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Articles de revues sur le sujet « Alain of Lille »

Auteur : Grafiati
Publié le 10 mars 2023

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1

Castellani, Marie-Madeleine. « Alain de Lille ». Nord' N°75, no 1 (2020) : 65. http://dx.doi.org/10.3917/nord.075.0065.

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Pejenaute Rubio, Francisco. « El Alain de Lille que conocemos sigue siendo Alain de Lille ». Helmántica, no 182 (1 janvier 2009) : 221–42. http://dx.doi.org/10.36576/summa.29422.

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SCATTERGOOD. « ALAIN DE LILLE AND THE PROLOGUE TO "PATIENCE" ». Medium Ævum 61, no 1 (1992) : 87. http://dx.doi.org/10.2307/43632172.

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Ferreira Filho, Pedro Calixto, et Antonio Henrique Campolina Martins. « LA TRANSLATIO SEMANTICAE ET GRAMMAIRE CHEZ ALAIN DE LILLE ». Revista Ética e Filosofia Política 2, no 21 (10 janvier 2019) : 194–247. http://dx.doi.org/10.34019/2448-2137.2018.17866.

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Résumé : Dans le néoplatonisme grec, le fait d'avoir érigé un principe non-ontique rompt avec la supériorité de l'affirmation sur la négation lorsqu'il s'agit d'énoncer le divin. Cependant, à cause des thèses exprimées sur la transcendance radicale de l'Un, la réflexion sur le discours portant sur la divinité s'achève la plupart du temps par la dénonciation d'une inaptitude profonde du discours à signifier une quelconque réalité divine, et aboutit systématiquement à l'apologie du silence. L’apophase a comme objectif de dépouiller l’âme de toute détermination afin qu’elle puisse s’unir au Principe qui est au-delà de toute détermination. Au XIIème siècle la conscience de la supériorité de la négation sur l'affirmation in divinis, qui avait donné l’origine à la translatio nominis chez Denys et à une translatio categoriae chez Erigène, donne lieu à une théorie grammaticale que l'on a qualifiée de translatio semanticae. C'est cette question du tranfert sémantique des noms et de la proposition qui constituera l’objet d'analyse de ce chapitre. Nous nous proposons d’étudier les éléments de cette sémantique et de cette syntaxe néoplatoniciennes dans les maximes de grammaire contenues dans les Règles de Théologie d'Alain de Lille écrites au XIIème siècle.Mots-clef : Alain de Lille, grammaire, sémantique, translatio, kataphase, apophase.
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Calixto, Pedro. « La sémantique propositionnelle in divinis chez Alain de Lille ». Revue des sciences philosophiques et théologiques TOME 91, no 1 (2007) : 23. http://dx.doi.org/10.3917/rspt.911.0023.

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Wahlgren-Smith, Lena. « Alain de Lille (?) : Letters familières (1167-1170). Françoise Hudry ». Speculum 81, no 2 (avril 2006) : 536–37. http://dx.doi.org/10.1017/s0038713400003080.

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McCurdy, Harold. « Omnis Mundi Creatura (Alain of Lille, c. 1128–1202) ». Theology Today 44, no 3 (octobre 1987) : 371. http://dx.doi.org/10.1177/004057368704400310.

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Benedict, Philip. « Lille : Citadelle de la Contre-Réforme ? (1598-1668). Alain Lottin ». Journal of Modern History 58, no 3 (septembre 1986) : 724–25. http://dx.doi.org/10.1086/243058.

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CAIRNS. « 'ALAIN DE LILLE AND THE PROLOGUE TO "PATIENCE"' : A BIBLIOGRAPHICAL CORRECTION ». Medium Ævum 62, no 2 (1993) : 292. http://dx.doi.org/10.2307/43629562.

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Bain, Emmanuel. « Les hérétiques du prince : Alain de Lille et les hérétiques méridionaux ». Cahiers de Fanjeaux 55, no 1 (2020) : 173–95. http://dx.doi.org/10.3406/cafan.2020.2431.

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Eckhardt, Caroline D. « Another Manuscript of the Commentary on Prophetia Merlini Attributed to Alain de Lille ». Manuscripta 29, no 3 (novembre 1985) : 143–47. http://dx.doi.org/10.1484/j.mss.3.1157.

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Miatello, André Luis Pereira. « A política dos sermões ou os sermões na política : a pregação nas cidades comunais da Baixa Idade Média ». Diálogos 21, no 1 (26 mai 2017) : 98. http://dx.doi.org/10.4025/dialogos.v21i1.37332.

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Este artigo propõe os sermões da Baixa Idade Média ocidental como parte da linguagem política das comunas italianas. Junto com os discursos de assembleia (conciones), os sermões compunham uma retórica de natureza religiosa com validade cívica apta para os governos citadinos e para o modo de vida urbano. Estuda-se a Summa de Arte Praedicatoria, de Alain de Lille, os Li livres dou Trésor, de BrunettoLatini, os sermões de Giordano de Pisa e a Crônica de Rolandino de Pádua para mostrar como, de um ponto de vista político e cívico, os sermões eram peças importantes do ordenamento social e da resolução de conflitos.
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Pejenaute Rubio, Francisco. « Observaciones al pretendido Prólogo, en prosa, al de De plactu Naturae de Alain de Lille ». Helmántica 51, no 155 (1 janvier 2000) : 471–98. http://dx.doi.org/10.36576/summa.3627.

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Albert, Jean-Pierre. « Alain Lottin, Être et croire à Lille et en Flandre, XVIe-XVIIIe siècles. Recueil d’études ». Archives de sciences sociales des religions, no 122 (1 avril 2003) : 59–157. http://dx.doi.org/10.4000/assr.1440.

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Alves, Aléssio Alonso. « PRAEDICATIO EST : HUMBERT OF ROMANS, JACOBUS OF FUSIGNANO AND GIORDANO DA PISA ON THE PREACHING OF THE ORDER OF THE FRIAR PREACHERS IN THE LATE XIIITH AND EARLY XIVTH CENTURY ». Revista de Historia Social y de las Mentalidades 24, no 2 (14 décembre 2020) : 1–40. http://dx.doi.org/10.35588/rhsm.v24i2.4426.

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The purpose of this article is to establish a synthetic concept of preaching according with the statements expressed by three Friars Preachers in the second half of the thirteenth and early fourteenth century. Starting with the definition by the theologian Alain de Lille (1128-1202), today taken as paradigmatic, three works of different natures are analysed and compared: De eruditione religiosorum praedicatorum (1263), by Humbert of Romans (1190-1277); the Libellus artis predicatorie (1290), by Jacobus of Fusignano (? -1333); and the reportationes of two sermons (1304) by Giordano da Pisa (c. 1260-1311). As conclusion, preaching is synthesized into a concept as an instruction on the Holy Scriptures, divine things, faith and truth; as well as about morals, vices and sins, whose goal is the salvation of its audience.
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Ótott, Noémi. « Az Il Tesoretto forrásainak tükrében ». Antikvitás & ; Reneszánsz, no 5 (1 mai 2020) : 15–33. http://dx.doi.org/10.14232/antikren.2020.5.15-33.

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Brunetto Latini firenzei irodalmár és politikus Il Tesoretto című allegorikus-didaktikus költeménye feltehetően az 1260-as évek második felében, franciaországi száműzetése idején keletkezett. A költemény a szerző által egyes szám első személyben elmesélt allegorikus látomás története. Kritikusai mindig is azt vetették Latini szemére, hogy egyszerű kompilátor volt, aki forráskritika nélkül átvett mindent modelljeitől. Az világosan látszik, hogy gyakran és módfelett tudatosan utánozta elődeit, főként Alain de Lille-t, Boethiust és a Rózsaregény szerzőjét (szerzőit), mind szó szerinti szövegátvételekkel és tartalmi párhuzamokkal, mind pedig a műfajok és stílusbeli hangnemek átvételével.Jelen tanulmány célja, hogy átfogó képet adjon az Il Tesoretto forrásairól, valamint a szakirodalom által eddig feltárt adatokon túl további egyezéseket, sőt különbségeket és módosításokat mutasson be és vizsgáljon meg. A tanköltemény elemzése és valódi értékeinek keresése során ugyanis fontos látni, hogyan alkalmazta Latini elődeinek műveit, és hogyan illesztette be ezeket saját költői víziójába.
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Vion, Daniel. « Allocution prononcée par le doyen Daniel Vion lors des funérailles du professeur Alain BRICE, (Lille, le 10 juin 2000) ». Journal européen d’hydrologie 31, no 1 (2000) : 9–10. http://dx.doi.org/10.1051/water/20003101009.

