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Objectives: The main objective was to generate a GLobal OMERACT Ultrasound DActylitis Score (GLOUDAS) in psoriatic arthritis and to test its reliability. To this end, we assessed the validity, feasibility and applicability of ultrasound assessment of finger entheses to incorporate them into the scoring system., Methods: The study consisted of a stepwise process. First, in cadaveric specimens, we identified enthesis sites of the fingers by ultrasound and gross anatomy, and then verified presence of entheseal tissue in histological samples. We then selected the entheses to be incorporated into a dactylitis scoring system through a Delphi consensus process among international experts. Next, we established and defined the ultrasound components of dactylitis and their scoring systems using Delphi methodology. Finally, we tested the interobserver and intraobserver reliability of the consensus- based scoring systemin patients with psoriatic dactylitis., Results: 32 entheses were identified in cadaveric fingers. The presence of entheseal tissues was confirmed in all cadaveric samples. Of these, following the consensus process, 12 entheses were selected for inclusion in GLOUDAS. Ultrasound components of GLOUDAS agreed on through the Delphi process were synovitis, tenosynovitis, enthesitis, subcutaneous tissue inflammation and periextensor tendon inflammation. The scoring system for each component was also agreed on. Interobserver reliability was fair to good (κ 0.39-0.71) and intraobserver reliability good to excellent (κ 0.80-0.88) for dactylitis components. Interobserver and intraobserver agreement for the total B-mode and Doppler mode scores (sum of the scores of the individual abnormalities) were excellent (interobserver intraclass correlation coefficient (ICC) 0.98 for B-mode and 0.99 for Doppler mode; intraobserver ICC 0.98 for both modes)., Conclusions: We have produced a consensus-driven ultrasound dactylitis scoring system that has shown acceptable interobserver reliability and excellent intraobserver reliability. Through anatomical knowledge, small entheses of the fingers were identified and histologically validated., Competing Interests: Competing interests: EN: Speaker fees from Abbvie, Lilly, Novartis, Pfizer; research grant from Lilly and Abbvie; support for attending meetings from Novartis and Fresenius Kabi. MADA: Speaker fees from Abbvie, Amgen, BMS, Galapagos, Novartis, Lilly, Janssen, and UCB; consulting fees from Abbvie, Amgen, BMS, Galapagos, Novartis, Lilly, Janssen, UCB; research grant from Abbvie, Amgen, Pfizer; royalty from Elsevier; support for attending meetings from Novartis and Janssen. LT: Speaker fees from Janssen, Lilly, Novartis, Pfizer; advisory board for Janssen and UCB. CP: No competing interests. MM: No competing interests. JB: No competing interests. GAWB: No competing interests. MCK: No competing interests. PM: Speaker fees from Janssen, Lilly, Novartis, AbbVie; research grant from AbbVie and Novartis. RN: Speaker fees from Abbvie, Novartis, Pfizer, Marcin Szkudlarek: Speaker fees from Novartis; meeting support from Pfizer. PT: Speaker fees from AbbVie, Novartis, Sandoz; advisory board for Novartis. VV: No competing interests. PW: No competing interests. CB: Speaker and/or Consultancy fees from: Janssen, Lilly, Novartis, AbbVie, Pfizer, UCB, Sanofi. EF: Speaker fees from AbbVie, Amgen, Bristol-Myers Squibb, Janssen-Cilag, Lilly, Novartis, Pfizer, Union Chimique Belge Pharma. AZ: Speaker bureau from AbbVie, Novartis, Janssen, Lilly, UCB, and Amgen; paid instructor from AbbVie, Novartis, UCB. MM: Speaker fees from Eli Lilly, SC Angelini Pharmaceuticals Romania SRL, KRKA; consulting fees from Eli Lilly, Galapagos. FAV: Speaker fees from Abbvie, Ewopharma BMS, Novartis, Lilly, Janssen, Pfizer, Zentiva, UCB; advisory board Abbvie, Ewopharma, Lilly, Janssen, Pfizer. MAM: No competing interests. JAM: Speaker fees from Janssen, Novartis, UCB; advisory board for Novartis. CAG-A: Speaker fees from Janssen, Abbvie, Novartis, Pfizer; advisory fees from Novartis, Galápagos, UCB; support for attending meetings from Pfizer, Janssen, Novartis. OO-V: Speaker fees from GSK and Novartis; support for attending meetings from Pfizer, Janssen, Gebro Pharma. AI: Grants from Abbvie, Pfizer, Novartis; Honoraria from AbbVie, Alfa-sigma, BMS, Celgene, Celltrion, Eli-Lilly, Galapagos, Gilead, Janssen, MSD, Novartis, Pfizer, Sanofi Genzyme, SOBI; Consulting fees from Abbvie, BMS, Pfizer, Eli-Lilly; Leadership or fiduciary roles as EULAR Immediate Past President; EULAR Presidency member; EULAR Board member; EULAR Advocacy Committee Member; EULAR Advocacy Committee Advisor. PH: No competing interests. IT: No competing interests. PVB: Speaker fees from Abbvie, Eli Lilly, Jannsen, Novartis, Richter, Sandoz; support for attending meetings from Abbvie, Janssen, Novartis, Eli Lilly, Sandoz. SZA: Speaker fees from Abbvie, Novartis, Pfizer, Janssen, UCB; research grant from Abbvie, Novartis, Pfizer, Janssen, Lilly, Fresenius Kabi; support for attending meetings from Abbvie, Pfizer, UCB and Fresenius Kabi. DK: Speaker fees from Abbvie, Galapagos, Janssen, Novartis; support for attending meetings from Novartis, Abbvie, and Janssen. HIK: Clinical trials Roche, Abbvie, Sun, Emerald, Novartis, Biogen, Sanofi, and Suneos. GSK: Research grants from Abbvie, Bristol Myers Squibb, Galapagos, Novartis, JannsenIngrid Möller: No competing interests., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ on behalf of EULAR.)

