BackgroundUltrasound (US) is a valid imaging tool to detect signs of giant cell arteritis (GCA). Although the halo sign has always been considered the most useful finding for GCA diagnosis, modern high frequency transducers are able to precisely measure the intima-media thickness (IMT) of cranial and extracranial arteries. However, data on optimal cut-off values for IMT to differentiate patients and controls in clinical practice are limited.ObjectivesTo determine the optimal cut-off value for IMT of cranial and extracranial arteries in patients with suspected GCA.MethodsThis is a retrospective observational study of patients referred to our US fast-track clinic with suspected GCA. All patients underwent bilateral US examination of the cranial and extracranial (carotid, subclavian and axillary) arteries within 24 hours per protocol. The exam was performed using an EsaoteMyLab8 with a 12-18 MHz frequency transducer for cranial arteries and an 8-14 frequency transducer for extracranial arteries. The IMT was measured in gray scale mode and the presence of a non-compressible halo sign was checked in all arteries. The gold standard for GCA diagnosis was clinical confirmation by the referring rheumatologist after 6 months follow-up. Mean IMT values of each artery were compared between patients with and without GCA by independent samples T-test. Receiver operating characteristics analysis was performed and the Youden index was used to determine the optimal cut-off value for IMT of each artery.ResultsOf the 157 patients with suspected GCA (67.5% female, mean age 73.7 years) referred to the fast-track clinic, 47 (29.9%) had GCA clinical confirmation after 6 months. 41 (87.2%) patients with GCA had positive US findings (61.7% had cranial involvement, 44.7% extracranial involvement and 19.1% a mixed pattern of cranial and extracranial arteries). The following IMT cut-off values showed the highest diagnostic accuracy: 0.44mm for the common superficial temporal artery; 0.34 mm for the frontal branch; 0.36 mm for the parietal branch; 1.1 mm for the carotid artery: 1 mm for the subclavian and axillary arteries. The area under the ROC curve of the IMT for a clinical diagnosis of GCA was 0.984 (95% CI 0.959 - 1) for common superficial temporal artery, 0.989 (95% CI 0.976 -1) for frontal branch, 0.991 (95% CI 0.980 - 1) for parietal branch, 0.977 (95% CI 0.961 – 0.993) for carotid, 0.99 (95% CI 0.979 - 1) for subclavian and 0.996 (95% CI 0.991 -1) for axillary arteries (Table 1).Table 1.Optimal IMT cut-off values for cranial and extracranial arteriesArterySidePatients without GCAPatients with GCACut-off (mm)AUC (CI 95%)Sensitivity (%)Specificity (%)Common superficialtemporal artery mm, mean (SD)Right0.33 (0.06)0.68 (0.28)0.430.997 (0.988 -1)10097.1Left0.35 (0.11)0.57 (0.21)0.450.966 (0.905 -1)10092.3Both0.34 (0.08)0.63 (0.25)0.440.984 (0.959 -1)94.795.1Frontal branch mm, mean (SD)Right0.26 (0.05)0.4 (0.18)0.340.994 (0.983 -1)10097.1Left0.27 (0.05)0.4 (0.18)0.340.985 (0.962 -1)10096.1Both0.26 (0.05)0.4 (0.18)0.340.989 (0.976 -1)10096.6Parietal branch mm, mean (SD)Right0.27 (0.05)0.43 (0.18)0.360.994 (0.981 -1)10098.9Left0.27 (0.05)0.41 (0.16)0.360.987 (0.967 -1)10097.6Both0.27 (0.05)0.42 (0.17)0.360.991 (0.980 -1)10098.3Carotid mm, mean (SD)Right0.8 (0.17)0.88 (0.29)10.974 (0.949 – 0.999)10092.6Left0.82 (0.15)1 (0.42)1.20.982 (0.961 - 1)90.996.2Both0.81 (0.16)0.96 (0.36)1.10.977 (0.961 – 0.993)9094Subclavian mm, mean (SD)Right0.74 (0.18)0.99 (0.44)10.987 (0.97 - 1)10093.4Left0.67 (0.17)0.9 (0.35)1.10.991 (0.975 - 1)10098.3Both0.7 (0.18)0.94 (0.4)10.99 (0.979 - 1)10096Axillary mm, mean (SD)Right0.69 (0.16)0.99 (0.5)10.992 (0.982 - 1)10096Left0.67 (0.17)0.99(0.49)10.998 (0.995 -1)10098.3Both0.68 (0.17)0.99 (0.49)10.996 (0.991 -1)10097.1ConclusionDifferent IMT cut-off values for each artery are necessary to establish a correct US diagnosis of GCA. These proposed IMT cut-off values may help to improve the diagnostic accuracy of US in clinical practice.Disclosure of InterestsNone declared