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Pini, Giorgio. « Logic, Theology, and Poetry in Boethius, Abelard, and Alain of Lille : Words in the Absence of Things. By Eileen C. Sweeney ». International Philosophical Quarterly 52, no 2 (2012) : 252–54. http://dx.doi.org/10.5840/ipq201252223.

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Le Goff, T. J. A. « Histoire de Lille de Charles Quint à la conquête française (1500-1715). Jean-Jacques Duthoy , Alain Lottin , Hervé Oursel , Louis Trenard ». Journal of Modern History 57, no 2 (juin 1985) : 361–63. http://dx.doi.org/10.1086/242845.

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Wille, Clara. « La Symbolique animale de la Prophetia Merlini de Geoffroy de Monmouth selon un commentaire de XII² siècle attribué à Alain de Lille ». Reinardus / Yearbook of the International Reynard Society 15 (8 novembre 2002) : 175–90. http://dx.doi.org/10.1075/rein.15.14wil.

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Perloff, Marjorie. « Presidential Address 2006 : It Must Change ». PMLA/Publications of the Modern Language Association of America 122, no 3 (mai 2007) : 652–62. http://dx.doi.org/10.1632/pmla.2007.122.3.652.

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This year marks the centennial of Samuel Beckett's birth, and the celebrations around the world have been a wonder to behold. From Buenos Aires to Tokyo, from Rio de Janeiro to Sofia, from South Africa (where Beckett did not permit his plays to be performed until apartheid was ended) to New Zealand, from Florida State University, in Tallahassee, to the University of Reading, from the Barbican Theatre, in London, to the Pompidou Center, in Paris, from Hamburg and Kassel and Zurich to Aix-en-Provence and Lille, from Saint Petersburg to Madrid to Tel Aviv, and of course most notably in Dublin, 2006 has been Beckett's year. Most of the festivals have included not only performances of the plays but also lectures, symposia, readings, art exhibitions, and manuscript displays. Paris Beckett 2006, for example, cosponsored by the French government and New York University's Center for French Civilization and Culture, has featured productions of Beckett's entire dramatic oeuvre, mounted in theaters large and small all over Paris, and lectures by such major figures as the novelist-theorists Philippe Sollers and Hélène Cixous, the playwrights Fernando Arrabal and Israel Horovitz, and the philosopher Alain Badiou. To round things out, in 2007 the Pompidou Center will host a major exhibition of and on Beckett's work.
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VINCENT, NICHOLAS. « Alain de Lille (?). Lettres familières (1167–1170). Edited by Françoise Hudry, with a preface by Pascale Bourgain. (Études et rencontres de l’École des Chartes, 14.) Pp. 189. Paris : Vrin/École des Chartes, 2003. €25. 2 7116 4332 0 ». Journal of Ecclesiastical History 56, no 3 (juillet 2005) : 572–74. http://dx.doi.org/10.1017/s0022046905604381.

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Beltai, A., B. Combe, A. Coffy, C. Gaujoux-Viala, C. Lukas, A. Saraux, M. Dougados, J. P. Daures et C. Hua. « POS0306 IMPACT OF MULTIMORBIDITY ON DISEASE MODIFYING ANTI-RHEUMATIC DRUG THERAPY IN EARLY RHEUMATOID ARTHRITIS : DATA FROM THE ESPOIR COHORT ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 379.2–379. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2868.

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Background:Multimorbidity is frequent in rheumatoid arthritis (RA) and could interfere with the therapeutic response.Objectives:The aim of this study was to evaluate multimorbidity in the French cohort of early arthritis (ESPOIR cohort) and its possible impact on the therapeutic response.Methods:We included patients fulfilling 2010 ACR/EULAR criteria for RA. An adapted MultiMorbidity Index (aMMI) was developed [1]. Each patient was assigned scores of binary aMMI (0= no comorbidity, 1= at least 1 comorbidity) and counted and weighted aMMI. The primary endpoint was achievement of Clinical Disease Activity Index (CDAI) low disease activity after initiation of a first disease-modifying anti-rheumatic drug (DMARD) according to the aMMI. Secondary endpoints were other disease activity scores and response criteria. We collected data from the visit preceding the first DMARD initiation (baseline visit) and the visit after at least 3 months of treatment (follow-up visit). The impact of aMMI on therapeutic maintenance at 1, 3, 5 and 10 years was evaluated.Results:Analyses involved 472 patients: 302 (64%) had at least 1 comorbidity. Overall, 45.3% and 44.7% with binary aMMI= 0 or 1, respectively (p= 0.9), achieved CDAI low disease activity (Table 1). Similar results were found with counted and weighted aMMI. Use of other disease activity scores or response criteria did not show a significant impact of multimorbidity on the therapeutic response. Therapeutic maintenance was significantly better with binary aMMI = 1 than binary aMMI = 0. Increased counted aMMI was associated with increased probability of still being on the first initiated DMARD at each time point (Table 2).Table 1.Impact of aMMIs on CDAI, DAS28 and SDAI low disease activity (LDA) achievement at follow-up visit (univariate analyses)LDA achievementCDAIpDAS28pSDAIpYesNoYesNoYesNoBinary aMMI, n (%)077 (45.3)93 (54.7)0.9*85 (50.0)85 (50.0)0.2*80 (47.1)90 (52.9)0.9*1135 (44.7)167 (55.3)131 (43.4)171 (56.6)141 (46.7)161 (53.3)Counted aMMI, mean (SD)1.0 (1.1)1.1 (1.1)0.71.0 (1.1)1.1 (1.1)0.21.1 (1.1)1.1 (1.1)1.0Weighted aMMI, mean (SD)4.1 (5.2)4.0 (4.7)0.94.0 (5.2)4.1 (4.7)0.34.0 (5.0)4.0 (4.9)1.0aMMI= adapted MultiMorbidity Index; CDAI= Clinical Disease Activity Index; SDAI= Simplified Disease Activity Index* Proportion of patients achieving LDA between patients with binary aMMI= 0 and binary aMMI= 1. Because of no statistically significant results, no multivariate analysis was performed.Table 2.Probability of first DMARD maintenance at 1, 3, 5 and 10 years (multivariate analysis)Time pointFirst DMARD maintained or stoppedBinary aMMI#Counted aMMI§011 year(n= 530)Maintenance (n= 300)22981.71 (0.93)OR [95% CI]*> 999 [286.2->999]221.3 [84.0-583.0]Withdrawal (n= 230)205250.12 (0.37)3 years(n= 493)Maintenance (n= 285)102751.66 (0.94)OR [95% CI]*153.9 [73.0-324.5]26.1 [15.1-45.3]Withdrawal (n= 208)175330.22 (0.64)5 years(n= 459)Maintenance (n= 116)91071.72 (1.05)OR [95% CI]*10.9 [5.1-23.3]2.2 [1.8-2.7]Withdrawal (n= 343)1631800.82 (1.0)10 years(n= 415)Maintenance (n= 40)2381.58 (0.84)OR [95% CI]*14.0 [3.3-59.1]1.6 [1.2-2.0]Withdrawal (n= 375)1582170.99 (1.12)#data are number of patients§ data are mean (standard error)* data are odds ratios (ORs) and 95% confidence intervals (95% CI) of still being on the first initiated DMARD at 1, 3, 5 and 10 years between patients with binary aMMI = 1 and binary aMMI = 0 and according to counted aMMI, per additional point.Conclusion:In the ESPOIR cohort, therapeutic response to a first DMARD was not affected by multimorbidity but therapeutic maintenance was better in multimorbid patients.References:[1]Radner H, Yoshida K, Mjaavatten MD, et al. Development of a multimorbidity index: Impact on quality of life using a rheumatoid arthritis cohort. Semin Arthritis Rheum 2015;45:167–73.The variables included in multivariate analyses were sex, rheumatoid factor and/or anti-citrunillated peptide antibody positivity, age, CDAI at baseline visit, number of treatments at baseline visit.Acknowledgements:We are grateful to Nathalie Rincheval (Montpellier) for expert monitoring and data management and all the investigators who recruited and followed the patients (F. Berenbaum, Paris-Saint Antoine; MC. Boissier, Paris-Bobigny; A. Cantagrel, Toulouse; B. Combe, Montpellier; M. Dougados, Paris-Cochin; P. Fardellone and P. Boumier, Amiens; B. Fautrel, Paris-La Pitié; RM. Flipo, Lille; Ph. Goupille, Tours; F. Liote, Paris- Lariboisière; O. Vittecoq, Rouen; X. Mariette, Paris-Bicêtre; P. Dieude, Paris Bichat; A. Saraux, Brest; T. Schaeverbeke, Bordeaux; and J. Sibilia, Strasbourg).Disclosure of Interests:Aurélie BELTAI: None declared, Bernard Combe Speakers bureau: AbbVie; Bristol-Myers Squibb; Gilead; Janssen; Lilly; Merck; Novartis; Pfizer; Roche-Chugai; and Sanofi, Consultant of: AbbVie; Bristol-Myers Squibb; Gilead; Janssen; Lilly; Merck; Novartis; Pfizer; Roche-Chugai; and Sanofi, Grant/research support from: Novartis, Pfizer, and Roche, Amandine Coffy: None declared, Cécile Gaujoux-Viala: None declared, Cédric Lukas Speakers bureau: Abbvie, Amgen, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai and UCB, Consultant of: Abbvie, Amgen, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai and UCB, Grant/research support from: Pfizer, Novartis and Roche-Chugai, Alain Saraux Speakers bureau: AbbVie; Bristol-Myers Squibb; Lilly; Nordic; Novartis; Pfizer; Roche-Chugai; Sanofi and UCB, Consultant of: AbbVie; Bristol-Myers Squibb; Lilly; Nordic; Novartis; Pfizer; Roche-Chugai; Sanofi and UCB, Grant/research support from: AbbVie; Bristol-Myers Squibb; Lilly; Nordic; Novartis; Pfizer; Roche-Chugai; Sanofi and UCB, Maxime Dougados Speakers bureau: Pfizer, Abbvie, Lilly, UCB, Merck, BMS, Roche, Biogen, Sanofi, Novartis, Sandoz, Consultant of: Pfizer, Abbvie, Lilly, UCB, Merck, BMS, Roche, Biogen, Sanofi, Novartis, Sandoz, Grant/research support from: Pfizer, Abbvie, Lilly, UCB, Merck, BMS, Roche, Biogen, Sanofi, Novartis, Sandoz, Jean-Pierre DAURES: None declared, Charlotte Hua: None declared
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Andrianova, Irina, Elena Vyal, Marina Zavarkina et Lyubov Alekseeva. « In memory of Louis Allain ». Неизвестный Достоевский 9, no 1 (mars 2022) : 156–57. http://dx.doi.org/10.15393/j10.art.2022.6041.