Background: The transition from psoriasis (PsO) to psoriatic arthritis (PsA) and the early diagnosis of PsA is of considerable scientific and clinical interest for the prevention and interception of PsA., Objective: To formulate EULAR points to consider (PtC) for the development of data-driven guidance and consensus for clinical trials and clinical practice in the field of prevention or interception of PsA and for clinical management of people with PsO at risk for PsA development., Methods: A multidisciplinary EULAR task force of 30 members from 13 European countries was established, and the EULAR standardised operating procedures for development for PtC were followed. Two systematic literature reviews were conducted to support the task force in formulating the PtC. Furthermore, the task force proposed nomenclature for the stages before PsA, through a nominal group process to be used in clinical trials., Results: Nomenclature for the stages preceding PsA onset, 5 overarching principles and 10 PtC were formulated. Nomenclature was proposed for three stages towards PsA development, namely people with PsO at higher risk of PsA, subclinical PsA and clinical PsA. The latter stage was defined as PsO and associated synovitis and it could be used as an outcome measure for clinical trials evaluating the transition from PsO to PsA. The overarching principles address the nature of PsA at its onset and underline the importance of collaboration of rheumatologists and dermatologists for strategies for prevention/interception of PsA. The 10 PtC highlight arthralgia and imaging abnormalities as key elements of subclinical PsA that can be used as potential short-term predictors of PsA development and useful items to design clinical trials for PsA interception. Traditional risk factors for PsA development (ie, PsO severity, obesity and nail involvement) may represent more long-term disease predictors and be less robust for short-term trials concerning the transition from PsO to PsA., Conclusion: These PtC are helpful to define the clinical and imaging features of people with PsO suspicious to progress to PsA. This information will be helpful for identification of those who could benefit from a therapeutic intervention to attenuate, delay or prevent PsA development., Competing Interests: Competing interests: AZ: speakers bureau: AbbVie, Novartis, Janssen, Lilly, UCB, Amgen, paid instructor for: AbbVie, Novartis, UCB, all support for the present manuscript: EULAR fellowship; GDM: EULAR fellowship; LG: consultant of: AbbVie, Amgen, BMS, Celltrion, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Sandoz, UCB, grant/research support from: Sandoz, UCB; XB: speakers bureau: AbbVie, BMS, MSD, Sandoz, Novartis, Pfizer, Galapagos, UCB, Lilly, paid instructor for: AbbVie, BMS, MSD, Sandoz, Novartis, Pfizer, Galapagos, UCB, Lilly, consultant of: AbbVie, BMS, MSD, Sandoz, Novartis, Pfizer, Galapagos, UCB, Lilly, grant/research support from: AbbVie, MSD, Novartis; leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid: Editorial Board Member of Annals of Rheumatic Diseases, ASAS President. DA received grants, speaker fees or consultancy fees from AbbVie, Gilead, Galapagos, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Sandoz and Sanof; AI: payment or honoraria for lectures, presentations, speakers bureau, manuscript writing or educational events AbbVie, Alfa-sigma, BMS, Celgene, Celltrion, Eli Lilly, Galapagos, Gilead, Janssen, MSD, Novartis, Pfizer, Sanofi Genzyme, SOBI grant/research support from: Pfizer, AbbVie, Novartis; leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid: EULAR President, member of the EULAR Board, member of EULAR Advocacy Committee; PG: payment or honoraria for lectures, presentations, speakers bureau, manuscript writing or educational events AbbVie, Almirall, Amgen, UCB, Sanofi, Pfizer, Novartis, Eli Lilly, Jannsen, Leo Pharma; PVB: none; HB: none declared; W-HB: speakers bureau: AbbVie, Almirall, BMS, Janssen, Leo, Lilly, Novartis and UCB, consultant of: AbbVie, Almirall, BMS, Janssen, Leo, Lilly, Novartis and UCB; NSD: none declared; MdW: payment or honoraria for lectures, presentations, speakers bureau, manuscript writing or educational events: UCB; EE: consultant of: AbbVie, Janssen, Novartis, Amgen; HM-O: speakers bureau: AbbVie, Biogen, Eli Lilly, Janssen, Moonlake, Novartis, Pfizer, Takeda and UCB Pharma, consultant of: AbbVie, Biogen, Eli Lilly, Janssen, Moonlake, Novartis, Pfizer, Takeda and UCB Pharma, grant/research support from: Janssen, Novartis and UCB; MP: support for attending meetings and/or travel: Pfizer, AbbVie, UCB; LP: speakers bureau: Janssen, Lilly, Novartis, UCB, consultant of: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Janssen, Leo Pharma, Lilly, Novartis, Pfizer, Sandoz, Sanofi, UCB, grant/research support from: AbbVie, Almirall, Amgen, Boehringer Ingelheim, Leo Pharma, Lilly, Novartis, Pfizer, Sanofi, UCB; RQ: grants or contracts from any entity: Novartis, Janssen, Pfizer; payment or honoraria for lectures, presentations, speakers bureau, manuscript writing or educational events: Amgen, Janssen, Eli Lilly, Novartis, UCB, Pfizer; PR: none declared; LS: speakers bureau: AbbVie, Almirall, Amgen, Aspire Pharma, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Celltrion, Fresensius Kabi, Galderma, Janssen, Leo, Lilly, Novartis, Pfizer, MSD, Sanofi, Takeda, UCB, Consultant of: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Fresensius Kabi, Janssen, Lilly, Novartis, UCB, grant/research support from: Janssen, Pfizer; GS: none declared; SS: speakers bureau: AbbVie, GSK, Janssen, UCB, consultant of: AbbVie, Amgen, Eli Lilly, Janssen, UCB, grant/research support from: Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, GSK, Janssen and UCB; TAS: speakers bureau: AbbVie, Roche, Sanofi, Takeda and Novartis, grant/research support from: AbbVie and Roche; PS: speakers bureau: AstraZeneca; IT: speakers bureau: Janssen, Pfizer; FEVdB: none declared; AvdH-vM: none declared; AW: payment or honoraria for lectures, presentations, speakers bureau, manuscript writing or educational events: Janssen Neopharm, Eli Lilly Novartis, AbbVie; consulting fees: Novartis, AbbVie, Janssen; JSS: consulting fees: AbbVie,Galapagos/Gilead, Novartis-Sandoz, BMS, Samsung Sanofi, Chugai R-Pharma, Lilly; payment or honoraria for lectures, presentations, speakers bureau, manuscript writing or educational events: Samsung, Lilly, Chugai R-Pharma, MSD, Janssen Novartis-Sandoz; DGMcG: speakers bureau: AbbVie, Celgene, Janssen, Merck, Novartis, Pfizer, UCB, consultant of: AbbVie, Celgene, Janssen, Merck, Novartis, Pfizer, UCB, grant/research support from: AbbVie, Celgene, Janssen, Merck, Novartis, Pfizer., (© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives: This study aimed to determine the prevalence of ultrasound-detected tendon abnormalities in healthy subjects (HS) across the age range., Methods: Adult HS (age 18-80 years) were recruited in 23 international Outcome Measures in Rheumatology ultrasound centres and were clinically assessed to exclude inflammatory diseases or overt osteoarthritis before undergoing a bilateral ultrasound examination of digit flexors (DFs) 1-5 and extensor carpi ulnaris (ECU) tendons to detect the presence of tenosynovial hypertrophy (TSH), tenosynovial power Doppler (TPD) and tenosynovial effusion (TEF), usually considered ultrasound signs of inflammatory diseases. A comparison cohort of patients with rheumatoid arthritis (RA) was taken from the Birmingham Early Arthritis early arthritis inception cohort., Results: 939 HS and 144 patients with RA were included. The majority of HS (85%) had grade 0 for TSH, TPD and TEF in all DF and ECU tendons examined. There was a statistically significant difference in the proportion of TSH and TPD involvement between HS and subjects with RA (HS vs RA p<0.001). In HS, there was no difference in the presence of ultrasound abnormalities between age groups., Conclusions: Ultrasound-detected TSH and TPD abnormalities are rare in HS and can be regarded as markers of active inflammatory disease, especially in newly presenting RA., Competing Interests: Competing interests: There are no declared competing interests from authors except the following: CC declared grants from NIHR Versus Arthritis, Lilly sponsored EULAR conference travel, Modern Biosciences payment as DSM committee member, Roche consultancy fee and Novartis sponsored writing of one medical paper. KI declared a Mitsubishi-Tanabe research grant for RA; Abbvie, Eli Lilly, Mitsubishi-Tanabe, Bristol-Myers-Squib and Novartis speaker’s fees; and participation on a DSM board for Abbvie, Eli Lilly and Mitsubishi-Tanabe. RK declared support from Abbvie, Roche, Novartis and UCB with payments for travel to meetings/lectures, presentations, speakers’ bureaus, manuscript writing/educational events., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY. Published by BMJ.)