Background:Juvenile idiopathic arthritis (JIA) requires frequent systemic treatments, the ideal goal being to achieve remission. Questions remain as to when treatment can be stopped and how to balance the risks and benefits of continuing medications against the possibility of a flare after discontinuation. There is currently little conclusive evidence on the management of JIA in remission.Objectives:To determine the time to remission and frequency of flares in patients with JIA after withdrawal of systemic treatment in a single-centre cohort.Methods:Patients with JIA visited in the last 15 years were included. A retrospective cross-sectional study was performed. Demographic data such as sex, age at diagnosis, current age, subcategories of JIA were collected. Systemic treatment was also collected (date of discontinuation, date of flare after discontinuation, time in remission, time of treatment until discontinuation, discontinuation of biologic therapy while maintaining methotrexate). For the analysis of qualitative variables, absolute and relative frequencies were used; for quantitative variables, median and IR; for comparative analysis, Chi-square and Mann-Whitney U test.Results:We included 146 patients with JIA. Demographic data are shown in Table 1. 134 (90.4%) patients required systemic treatment (synthetic and/or biological DMARDs), of which 61 (45.5%) discontinued treatment completely at some point. Of the total number of patients who discontinued all systemic treatment, 19 (31.1%) had a flare with a median time in remission of 4.1 years (IR 1.3-9.1). 17 of the 134 patients (12.7%) with systemic treatment discontinued biologic therapy while maintaining methotrexate, of which 12 (70.6%) patients had a flare with a median time in remission of 0.9 years (IR 0.6-1.2). The differences between the frequency of flares and median time in remission between both treatment discontinuation groups (all systemic treatment versus discontinuation of biologic while maintaining methotrexate) were statistically significant (p<0.001). The median time from systemic treatment to complete withdrawal was 3.2 years (IR 1.9-4.8).Table 1.Demographic characteristics of patients with JIAVariables N 146Sex: Women n (%) 89 (60.3)Age at onset (years, median (IR)) 4.6 (2.5-9.2)Current age (years, median (IR))16.7 (11.1-20.9)Types of JIA:Persistent oligoarticular n (%) 66 (45.2)Extended oligoarticular n (%) 11 (7.5)Polyarticular RF - n (%) 29 (19.9)Polyarticular RF + n (%) 3 (2.1)Enthesitis-related n (%) 12 (8.2)Psoriatic n (%) 9 (6.2)Systemic n (%) 16 (11.0)Conclusion:One third of the patients in whom all systemic treatment was withdrawn had a flare (70% remain in remission without medication) with a median time in remission of 4 years. On the other hand, two-thirds of patients in whom biologic therapy was withdrawn while maintaining methotrexate had a flare, with a shorter time in remission. The differences between both groups with withdrawal of systemic treatment are statistically significant (p<0.001).References:[1]Halyabar O, Mehta J, Ringold S, Rumsey DG, Horton DB. Treatment Withdrawal Following Remission in Juvenile Idiopathic Arthritis: A Systematic Review of the Literature. Paediatr Drugs. 2019 Dec;21(6):469-492. doi: 10.1007/s40272-019-00362-6.[2]Simonini G, Ferrara G, Pontikaki I, Scoccimarro E, Giani T, Taddio A, Meroni PL, Cimaz R. Flares After Withdrawal of Biologic Therapies in Juvenile Idiopathic Arthritis: Clinical and Laboratory Correlates of Remission Duration. Arthritis Care Res (Hoboken). 2018 Jul;70(7):1046-1051. doi: 10.1002/acr.23435.[3]Chhabra A, Robinson C, Houghton K, Cabral DA, Morishita K, Tucker LB, Petty RE, Larché M, Batthish M, Guzman J. Long-term outcomes and disease course of children with juvenile idiopathic arthritis in the ReACCh-Out cohort: a two-centre experience. Rheumatology (Oxford). 2020 Dec 1;59(12):3727-3730. doi: 10.1093/rheumatology/keaa118.Disclosure of Interests:None declared