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On January 15, Louis Allain, one of the leading French Slavists, a researcher of F. M. Dostoevsky's work and literature of the Silver Age, honorary professor at the University of Lille, a member of the editorial board of "The Unknown Dostoevsky" journal, passed away after a prolonged illness at the age of 88. Professor Allen's interests centered on Russian literature from Pushkin to Blok, but he is most renowned as the author of works dedicated to the work of Dostoevsky. An evening in memory of Louis Allain will be held at the Institute of Slavic Studies in Paris on April 13. Members of the Editorial Board of our journal express their deepest condolences to the relatives, friends and colleagues of Professor Allain. We grieve together with you for the irreparable loss. May this brilliant and wonderful man, researcher and educator stay in our memory forever!
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Ramiro, S., R. B. M. Landewé, D. Van der Heijde, A. Sepriano, O. Fitzgerald, M. Østergaard, J. Homik et al. « POS0111 MORE METICULOUSLY FOLLOWING TREAT-TO-TARGET IN RA DOES NOT LEAD TO LESS RADIOGRAPHIC PROGRESSION : A LONGITUDINAL ANALYSIS IN BIODAM ». Annals of the Rheumatic Diseases 81, Suppl 1 (23 mai 2022) : 279–81. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2161.

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BackgroundA Treat-to-Target approach (T2T) is broadly considered to lead to better clinical outcomes and recommended in patients with RA. However, very few studies have analyzed the effect of T2T on radiographic progression, and any such studies have provided inconsistent results.ObjectivesTo investigate whether meticulously following a treat-to-target (T2T)-strategy in daily clinical practice leads to lower radiographic progression in RA.MethodsPatients from the multicenter RA-BIODAM cohort with ≥2 consecutive visits with radiographs available were included. In RA-BIODAM patients were enrolled as they were initiating a new csDMARD/bDMARD treatment were followed-up with the intention to benchmark and intensify treatment. The primary outcome of this analysis was the change in Sharp-van der Heijde score (SvdH, 0-448), assessed every 6 months, using average scores from 2 readers (scores with known chronological order). Following a DAS44-T2T remission strategy, which was defined at each 3-month visit, was the main variable of interest. Patients were categorized based on the proportion of visits in which T2T was followed according to our definition: very low (≤40% of the visits, low (>40%, <62.5%), high (≥62.5%, ≤75%) and very high (>75%). Radiographic progression at 2 years was visualized across groups by cumulative probability plots. Per 3-month interval T2T could be followed zero, one or two times (in a total of 2 visits). Associations between the number of visits with T2T in an interval and radiographic progression, both in the same and in the subsequent 6-month interval, were analysed by generalised estimating equations, adjusted for age, gender, disease duration and country.ResultsIn total, 511 patients were included (mean (SD) age: 56 (13) years; 76% female). After 2 years, patients showed on average 2.2 (4.1) units progression (median:1 unit). Mean (SD) 2-year progression was not significantly different across categories of T2T: very low: 2.1 (2.7)-units; low: 2.8 (6.0); high: 2.4 (4.5), very high: 1.6 (2.2) (Figure 1). Meticulously following-up T2T in a 3-month interval neither reduced progression in the same 6-month interval (parameter estimates (for yes vs no): +0.15 units (95%CI: -0.04 to 0.33) for 2 vs 0 visits; and +0.08 units (-0.06;0.22) for 1 vs 0 visits) nor did it reduce progression in the subsequent 6-month interval (Table 1).Table 1.Effect of following DAS44-remission-T2T strategy on 6-month radiographic progression over 2 yearsChange in radiographic damage(regression coefficient (95% CI))N=506T2T during 3 months on radiographic progression in the same 6-month period 2 visits vs 0 followed0.15 (-0.04; 0.33) 1 visit vs 0 followed0.08 (-0.06; 0.22)T2T during 3 months on radiographic progression in the subsequent 6-month period 2 visits vs 0 followed-0.09 (-0.28; 0.10) 1 visit vs 0 followed-0.10 (-0.24; 0.05)Figure 1.Cumulative probability plot with 2-year radiographic progression according to the proportion of 3-monthly visits with T2T followedConclusionIn this daily practice cohort, more meticulously following T2T principles did not result in more reduction of radiographic progression than a somewhat more liberal attitude toward T2T. One possible interpretation of these results is that the intention to apply T2T already suffices and that a more stringent approach does not further improve outcome.AcknowledgementsBIODAM was financially supported by an unrestricted grant from AbbVieDisclosure of InterestsSofia Ramiro Speakers bureau: Eli Lilly, MSD, Novartis, UCB, Consultant of: AbbVie, Eli Lilly, MSD, Novartis, Pfizer, UCB, Sanofi, Grant/research support from: AbbVie, Galapagos, Novartis, Pfizer, UCB, Robert B.M. Landewé Speakers bureau: AbbVie, BMS, Gilead, Galapagos, GSK,Janssen, Lilly, Novartis, Pfizer, UCB, Consultant of: AbbVie, BMS, Gilead, Galapagos, GSK,Janssen, Lilly, Novartis, Pfizer, UCBDr Landewé owns Rheumatology Consultancy BV, Désirée van der Heijde Consultant of: AbbVie, Bayer, BMS, Cyxone, Eisai, Galapagos, Gilead, Glaxo-Smith-Kline, Janssen, Lilly, Novartis, Pfizer, UCB Pharma. Director of Imaging Rheumatology bv., Alexandre Sepriano Speakers bureau: Novartis, Consultant of: UCB, Oliver FitzGerald Speakers bureau: Biogen, Novartis, AbbVie, BMS, Pfizer, Grant/research support from: BMS, Novartis, UCB, Pfizer, Lilly, Janssen, Mikkel Østergaard Speakers bureau: Abbvie, BMS, Celgene, Eli-Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Orion, Pfizer, Roche and UCB, Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi and UCB, Grant/research support from: Abbvie, Amgen, BMS, Merck, Celgene and Novartis, Joanne Homik: None declared, Ori Elkayam Speakers bureau: Pfizer, Lilly, Novartis, Abbvie, BI, Janssen, Consultant of: Pfizer, Lilly, Novartis, Abbvie, BI, Janssen, Grant/research support from: Pfizer, Abbvie, Janssen, Carter Thorne Consultant of: Abbvie, Organon, Pfizer, Sandoz, Maggie Larché Speakers bureau: AbbVie, Actelion, Amgen, BMS, Boehringer-Ingelheim, Fresenius-Kabi, Gilead, Janssen, Mallinckrodt, Merck, Novartis, Pfizer, Roche, Sandoz, Sanofi, Sobi, UCB, Grant/research support from: Abbvie, BMS, Gianfranco Ferraccioli Speakers bureau: SOBI, Consultant of: Abbivie, Marina Backhaus: None declared, Gilles Boire Speakers bureau: Abbvie Canada, BMS Canada, Lilly Canada, Janssen Canada, Merck Canada, Pfizer Canada, Viatris, Consultant of: Abbvie Canada, Amgen Canada, BMS Canada, Celgene, GileadSciences, Janssen Canada, Lilly Canada, Merck Canada, Mylan Canada, Novartis Canada, Pfizer Canada, Roche Canada, Samsung Bioepis, Sanofi Canada, Teva, Grant/research support from: Lilly Canada, BMS Canada, Pfizer, Sandoz Canada, UCB Canada, Merck Canada, Novartis Canada, Roche Canada, Bernard Combe Speakers bureau: Abbvie, BMS,Celltrion,Galapgos-Gilead, Janssen, Lilly, MERCK, Pfizer,Roche-Chugai, Consultant of: Abbvie, Celltrion,Galapgos-Gilead, Janssen, Lilly, MERCK, Roche-Chugai, Grant/research support from: Pfizer, Roche-chugai, Thierry Schaeverbeke: None declared, Alain Saraux Speakers bureau: Abbvie, Lilly, Nordic, Novartis, Pfizer, Roche-Chugai, Sanofi, UCB, Consultant of: Abbvie, Lilly, Nordic, Novartis, Pfizer, Roche-Chugai, UCB, Grant/research support from: Novartis, Fresenius, Lilly, Maxime Dougados Consultant of: Pfizer, AbbVie, UCB, Merck, Lilly, Novartis, BMS, Galapagos, Biogen, Roche, Grant/research support from: Pfizer, AbbVie, UCB, Merck, Lilly, Novartis, BMS, Galapagos, Biogen, Roche, Maurizio Rossini Speakers bureau: Amgen, Abbvie, BMS, Eli-Lilly, Galapagos,MSD, Novartis, Pfizer, Sandoz, Theramex, UCB, Marcello Govoni Speakers bureau: Abbvie, Pfizer, Galapagos, BMS, Eli-Lilly, Paid instructor for: Pfizer, Consultant of: Abbvie, BMS, Novartis, Astrazeneca, Pfizer, Luigi Sinigaglia: None declared, Alain Cantagrel Speakers bureau: Abbvie, Amgen, Biogen, BMS, Janssen, Lilly France, Médac, MSD France, Nordic-Pharma, Novartis, Pfizer, Sanofi Aventis, UCB, Consultant of: BMS, Janssen, Lilly France, MSD France, Sandoz, Grant/research support from: MSD France, Novartis, Pfizer, Cornelia Allaart: None declared, Cheryl Barnabe Speakers bureau: Sanofi Genzyme, Pfizer, Fresenius Kabi, Janssen, Consultant of: Gilead, Celltrion Healthcare, Clifton Bingham Consultant of: AbbVie, BMS, Eli Lilly, Janssen, Moderna, Pfizer, Sanofi, Grant/research support from: BMS, Dirkjan van Schaardenburg: None declared, Hilde Berner Hammer Speakers bureau: AbbVie, Novartis, Lilly, Rana Dadashova: None declared, Edna Hutchings: None declared, Joel Paschke: None declared, Walter P Maksymowych Speakers bureau: Abbvie, Janssen, Novartis, Pfizer, UCB, Consultant of: Abbvie, Boehringer Ingelheim, Celgene, Eli-Lilly, Galapagos, Novartis, Pfizer, UCB, Grant/research support from: Abbvie, Novartis, Pfizer
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Combe, B., N. Rincheval, F. Berenbaum, P. Boumier, A. Cantagrel, P. Dieudé, M. Dougados et al. « OP0181 CURRENT FAVOURABLE 10-YEAR OUTCOME OF PATIENTS WITH EARLY RHEUMATOID ARTHRITIS : DATA FROM THE ESPOIR COHORT ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 109–10. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1063.