Objectives: Dactylitis is one of the most typical features of psoriatic arthritis (PsA), with a high lifetime prevalence and inclusion in PsA clinical indices. Musculoskeletal ultrasonography (Msk-US) can readily detect inflammatory involvement of finger anatomical structures particular to dactylitis and monitor therapeutic effects. In this study, we aim to identify the characteristic lesions in PsA dactylitis of the hands, assess the reliability of Msk-US in scoring those lesions and develop a DACTylitis glObal Sonographic (DACTOS) score., Methods: After a systematic literature review on the use of Msk-US in PsA dactylitis, 12 rheumatologists participated in a three-round Delphi procedure and consensus meeting to agree on the sonographic elementary lesions characterising dactylitis and on the composition of a global sonographic score. Then, a web-based and a patient-based intra-rater and inter-rater reliability exercise was performed to assess those lesions included in the score., Results: DACTOS score was obtained by summing the scores of each lesion selected in the Delphi survey: subcutaneous soft tissue oedema, flexor tenosynovitis, peritendon extensor inflammation and synovitis. The DACTOS score ranges from 0 to 25. In the reliability exercises, we obtained moderate-to-excellent agreement for the sonographic lesions included in the score., Conclusions: The novel DACTOS score is a reliable measure to interpret the multiple characteristic sonographic features of dactylitis. The DACTOS score provides a useful global analysis of dactylitis of the hand and can represent a support to clinical diagnosis as well as a useful tool for the management and research in patients with PsA with dactylitis., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives: Skin and joint involvement in psoriasis (PsO) and psoriatic arthritis (PsA) are thought to relate to the so-called Koebner response. Given that dactylitis is non-randomly distributed in the digits, this study tested the hypothesis that the accessory pulleys linked to the flexor tendons were thickened in PsA and thus exhibited koebnerisation., Methods: Ninety-six subjects (27 PsA, 27 rheumatoid arthritis (RA), 23 PsO and 19 healthy controls (HCs)) were enrolled. The A1, A2 and A4 pulley thickness was measured using a high-resolution probe (22 MHz). All patients were in remission or low disease activity with current dactylitis being excluded., Results: Within 864 pulleys investigated, patients with PsA had thicker pulleys in every digit compared with both RA (P<0.001 and P=0.003) and HCs (P<0.001). RA and PsO groups had some pulleys in some digits thicker than HCs whereas some others were comparable. The second digit A1 pulley thickness was higher in patients with PsA with previous dactylitis (P=0.020). More pulleys were thickened in the PsA group (165/243, 68%) than RA (41/243, 17%; P<0.001) and HCs (13/171, 7.6%; P<0.001)., Conclusions: In established PsA, the accessory pulleys are thickened compared with RA, PsO or HCs and especially in subjects with a history of dactylitis. These findings implicate the involvement of pulleys in PsA-related tenosynovitis and dactylitis supporting the idea of deep koebnerisation in dactylitis and sites of high physical stress., Competing Interests: Competing interests: DMG received grants and/or honoraria from Abbvie, Celgene and Janssen. SZA received grants and/or honoraria from Abbvie, Novartis, UCB, Sanofi and Pfizer., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objective: Subclinical enthesopathy is recognised in both psoriasis and psoriatic arthritis (PsA). This study used ultrasonography with power Doppler (PD) to test the hypothesis that subclinical enthesopathy in PsA was associated with an 'inflammatory' or vascular phenotype compared to that seen in psoriasis., Methods: 100 patients with a mean age of 46.3 years (SD 15) (42 with psoriasis and 58 with PsA) and 23 matched healthy controls (HC) from two centres were included. 