Background:Patients with inflammatory arthralgia (IA) are considered to be at increased risk for progression to RA. Ultrasound (US) has shown high sensitivity to detect synovitis compared with physical examination. Thus, US is recommended to identify subclinical synovitis in patients without clinical signs of inflammation.Objectives:To determine the frequency and pattern of US detected active inflammation in patients with IA and investigate factors contributing to predict this outcome.Methods:An US clinic is scheduled in an academic center running twice every week. A retrospective analysis of our US unit cohort during a period of 12 months was undertaken. Patients with IA and no previous diagnosis of inflammatory arthropathies were included for analysis. Inclusion criteria of IA definition included: severe symptoms presenting in the morning, duration of morning stiffness ≥60 min, symptoms predominantly located in MCP joints and absence of clinically detected synovitis by the referral rheumatologist. The following routinely collected variables were included in the analysis: demographics, clinical features and laboratory tests. Patients underwent bilateral US examination of hands and/or feet according to the European League Against Rheumatism (EULAR) guidelines. The presence of synovitis and tenosynovitis was assessed on a semi quantitative scale (0–3) for Grey Scale(GS)/Power Doppler(PD). Active inflammation was defined as PD synovitis and/or tenosynovitis >1 at any location. First, differences between groups were tested using chi-squared/Fisher and Student-t tests in the univariate analysis. Second, multivariate logistic regression models were employed to investigate the association between possible predictive factors of US active inflammation.Results:A total of 110 patients were included in the analysis. Mean age was 53.6±15.6 years, 80 (72.7%) were females, and mean symptoms duration was 11.7±9.9 months (Table1). A total of 76 (69.1%) patients presented with a polyarticular arthralgia pattern. US active inflammation were present in 38 (34.5%) patients (28.2% showed PD synovitis and 19.1% PD tenosynovitis). Hands were most commonly involved with PD synovitis at wrists in 18.2% and at MCP in 14.5% of patients. For PD tenosynovitis, the flexor MCP 2-5 (4.5%) and 6th extensor tenosynovitis (5.5 %) were the most frequent affected locations. Only 9 (8.2%) patients had erosions in hands and/or feet at baseline examination. In the univariate analysis, the higher ESR values, the shorter time from symptoms onset and the presence of ACPA were significantly associated with the presence of US active inflammation (p<0.001, p=0.035 and p=0.01, respectively). In the multivariate analysis, only ACPA and ESR values (OR=1,0003; 95%CI 1,000-1,006 and OR=1.054; 95%CI 1.016-1.094), remained significantly associated with the detection of US active inflammation.Conclusion:US features of active inflammation are found in 1 over 3 patients with IA being PD synovitis the most common finding, specially at the wrists and MCP joints. Higher ESR and ACPA values are significantly associated with the presence of US active inflammation. Thus, we strongly recommend the use of PD US to detect subclinical inflammation in at-risk patients with IA with no sign of inflammation on clinical examination, especially those with high ESR and ACPA values.Table 1.Baseline characteristics of patients with IATotaln= 110US inflammatoryfindingsn= 38 (34.5%)Non-US inflammatoryfindingsn=72 (65.5%)pAge53.6 ± 15.657.2±16.251.6±13.40.071SexFemale80 (72.7%)26 (68.4%)54 (75%)0.461Smokingn= 87Non smoker45 (51.7%)12 (44.4%)33 (55%)0.412Smoker34 (39.1%)11 (40.7%)23 (38.3%)Former smoker8 (9.2%)4 (14.8%)4 (6.7%)ExtensionMonoarticular12 (10.9%)6 (15.8%)6 (8.3%)0.176Oligoarticular 22 (20%)10 (26.3%)12 (16.7%)Polyarticular76 (69.1%)22 (57.9%) 54 (75%)Time (months)from symptoms onset11.7 ± 9.99.1±8.113±10.50.035ESR (mm/h) n=4524.7 ± 18.233.1±21.820.3 ±14.4<0.001RF (IU/mL) n=5339.1 ± 230.528.5±5645.1±286.10.647ACPA (IU/mL) n=5698.1 ± 331.2209.4±488.426±125.20.01Disclosure of Interests:None declared