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Background:ESPOIR is a longitudinal prospective cohort of adults with possible early RA (ClinicalTrials.gov: NCT03666091). Patients were referred by rheumatologists and general practitioners to one of the 14 regional centers in France. The objective and design of the cohort are described elsewhere (1). Patients received standard of care by their rheumatologists and were followed without predefined therapeutic strategiesObjectives:To report the current 10-year outcome of patients with early rheumatoid arthritis (RA) in the ESPOIR cohort, and predictors of outcome.Methods:From 2003 to 2005, 813 patients were included if they had early arthritis (< 6 months) with a high probability of RA developing and had never been prescribed disease modifying anti-rheumatic drugs (DMARDs). Multivariate logistic regression analysis was used to evaluate predictors of outcome.Results:In total, 521 (64.1%) RA patients were followed up for 10 years and 35 (4.3%) died, which appears similar to the French general population. Overall, 480 (92.1%) patients received a DMARD; 174/521 (33.4%) received at least one biologic DMARD, 13.6 and 23.4% within 2 and 5 years. At year 10 (Table), mean DAS28 ESR was 2.5 ± 1.3; 273 (52.4%) patients were in DAS28 remission, 39.7% in CDAI remission, 40.1% in DAS28 sustained remission, and 14.1% in drug-free remission. Disability was well controlled overtime (Figure) and half of the patients achieved a HAQ Disability Index < 0.5; the SF-36 physical component and pain were well controlled. Structural progression was weak, with a mean change from baseline in modified Sharp score of 11.0 ± 17.9. A total of 82 (16.5%) patients required joint surgery including arthroplasty or arthrodesis in only 6.5% of the cases. A substantial number of patients showed new comorbidities, mainly cardiovascular or metabolic diseases over 10 years. Finally, positivity for anti-citrullinated protein antibodies was confirmed as a robust predictor of long-term outcome in patients with early RA.Table 1.Outcome in ESPOIR cohort and 1993 cohort at 10 yearsESPOIR cohort n=5211993 cohort n=112DAS28 ESR2.5 ± 1.3DAS44-2.2 ± 0.9SDAI7.5 ± 8.7CDAI6.8 ±8.3DAS28 ESR remission (n (%)273 (52.4)CDAI remission207 (39.7)DAS28 sustained remission, n (%)209 (40.1)DAS28 drug-free remission, n (%)75 (14.1)DAS28 ESR LDA336 (64.5)Rheumatoid nodules39 (7.5)Sicca syndrome314 (60.3)Patient global assessment24.0 ± 24.0HAQ DI score0.5 ± 0.60.75 ± 0.71HAQ DI < 0.5, n (%)280 (54.5)SF36 MCS46.7 ± 10.5SF36 PCS44.6 ± 9.2Pain (mm, VAS)16.6 ± 20.6Fatigue (mm, VAS)31.4 ± 27.023.2 ± 23.0ESR (mm/hr)14.4 ± 13.818.4 ± 16.5CRP level (mg/l)6.4 ± 16.59.3 ± 11.7Normal CRP (< 5 mg/l), n (%)336 (67.6)Total mSharp score*13.8 ± 19.635.4 ± 46.1Erosion score4.9 ± 9.418.4 ± 26.5)Joint narrowing score8.9 ± 12.132.1 ±23.2Joint surgery82 (16.5)26 (23.2)Joint arthroplasty/arthrodesis34 (6.5)20 (17.9)Data are mean (SD)DAS28, disease activity in 28 joints; HAQ DI, Health Assessment Questionnaire Disability Index; SF36 MCS, Medial Outcomes Study 36-item Short Form mental component summary; SF36 PCS, Medical Outcomes Study 36-item Short Form physical component summary; ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; VAS, visual analog scale; CDAI, Clinical Disease Activity Index; SDAI, Simple Disease Activity Index; *van der Heijde-modified Total Sharp scoreFigure 1.Health Assessment Questionnaire Disability Index (HAQ-DI) over 10 years Data are mean (SD).Conclusion:We report a very mild 10-year outcome of a large inception cohort of patients with early RA diagnosed in the early 2000s, which was much better than results for a previous cohort of early RA patients who were recruited in 1993. This current favourable outcome may be related to more intensive care for real-life patients than previously.References:[1]Combe B et al. Jt Bone Spine Rev Rhum. 2007;74:440–5Acknowledgements:We thank MC Boissier, G Falgaronne and F. Lioté for help in patient recruitment. An unrestricted grant from Merck Sharp and Dohme (MSD) was allocated for the first 5 years of the cohort study. Two additional grants from INSERM supported part of the biological database. The French Society of Rheumatology, Abbvie, Pfizer, Lilly and more recently Fresenius and Biogen supported the ESPOIR cohort.Disclosure of Interests:Bernard Combe Speakers bureau: AbbVie; BMS; Gilead; Lilly; Merck; Pfizer; Roche-Chugai;, Consultant of: AbbVie; BMS; Gilead; Janssen; Lilly; Merck; Novartis; Pfizer; Roche-Chugai; and Sanofi;, Grant/research support from: Fresenius, Novartis, Pfizer, and Roche-Chugai., Nathalie Rincheval: None