk, Sanofi and Zealand Pharma, Consultant of: Amgen, AstraZeneca, Boehringer Ingelheim, Carmot Therapeutics, Eli Lilly, MSD/Merck, Mundipharma, Novo Nordisk, Sanofi and Zealand Pharma., Speakers bureau: AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly, MedImmune, MSD/Merck, Mundipharma, Norgine, Novo Nordisk, Sanofi and Zealand Pharma., Lars Erik Kristensen Consultant of: UCB Pharma (Advisory Board), Sannofi (Advisory Board), Abbvie (Advisory Board), Biogen (Advisory Board), Speakers bureau: AbbVie, Amgen, Biogen, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Forward Pharma, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, and UCB Pharma

Karen Rokkedal Lausch,1 Mette Søgaard,2,3 Flemming Schønning Rosenvinge,4,5 Helle Krogh Johansen,6 Trine Boysen,7 Bent Løwe Røder,8 Klaus Leth Mortensen,1,9Lene Nielsen,10 Lars Lemming,9 Bente Olesen,10 Christine Leitz,11 Lise Kristensen,9,12 Esad Dzajic,13 Lars Jørgen Østergaard,1 Henrik Carl Schønheyder,14,15 Maiken Cavling Arendrup6,16,17 1Department of Infectious Disease, Aarhus University Hospital, 8200 Aarhus, Denmark; 2Department of Cardiology, Aalborg University Hospital, 9000 Aalborg, Denmark; 3Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Faculty of Health, Aalborg University, 9000 Aalborg, Denmark; 4Department of Clinical Microbiology, Odense University Hospital, 5000 Odence C, Denmark; 5Department of Clinical Microbiology, Lillebaelt Hospital, 5500 Middelfart, Denmark; 6Department of Clinical Microbiology, Rigshospitalet, 2100 Copenhagen, Denmark; 7Department of Clinical Microbiology, Hvidovre Hospital, 2650 Hvidovre, Denmark; 8Department of Clinical Microbiology, Hospital of Slagelse, Slagelse Sygehus, 4200 Slagelse, Denmark; 9Department of Clinical Microbiology, Aarhus University Hospital, 8200 Aarhus, Denmark; 10Department of Clinical Microbiology, Herlev and Gentofte Hospital, University of Copenhagen, 2730 Herlev, Denmark; 11Department of Clinical Microbiology, Viborg Regionshospital, 8800 Viborg, Denmark; 12Department of Clinical Microbiology, Herning Regionshospital, 7400 Herning, Denmark; 13Department of Clinical Microbiology, Sydvestjysk Sygehus, 6700 Esbjerg, Denmark; 14Department of Clinical Microbiology, Aalborg University Hospital, 9000 Aalborg, Denmark; 15Department of Clinical Medicine, University of Aalborg, 9000 Aalborg, Denmark; 16Unit of Mycology, Statens Serum Institute, 2300 København, Denmark; 17Department of Clinical Medicine, University of Copenhagen, 2200 Copenhagen, Denmark Background: In accordance with international guidelines, primary antifungal treatment (AFT) of candidemia with echinocandins has been nationally recommended in Denmark since 2009. Our nationwide cohort study describes the management of candidemia treatment focusing on the impact of prophylactic AFT on species distribution, the rate of adherence to the recommended national guidelines for AFT, and the effect of AFT on patient outcomes.Materials and methods: Incident candidemia cases from a 2-year period, 2010–2011, were included. Information on AFT was retrospectively collected from patient charts. Vital status was obtained from the Danish Civil Registration System. HRs of mortality were reported with 95% CIs using Cox regression.Results: A total of 841 candidemia patients was identified. Prior to candidemia diagnosis, 19.3% of patients received AFT (162/841). The risk of non-albicans candidemia increased after prior AFT (59.3% vs 45.5% among nontreated). Echinocandins as primary AFT were given for 44.2% (302/683) of patients. Primary treatment with echinocandins resulted in adequate treatment in a higher proportion of patients (97.7% vs 72.1%) and was associated with lower 0- to 14-day mortality compared with azole treatment (adj. HR 0.76, 95% CI: 0.55–1.06). Significantly lower 0- to 14-day mortality was observed for patients with Candida glabrata and Candida krusei with echinocandin treatment compared with azole treatment (adj. HR 0.50, 95% CI: 0.28–0.89), but not for patients with Candida albicans or Candida tropicalis.Conclusion: The association shown between prior AFT and non-albicans species underlines the importance of treatment history when selecting treatment for candidemia. Compliance with national recommendations was low, but similar to previously reported international rates. Primary treatment of candidemia with echinocandins compared with azoles yielded both a higher proportion of adequately treated patients and improved mortality rates. This real-life setting supports guidelines recommendation, and further focus on compliance with these seems warranted. Keywords: candidemia, candida, antifungal treatment, echinocandin, azole, Candida albicans, Candida glabrata