Background:Juvenile idiopathicarthritis (JIA) comprises a group of inflammatory diseases that frequently requires systemic treatments. There are some studies that evaluate the systemic drug survival in adults with JIA; but there is scarce data about the drug survival in paediatric population.Objectives:Our main objective was to study the drug survival of biologic therapies and synthetic DMARD in a monocentric cohort and the related factors influencing on it.Methods:Patients with JIA visited in the last 12 years were included. We carried out a retrospective, longitudinal study and collected data on treatment (start date, tapering and stop the treatment date; causes of finish and combined treatment or not). We also collected demographic data with date of birth, sex, symptoms onset data and JIA subcategory. We studied time to relapse since the drug suspension. The drug survival for each kind of treatment was analyzed with Kapplan-Meier curves.Results:We included 158 patients with JIA. Demographic data are shown in table 1. One hundred and thirty (82.3%) patients started methotrexate (MTX) with a half-life of 34.8 months; 79 (51.5%) patients started biologic therapy with half-life of 29 months and 14 (17.7%) patients started a second biologic with a half-life of 5 months. Time to first tapering of MTX was 12 months, for the first biologic was 10.5 months and for the second biologic was of 15 months. The main cause of suspension was remission for each group. Treatment according to different JIA subcategories is shown in table 2. In 45 patients (28.5%) systemic treatment was stopped and 11 (24.4%) had a disease flare in a mean time of 36 months. Taking into account only patients who flared, the mean time was 15.6 months.Table 1.Overview of patients with BSLE. BMZ: basal membrane zone MTP: methylprednisolone DDS: dapsoneTable 1.Demographic features of the patients.Total (n:158)Sex (female)96 (60,76%)Starting age (median y RI)4,9 (2,6-9,8)AAN positives91 (57,6%)JIA oligo persistent66 (41,77%)JIA oligo extended16 (10,13%)JIA enthesitis14 (8,86%)JIA psoriasic9 (5,7%)JIA systemic18 (11,39%)JIA poli FR-29 (18,35%)JIA poli FR+4 (2,53%)JIA undifferentiated2 (1,27%)Table 2.All diseases that are diagnosed in patients during the follow-up period.Group 1 (Systemic JIA n=18 (%)Group 2 (Oligoarticular JIA n=82 (%)Group 3 (Poliarticular JIA n=33 (%)Group 4 (Juvenil SpA n=23 (%)Synthetic DMARD(n:130)9 (50%)71 (86,6%)33 (100%)17 (74%)Biologic Therapy(n:79)6 (33,3%)34 (41,46%)22 (75%)17 (74%)No systemic treatment(n:21)7 (38,9%)10 (12,2%)04 (17.4%)Fig 1.Histology and DIF of BSLE H-Eaandb: subepidermal blisterscandd: abundant neutrophils are observede: DIF full house linear patternFig 2.skin lesions of BSLEa: tense serous blisters, scars and erosionsb: purpuric macules in palmsc: blisters in groind-g: blisters and hypopigmented scarsConclusion:The drug survival for systemic therapies in children with JIA is more than 2 years, without significant differences between synthetic DMARDs and biologics. Remission is the main cause for ending treatment. Biologic drug survival was significantly shorter between systemic JIA and the other subcategories. Only one fourth of patients had a flared after stopping the systemic treatment.Disclosure of Interests:Laura Trives Folguera Speakers bureau: ROCHE, Indalecio Monteagudo: None declared, Belén Serrano Benavente: None declared, Liz R. Caballero Motta: None declared, Ana Melissa Anzola: None declared, Katerine López Gloria: None declared, Juan Carlos Nieto Speakers bureau: Pfizer, Abbvie, MSD, Novartis, Janssen, Lilly, Nordic Pharma, BMS, Gebro, FAES Farma, Roche, Sanofi