declared, Francis Berenbaum Speakers bureau: Boehringer, Bone Therapeutics, Expanscience, Galapagos, Gilead, GSK, Merck Sereno, MSD, Nordic, Novartis, Regulaxis, Roche, Sandoz, Sanofi, Servier, UCB, Peptinov, TRB Chemedica, 4Moving Biotech, 4P Pharma, Consultant of: Boehringer, Bone Therapeutics, Expanscience, Galapagos, Gilead, GSK, Merck Sereno, MSD, Nordic, Novartis, Regulaxis, Roche, Sandoz, Sanofi, Servier, UCB, Peptinov, TRB Chemedica, 4Moving Biotech, 4P Pharma, Patrick BOUMIER: None declared, Alain Cantagrel Speakers bureau: AbbVie; Amgen, Bristol-Myers Squibb; Grunenthal; Lilly; Medac; MSD France; Novartis; Pfizer; Roche-Chugai; Sanofi;, Consultant of: AbbVie; Amgen, Bristol-Myers Squibb; Grunenthal; Lilly; Medac; MSD France; Novartis; Pfizer; Roche-Chugai; Sanofi;, Grant/research support from: Abbvie, Fresenius, MSD France, Novartis, Pfizer, and UCB, Philippe Dieudé Speakers bureau: Boehringer Ingelheim, Bristol-Myers Squibb, Chugai, Lilly, Medac, Novartis Roche-Genentech, Sanofi, Consultant of: Boehringer Ingelheim, Bristol-Myers Squibb, Chugai, Lilly, Medac, Novartis Roche-Genentech, Sanofi, Grant/research support from: Bristol-Myers Squibb, GlaxoSmithKline, Pfizer., Maxime Dougados Speakers bureau: Pfizer, Abbvie, Lilly, UCB, Merck, BMS, Roche, Biogen, Sanofi, Novartis, and Sandoz, Consultant of: Pfizer, Abbvie, Lilly, UCB, Merck, BMS, Roche, Biogen, Sanofi, Novartis, and Sandoz, Grant/research support from: Pfizer, Abbvie, Lilly, UCB, Merck, BMS, Roche, Biogen, Sanofi, Novartis, and Sandoz, Bruno Fautrel Speakers bureau: AbbVie, Amgen, Biogen, BMS, Celgene, Celltrion, Fresenius Kabi, Gilead, Janssen, Lilly, Medac, MSD, Mylan, NORDIC Pharma, Novartis, Pfizer, Roche, Sandoz, Sanofi-Genzyme, SOBI, UCB, Consultant of: AbbVie, Amgen, Biogen, BMS, Celgene, Celltrion, Fresenius Kabi, Gilead, Janssen, Lilly, Medac, MSD, Mylan, NORDIC Pharma, Novartis, Pfizer, Roche, Sandoz, Sanofi-Genzyme, SOBI, UCB, Grant/research support from: AbbVie, Lilly, MSD and Pfizer, René-Marc Flipo Speakers bureau: Abbvie, Biogen, BMS, Janssen, MSD, Nordic, Novartis, Pfizer, Roche-Chugai and Sanofi-Genzyme, Consultant of: Abbvie, Biogen, BMS, Janssen, MSD, Nordic, Novartis, Pfizer, Roche-Chugai and Sanofi-Genzyme, Grant/research support from: Abbvie, Janssen, Novartis, Pfizer and Roche-Chugai, Philippe Goupille Speakers bureau: AbbVie, Amgen, Biogen, BMS, Celgene, Chugai, Janssen, Lilly, Medac, MSD, Nordic Pharma, Novartis, Pfizer, Sanofi and UCB., Consultant of: AbbVie, Amgen, Biogen, BMS, Celgene, Chugai, Janssen, Lilly, Medac, MSD, Nordic Pharma, Novartis, Pfizer, Sanofi and UCB., Grant/research support from: Abbvie, Biogen, MSD, Pfizer, Xavier Mariette Speakers bureau: BMS, Galapagos, Gilead, GSK, Janssen, Lilly, Novartis, Pfizer, Servier, and UCB., Consultant of: BMS, Galapagos, Gilead, GSK, Janssen, Lilly, Novartis, Pfizer, Servier, and UCB., Grant/research support from: Servier, Alain Saraux Speakers bureau: AbbVie, Bristol-Myers Squibb, Lilly, Nordic, Novartis, Pfizer, Roche-Chugai, Sanofi and UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Lilly, Nordic, Novartis, Pfizer, Roche-Chugai, Sanofi and UCB, Grant/research support from: Roche-Chugai, Thierry Schaeverbeke Speakers bureau: AbbVie, BMS, Lilly, Novartis, Nordic Pharma, Pfizer, Roche, UCB, Consultant of: AbbVie, BMS, Lilly, Novartis, Nordic Pharma, Pfizer, Roche, UCB, Grant/research support from: Pfizer, AbbVie, BMS, Roche, UCB, Astra, MSD, Rigel, AB-sciences, Jean Sibilia Speakers bureau: AbbVie, Lilly, MSD, Amgen, Pfizer, BMS, Janssen, Roche, Sandoz, Sanofi-Genzyme, SOBI, UCB, Novartis., Consultant of: AbbVie, Lilly, MSD, Amgen, Pfizer, BMS, Janssen, Roche, Sandoz, Sanofi-Genzyme, SOBI, UCB, Novartis., Grant/research support from: AbbVie, Lilly, Pfizer, Roche, Olivier VITTECOQ Speakers bureau: AbbVie, Bristol-Myers Squibb, Gilead, Lilly, Merck, Novartis, Pfizer; Roche-Chugai, Mylan and Sanofi, Consultant of: AbbVie, Bristol-Myers Squibb, Gilead, Lilly, Merck, Novartis, Pfizer; Roche-Chugai, Mylan and Sanofi, Grant/research support from: Novartis, Pfizer, Merck, and Bristol-Myers Squibb, Jean-Pierre Daures: None declared
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Combe, B., F. Buttgereit, A. Ostor, R. Xavier, A. Saraux, C. Daridon, K. Famulla, Y. Song, I. Lagunes-Galindo et G. R. Burmester. « POS0654 IMPACT OF CONCOMITANT GLUCOCORTICOIDS ON THE CLINICAL EFFICACY AND SAFETY OF UPADACITINIB IN PATIENTS WITH RHEUMATOID ARTHRITIS : AN AD HOC ANALYSIS OF DATA FROM THREE PHASE 3 STUDIES ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 567–68. http://dx.doi.org/10.1136/annrheumdis-2021-eular.480.