1230 lower limb entheses were scanned by ultrasonographers blinded to clinical details. Both inflammatory and chronic features of enthesopathy were scored., Results: Psoriasis patients (with or without arthritis) were more likely to express a vascular phenotype, with higher inflammation-related enthesopathy scores than HC (for inflammation p<0.0001, for chronicity p=0.02, for total ultrasound scores p<0.0001). The PsA patients had higher ultrasound enthesopathy scores than psoriasis patients (inflammation p=0.04, chronicity p=0.02) and HC (inflammation p<0.0001, chronicity p=0.003). When symptomatic entheses were excluded, PsA patients still had higher PD scores than psoriasis patients (p=0.003). Doppler positivity in at least one entheseal site was observed more frequently in PsA (21/58, 36.2%) versus psoriasis (4/42, 9.5%; p=0.002)., Conclusions: This study shows that the ultrasound appearances of subclinical enthesitis in psoriasis differ from the subclinical enthesitis in PsA, with PsA patients having more PD. This is suggestive of a more inflammatory or vascular process in PsA, and offers potentially novel insights into the progression from skin to joint disease in psoriasis.

Objective: Caveolin-1 (CAV1) is an inhibitor of tissue fibrosis and has been implicated in the pathogenesis of systemic sclerosis (SSc). The aim of the study was to analyse the possible association of CAV1 gene single nucleotide polymorphisms (SNP) with SSc., Methods: A total population of 3974 individuals (1355 SSc patients, 2619 controls) was studied. Genotype data for 23 SNP spanning the CAV1-CAV2 gene locus were obtained from a genome-wide scan conducted in a French population (564 SSc patients, 1776 controls). Three CAV1 SNP (rs926198, rs959173, rs9920) displaying the most significant associations with SSc and/or clinical phenotypes were then genotyped in an Italian population (791 SSc patients, 843 controls). CAV1 protein expression in skin biopsies was investigated by immunohistochemistry and western blotting., Results: In the French population, the CAV1 rs959173 C minor allele showed a significant protective association with susceptibility to SSc (OR 0.71, 95% CI 0.59 to 0.86, p(adjusted)=0.009), and with the subset of patients with limited cutaneous SSc (OR 0.71, 95% CI 0.56 to 0.89, p(adjusted)=0.018). The association was replicated in the Italian population and strengthened in the combined populations through Cochran-Mantel-Haenszel meta-analysis (SSc: pooled OR 0.81, 95% CI 0.71 to 0.92, p=0.0018; limited cutaneous SSc: pooled OR 0.80, 95% CI 0.69 to 0.93, p=0.0053). Genotype/protein expression correlations revealed that the rs959173 C protective allele was associated with increased CAV1 protein expression., Conclusions: These results add CAV1 to the list of SSc susceptibility genes and provide further evidence for the contribution of this pathway in the fibrotic process that characterises SSc pathogenesis.

Objective: Enthesopathy is a major feature of psoriatic arthritis (PsA), which is supported by imaging studies. Given that nail disease often predates PsA and that the nail is directly anchored to entheses, the authors asked whether nail involvement in psoriasis equates with a systemic enthesopathy., Methods: Forty-six patients with psoriasis (31 with nail disease) and 21 matched healthy controls (HC) were recruited. 804 entheses of upper and lower limbs were scanned by an ultrasonographer blinded to clinical details., Results: Psoriasis patients had higher enthesitis scores than HC (median (range) 21 (0-65) vs 11 (3-39), p=0.005). Enthesopathy scores were higher in patients with nail disease (23 (0-65)) than in patients without nail disease (15 (5-26), p=0.02) and HC (11 (3-39), p=0.003). Inflammation scores of patients with nail disease (13 (0-34)) were higher than patients without nail disease (8 (2-15), p=0.02) and HC (5 (0-19), p<0.001). Modified nail psoriasis severity index scores were correlated to both inflammation (r(2)=0.45, p=0.005) and chronicity scores (r(2)=0.35, p=0.04). No link between the psoriasis area and severity index and enthesitis was evident., Conclusion: The link between nail disease and contemporaneous subclinical enthesopathy offers a novel anatomical basis for the predictive value of nail psoriasis for PsA evolution.