Background:Patients with inflammatory arthralgia (IA) are considered to be at increased risk for progression to RA. US has shown high sensitivity to detect synovitis compared with physical examination. Thus, US is recommended to identify subclinical synovitis in patients without clinical signs of inflammation.Objectives:The objective of our study is to determine the frequency and pattern of US detected inflammatory findings in patients with IA and investigate factors contributing to predict these findings.Methods:An US clinic is scheduled in an academic center running three days every week. A retrospective analysis of our US unit cohort during a period of 6 months was undertaken. Patients with IA and no previous diagnosis of inflammatory arthropathies were included for analysis. Inclusion criteria of IA definition included: severe symptoms presenting in the morning, duration of morning stiffness ≥60 min, symptoms predominantly located in MCP joints and abscense of clinically detected synovitis by the referral rheumatologist. The following routinely collected variables were included in the analysis: demographics, clinical features and laboratory tests. Patients underwent bilateral US examination in GS and PD mode of hands and/or feet according to the European League Against Rheumatism (EULAR) guidelines. The presence of synovitis, tenosynovitis and enthesitis was assessed on a semi quantitative scale (0–3) for Grey Scale(GS)/Power Doppler(PD) or using enthesitis OMERACT definition, respectively. Patients were stratified in two groups based on the presence of US inflammatory findings (synovitis, tenosynovitis or enthesitis with PD signal). First, differences between groups were tested using chi-squared and Student-t tests in the univariate analysis. Second, multivariate logistic regression models were employed to investigate the association between possible predictive factors of US detected inflammatory findings.Results:A total of 57 patients were included in the analysis. Mean age was 55.8±15.2 years, 41 (71.9%) were females, and mean symptoms duration was 11.4±10.4 months (Table 1). A total of 42 (73.7%) patients presented with a polyarticular arthralgia pattern. US inflammatory findings were present in 20 (35.1%) patients (26.3% PD synovitis, 21.1% PD tenosynovitis and 3.5% PD enthesitis). Hands were most commonly involved with PD synovitis at wrists in 19.3% and at MCP in 12.3% of patients (Table 2). For PD tenosynovitis, the flexor MCP 2-5 (5.3%) and compartment IV tenosynovitis (1.8 %) were the most frequent affected locations. Only two patients had PD enthesitis at feet and 6 (10.5%) had erosions in hands or feet at baseline examination. In the univariate analysis, the higher ESR values and the shorter time from symptoms onset were significantly associated with US detected inflammatory findings (p=0.044 and 0.049, respectively). In the multivariate analysis, only ESR values (OR=1,04; 95%CI 1,002-1,078), remained significantly associated with the presence of US inflammatory findings (Table 3).Table 3.Independent predictors of US detected inflammatory findingspOdds ratio95% C.I.LowerUpperESR (mm/h)0.0391.041.0021.078Time (months) from symptoms onset0.10.9240.8411.015Conclusion:PD US inflammatory findings are found in 1 over 3 patients with IA being PD synovitis the most common finding, specially at the wrists and MCP joints. Higher ESR values were significantly associated with the presence of US inflammatory findings. Our data highlights how the use of PD US may be useful to detect subclinical synovitis in patients with IA.Disclosure of Interests:Katerine López Gloria: None declared, Isabel Castrejon: None declared, Laura Trives Folguera Speakers bureau: ROCHE, Juan Carlos Nieto Speakers bureau: Pfizer, Abbvie, MSD, Novartis, Janssen, Lilly, Nordic Pharma, BMS, Gebro, FAES Farma, Roche, Sanofi, Belén Serrano Benavente: None declared, Julia Martínez-Barrio Consultant of: UCB Pharma, Javier Rivera: None declared, Carlos Gonzalez Consultant of: Gilead, Janssen, Novartis,, Speakers bureau: Abbvie, Celgene, Gilead, Janssen, Novartis, Pfizer, Roche, Indalecio Monteagudo: None declared, Jose-Maria Alvaro-Gracia Grant/research support from: Abbvie, Elli-Lilly, MSD, Novartis, Pfizer, Consultant of: Abbvie, BMS, Janssen-Cilag, Elli-Lilly, MSD, Novartis, Pfizer, Sanofi, Tigenix, Roche, UCB, Paid instructor for: Elli-Lilly, Pfizer, Roche, Speakers bureau: Abbvie, BMS, Janssen-Cilag, Elli-Lilly, Gedeon Richter, MSD, Novartis, Pfizer, Sanofi, Tigenix, Roche, UCB, Juan Molina Collada: None declared