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Background:Glucocorticoid (GC) therapy has strong anti-inflammatory effects and helps slow radiographic progression in RA1; however, GCs can be associated with adverse events (AEs) such as infection, especially with long-term use and higher doses.Objectives:To evaluate the impact of baseline GCs on the efficacy and safety of upadacitinib (UPA) with or without concomitant conventional synthetic DMARDs (csDMARDs).Methods:In this ad hoc analysis of three Phase 3 studies, patients with inadequate response to MTX (MTX-IR) receiving UPA 15 mg once daily (QD) or placebo (PBO) + csDMARDs in SELECT-NEXT, and MTX-IR/MTX-naïve patients receiving UPA 15 mg QD monotherapy or MTX monotherapy in SELECT-MONOTHERAPY/SELECT-EARLY, respectively, were included. Efficacy outcomes, including measures of remission and low disease activity (LDA) determined by DAS in 28 joints using CRP (DAS28[CRP]; <2.6/≤3.2) and Clinical Disease Activity Index (CDAI; ≤2.8/≤10), were assessed and stratified by baseline GC use. Patients were permitted to receive oral GCs ≤10 mg/day (prednisone equivalent) at baseline with no adjustment permitted until Week 24/26/48. Safety was reported as number and proportion of patients with AEs. Data were analyzed descriptively with no statistical comparisons between groups or doses.Results:Of 1,506 patients included in the analysis, 737 (48.9%) were receiving baseline GCs (mean dose 6.2 mg/day). Baseline characteristics were broadly similar across treatment groups; SELECT-EARLY, which enrolled MTX-naïve patients, generally had the shortest duration of RA and higher CRP levels. Across UPA treatment groups, concomitant GCs generally did not influence the proportions of patients achieving remission (Figure 1). In SELECT-NEXT, clinical responses with UPA 15 mg in combination with csDMARDs were similar irrespective of concomitant GC use (Figure 1). Within SELECT-MONOTHERAPY, responses in patients receiving UPA 15 mg without concomitant csDMARDs or GCs were higher than those in patients receiving MTX alone, but were numerically lower than in those receiving UPA 15 mg with GCs (Figure 1). However, this was not observed within SELECT-EARLY, where clinical responses in patients receiving UPA 15 mg monotherapy without GCs were higher than in those patients receiving UPA 15 mg with GCs for both DAS28(CRP) <2.6 (40.6% vs 29.9%, respectively) and CDAI ≤2.8 (20.0% vs 11.6%, respectively) (Figure 1). A similar trend was observed for LDA. Serious AEs, AEs leading to discontinuation, and AEs of special interest, including infections (such as herpes zoster), were broadly similar in the UPA groups irrespective of concomitant GC use (table of safety data will be presented).Conclusion:UPA 15 mg in combination with csDMARDs or as monotherapy was effective in achieving remission and LDA, irrespective of concomitant GC use. Safety of UPA, including incidence of infection, appeared largely unaffected by concomitant GC use.References:[1]Kirwan JR, et al. Cochrane Database Syst Rev 2007;1:CD006356.Acknowledgements:AbbVie funded this study and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship. Medical writing assistance was provided by Frances Smith, PhD, of 2 the Nth, which was funded by AbbVie.Disclosure of Interests:Bernard Combe Speakers bureau: AbbVie, Eli Lilly, Gilead, Janssen, Merck, Novartis, Pfizer, Roche-Chugai, Sanofi, and UCB Pharma, Consultant of: AbbVie, Eli Lilly, Gilead, Janssen, Merck, Novartis, Pfizer, Roche-Chugai, Sanofi, and UCB Pharma, Frank Buttgereit Speakers bureau: AbbVie, Eli Lilly, Pfizer, and Roche, Andrew Ostor Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, Gilead, Janssen, Novartis, Paradigm, Pfizer, Roche, and UCB Pharma., Ricardo Xavier Speakers bureau: AbbVie, Eli Lilly, Janssen, Novartis, Pfizer, Roche, and UCB Pharma, Consultant of: AbbVie, Eli Lilly, Janssen, Novartis, Pfizer, Roche, and UCB Pharma, Alain Saraux Speakers bureau: AbbVie, Bristol-Myers Squibb, Chugai, Eli Lilly, Nordic, Sanofi, and UCB Pharma, Consultant of: AbbVie, Bristol-Myers Squibb, Chugai, Eli Lilly, Nordic, Sanofi, and UCB Pharma, Capucine DARIDON Shareholder of: AbbVie, Employee of: AbbVie, Kirsten Famulla Shareholder of: AbbVie, Employee of: AbbVie, Yanna Song Shareholder of: AbbVie, Employee of: AbbVie, Ivan Lagunes-Galindo Shareholder of: AbbVie, Employee of: AbbVie, Gerd Rüdiger Burmester Speakers bureau: AbbVie, Eli Lilly, Gilead, Janssen, Merck, Pfizer, Roche, and UCB Pharma, Consultant of: AbbVie, Eli Lilly, Gilead, Janssen, Merck, Pfizer, Roche, and UCB Pharma
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Juge, P. A., B. Granger, M. P. Debray, E. Ebstein, F. Louis-Sidney, J. Kedra, T. Doyle et al. « POS0062 A RISK SCORE TO DETECT SUBCLINICAL RHEUMATOID ARTHRITIS-ASSOCIATED INTERSTITIAL LUNG DISEASE ». Annals of the Rheumatic Diseases 81, Suppl 1 (23 mai 2022) : 247.1–248. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3722.

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BackgroundDespite a high morbi-mortality rate, there are no definite strategy for subclinical interstitial lung disease (ILD) screening in patients with rheumatoid arthritis (RA).ObjectivesOur objectives were: 1. to identify risk factors for subclinical RA-ILD in a prospective discovery cohort (ESPOIR) 2.to develop a risk score for subclinical RA-ILD and 3. to validate the risk score in an independent replication cohort (TRANSLATE 2).MethodsPatients without pulmonary symptoms from 2 prospective RA cohorts who underwent chest HRCT scans were included. All patients were genotyped for MUC5B rs35705950. A risk score based on independent risk factors for subclinical RA-ILD was developed using multiple logistic regression in the discovery cohort. The risk score was tested for validation in the replication cohort.ResultsDiscovery and replication cohorts included 163 and 89 patients, respectively. Subclinical ILD was detected in 19.0% and 16.9% of the patients, respectively. In the discovery cohort, independent risk factors for subclinical RA-ILD were the MUC5B rs35705950 T risk allele (odds ratio [OR]=3.74; 95% confidence interval [CI] [1.37–10.39], male sex (OR=3.93; 95%CI [1.40–11.39]), older age at RA onset (for each year, OR=1.10; 95%CI [1.04–1.16]) and increased mean DAS28-ESR (for each unit, OR=2.03; 95%CI [1.24–3.42]). We developed a risk score for subclinical RA-ILD with AUC=0.82; 95%CI [0.70–0.94] (sensitivity (Se)=71.0%) and specificity (Sp)=79.6%). The risk score was validated in the replication cohort with AUC=0.78; 95%CI [0.65–0.92] (Se=86.7%, Sp=62.2%).ConclusionOur risk score could help identifying patients at high-risk for subclinical RA-ILD before the onset of pulmonary symptoms.Disclosure of InterestsPierre-Antoine Juge Speakers bureau: AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Consultant of: Bristol Myers Squibb, Benjamin Granger: None declared, Marie-Pierre Debray: None declared, Esther Ebstein: None declared, Fabienne Louis-Sidney: None declared, Joanna KEDRA: None declared, Tracy Doyle: None declared, Raphael Borie: None declared, Arnaud Constantin Consultant of: Abbvie, Amgen, Biogen, BMS, Boehringer Ingelheim, Fresenius Kabi, Galapagos, Janssen, Lilly, Medac, MSD, Mylan, Novartis, Pfizer, Procter & Gamble, Roche, Sanofi, UCB, Viatris, Bernard Combe Consultant of: AbbVie, BMS, Eli-Lilly, Gilead, Janssen, Merck, Novartis, Pfizer, Roche-Chugai, Sanofi, UCB, René-Marc Flipo Consultant of: Abbvie, Janssen, MSD and Pfizer. He reports research grants from Abbvie, Janssen, Novartis and Pfizer, Xavier Mariette Consultant of: BMS, Gilead, Janssen, Pfizer, Samsung, UCB, Olivier VITTECOQ: None declared, Alain Saraux: None declared, Guillermo CARVAJAL ALEGRIA: None declared, Jean Sibilia Consultant of: AbbVie, Lilly, MSD, Amgen, Pfizer, BMS, Janssen, Roche, Sandoz, Sanofi-Genzyme, SOBI, UCB, Novartis, Grant/research support from: AbbVie, Lilly, MSD, Amgen, Pfizer, BMS, Janssen, Roche, Sandoz, Sanofi-Genzyme, SOBI, UCB, Novartis, Francis Berenbaum: None declared, Caroline Kannengiesser: None declared, Catherine Boileau: None declared, Jeffrey Sparks Consultant of: AbbVie, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Optum, and Pfizer, Grant/research support from: National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant numbers R01 AR077607, P30 AR070253, and P30 AR072577), The R. Bruce and Joan M. Mickey Research Scholar Fund, Bristol Myers Squibb,Bruno Crestani Speakers bureau: Boehringer Ingelheim, AstraZeneca, Roche, Sanofi, Grant/research support from: MedImmune, Roche, Boehringer Ingelheim, Bruno Fautrel Consultant of: AbbVie, Amgen, Biogen, BMS, Celgene, Fresenius Kabi, Janssen, Lilly, Medac, MSD, NORDIC Pharma, Novartis, Pfizer, Roche, SOBI, UCB, Grant/research support from: AbbVie, Lilly, MSD, Pfizer, Philippe Dieudé Speakers bureau: Roche – Chugai, Bristol Myers Squibb, Consultant of: Pfizer, Roche – Chugai, Bristol Myers Squibb, Abbvie, MSD, Grant/research support from: Novartis
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Cramer, Anselm. « Confessiones Amantis : the Spiritual Exercises of the most Vertuous and Religious Dame Gertrude More (Analecta Cartusiana, Salzburg, general editors James Hogg, Alain Gerard, Daniel Le Blévec, 119–27), 2007 - Letters and Translations from Thomas a Kempis in the Lille Archives and elsewhere ; The Devotions of Dame Margaret Gascoigne (119–28), 2007 - Idiot’s Devotion—Directions : Parts 1 and 2 (119–29), 2008 - The Anchor of the Spirit ; The Apologie ; Summarie of Perfection (119–30), 2008 - Fr. Augustine BakerOSB , Remains (119–31), 2008 ». Recusant History 29, no 4 (octobre 2009) : 571–73. http://dx.doi.org/10.1017/s0034193200012437.

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Mease, P. J., L. C. Coates, F. Van den Bosch, D. D. Gladman, L. Gheyle, M. Trivedi, M. Alani et al. « POS1037 CORRELATION BETWEEN SKIN INVOLVEMENT, JOINT INVOLVEMENT AND ENTHESITIS IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS : POST-HOC ANALYSIS OF EQUATOR/EQUATOR2 ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 792.1–792. http://dx.doi.org/10.1136/annrheumdis-2021-eular.883.

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Background:Psoriatic arthritis (PsA) is a heterogeneous, inflammatory disease involving multiple clinical domains including arthritis/synovitis, enthesitis, dactylitis, spondylitis and psoriasis. Effects on each domain should be assessed to determine the overall quality of treatment. Filgotinib (FIL) is a novel preferential Janus kinase 1 inhibitor that is in development for inflammatory conditions including PsA. EQUATOR (NCT03101670) was a 16-week, Phase 2, double-blind, randomised, placebo (PBO)-controlled trial of FIL for patients with active PsA.1 EQUATOR2 (NCT03320876) is an open-label extension (OLE) of the study.Objectives:This post-hoc analysis of EQUATOR and EQUATOR2 assessed the patient-level correlation between changes over time in the three PsA clinical disease domains of skin, joint and enthesitis in patients treated with FIL.Methods:In EQUATOR, patients with active moderate-to-severe PsA (≥5 swollen joints and ≥5 tender joints, fulfilling Classification for PsA criteria) were randomised 1:1 to receive oral FIL 200 mg or PBO once daily (QD) for 16 weeks. At Week 16, patients could continue into the 304-week OLE, with all patients receiving FIL 200 mg QD regardless of previous treatment in EQUATOR. This post-hoc analysis was limited to patients with skin involvement (≥3% body surface area), joint involvement and enthesitis at baseline, with changes from baseline in the three domains assessed using the Psoriasis Area and Severity Index (PASI), swollen/tender joint count (S/TJC), and the Leeds Enthesitis Index (LEI) and Spondyloarthritis Research Consortium of Canada (SPARCC) index, respectively. Analyses that used LEI as the enthesitis index to assess change from baseline included patients with LEI score ≥1 at baseline; those using SPARCC included patients with SPARCC score ≥1 at baseline.Results:The EQUATOR study enrolled 131 patients and 122 patients continued into the EQUATOR2 OLE. Of the 131 patients enrolled in EQUATOR, 49 and 56 patients had PsA involving all three domains at core study baseline when enthesitis was assessed using LEI and SPARCC index, respectively. Pooled data for all patients receiving FIL during the OLE indicate that improvements from baseline in the clinical domains continued with long-term treatment, with 22/42 (52%) and 23/38 (61%) patients having both SJC66 and LEI resolution at Weeks 52 and 100, respectively. For the 22 patients with both SJC and LEI resolution at Week 52, the mean percent change from baseline for PASI was –64%; for the 23 patients with both SJC and LEI resolution at Week 100, the mean percent change from baseline for PASI was –60%. The Figure 1 shows correlation between SJC, LEI and PASI at Week 100. A relationship between the three clinical domains was observed at the individual level; within a single patient, an improvement in one domain was generally followed by improvements in the other two domains. With regard to the sequence in which changes were observed, joints improved first, followed by improvements in the skin and enthesitis. There were no notable differences between changes in LEI and SPARCC enthesitis index in terms of their correlation with improvements in joint and skin involvement. Similarly, there were no notable differences in correlation between the three domains when joints were assessed using TJC rather than SJC.Conclusion:Patients with improvements in skin, joints or enthesitis following treatment with FIL generally also had improvements in the other clinical domains of PsA. The joints were found to be the first of the three domains to improve.References:[1]Mease P et al. Lancet 2018;392:2367–77Acknowledgements:EQUATOR and EQUATOR2 were sponsored by Galapagos NV (Mechelen, Belgium) and co-funded by Galapagos NV and Gilead Sciences, Inc (Foster City, CA, USA). Medical writing/editorial support was provided by Debbie Sherwood, BSc, CMPP (Aspire Scientific, Bollington, UK), funded by Galapagos NV.Disclosure of Interests:Philip J Mease Speakers bureau: AbbVie, Amgen, Eli Lilly, Janssen, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, Galapagos, Gilead Sciences, GlaxoSmithKline, Janssen, Novartis, Pfizer, SUN and UCB, Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead Sciences, Janssen, Novartis, Pfizer, SUN and UCB, Laura C Coates Speakers bureau: AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Gilead, Janssen, Medac, Novartis, Pfizer and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer and UCB, Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Novartis, and Pfizer, Filip van den Bosch Consultant of: AbbVie, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Merck and UCB, Dafna D Gladman Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer and UCB, Lien Gheyle Shareholder of: Galapagos, Employee of: Galapagos, Mona Trivedi Shareholder of: Gilead Sciences, Amgen, Employee of: Gilead Sciences, Muhsen Alani Shareholder of: Gilead Sciences, Employee of: Gilead Sciences, Eline Vetters Employee of: Galapagos, Franck Olivier Le Brun Shareholder of: Galapagos, Employee of: Galapagos, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Philip Helliwell Speakers bureau: Janssen and Novartis, Paid instructor for: Pfizer, Consultant of: Eli Lilly.
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Helliwell, P., L. C. Coates, F. Van den Bosch, D. D. Gladman, L. Gheyle, M. Trivedi, M. Alani, F. O. Le Brun, R. Besuyen et P. J. Mease. « POS1038 THE EFFECT OF FILGOTINIB ON ENTHESITIS : 100-WEEK DATA FROM AN OPEN-LABEL EXTENSION STUDY IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 792.2–793. http://dx.doi.org/10.1136/annrheumdis-2021-eular.884.

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Background:Filgotinib (FIL), a novel preferential Janus kinase 1 inhibitor, was assessed in patients with active psoriatic arthritis (PsA) in the 16-week, Phase 2, EQUATOR trial (NCT03101670).1 EQUATOR2 (NCT03320876) is the open-label extension (OLE). As previously reported, an interim analysis of the OLE showed that the majority of patients had clinical resolution of enthesitis by Week 52.2Objectives:This post-hoc analysis evaluated the effect of FIL on clinical enthesitis after 100 weeks of treatment in the OLE, as assessed using the Leeds Enthesitis Index (LEI) and Spondyloarthritis Research Consortium of Canada (SPARCC) index, and evaluated the discriminatory capacity of the two indices. In addition, we assessed which of the sites included in LEI and SPARCC were most frequently involved and whether treatment effect was consistent across sites.Methods:In EQUATOR, patients with active moderate-to-severe PsA (≥5 swollen joints and ≥5 tender joints, fulfilling Classification for PsA criteria) were randomised 1:1 to receive oral FIL 200 mg or placebo (PBO) once daily (QD) for 16 weeks. At Week 16, all patients could continue into the OLE, receiving FIL 200 mg QD for up to an additional 304 weeks. We compared changes from core baseline in LEI and SPARCC measures, the effect on enthesitis at sites included in LEI and SPARCC assessments and the discriminatory capacity of both enthesitis indices.Results:Of 131 patients randomised to EQUATOR, 122 entered the OLE. There was strong agreement between LEI and SPARCC at baseline. While most patients had enthesitis at baseline according to either index (76/131 [58.0%] by LEI; 85/131 [64.9%] by SPARCC), a minority had enthesitis at a large number of sites (6.9% with 5–6 LEI sites; 12.2% with ≥9 SPARCC sites). The sites most frequently involved at baseline were the lateral epicondyle humerus and Achilles tendon, sites common to both LEI and SPARCC. There was greater variability in the change from baseline to Week 16 in SPARCC compared with LEI (Table 1). LEI showed a greater discriminatory capacity than SPARCC when change from baseline was compared for FIL vs PBO at Week 16, as shown by higher absolute standardised mean difference: −0.70 (LEI) and −0.30 (SPARCC) (observed cases; Table 1). Subgroup analyses indicated that the treatment effect of FIL vs PBO at Week 16 for all sites was consistent with the overall treatment effect seen for LEI or SPARCC, and indicative of an improvement with FIL vs PBO for nearly all sites. The proportion of patients with enthesitis decreased from baseline up to OLE Week 100 (Figure 1). There were no major differences in long-term effect on enthesitis between sites.Conclusion:FIL improved enthesitis consistently across sites compared with PBO. Rapid improvement in enthesitis was seen up to Week 16 of the core study and improvements continued up to Week 52, after which responses were generally stable up to Week 100. LEI assesses fewer locations than SPARCC, but reassuringly captured the sites most commonly affected by enthesitis; LEI also had greater discriminatory capacity.References:[1]Mease P, et al. Lancet 2018;392:2367–77[2]Mease P, et al. Arthritis Rheumatol 2020;72(suppl 10): abstract 0910Figure 1.Acknowledgements:EQUATOR and EQUATOR2 were sponsored by Galapagos NV (Mechelen, Belgium) and co-funded by Galapagos NV and Gilead Sciences, Inc (Foster City, CA, USA). Eline Vetters, Leen Gilles, Benjamin Pett and his team, all employees of Galapagos, provided assistance with statistical analyses. Medical writing/editorial support was provided by Debbie Sherwood, BSc, CMPP (Aspire Scientific, Bollington, UK), and funded by Galapagos NV.Disclosure of Interests:Philip Helliwell Speakers bureau: Janssen, Novartis, Paid instructor for: Pfizer, Consultant of: Eli Lilly, Laura C Coates Speakers bureau: AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Gilead, Janssen, Medac, Novartis, Pfizer and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Novartis, and Pfizer, Filip van den Bosch Consultant of: AbbVie, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Pfizer and UCB, Grant/research support from: AbbVie, Merck and UCB, Dafna D Gladman Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer and UCB, Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer and UCB, Lien Gheyle Shareholder of: Galapagos, Employee of: Galapagos, Mona Trivedi Shareholder of: Gilead Sciences, Amgen, Employee of: Gilead Sciences, Muhsen Alani Shareholder of: Gilead Sciences, Employee of: Gilead Sciences, Franck Olivier Le Brun Shareholder of: Galapagos, Employee of: Galapagos, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Philip J Mease Speakers bureau: AbbVie, Amgen, Eli Lilly, Janssen, Novartis, Pfizer and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol-Myers Squibb, Eli Lilly, Galapagos, Gilead Sciences, GlaxoSmithKline, Janssen, Novartis, Pfizer, SUN and UCB, Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead Sciences, Janssen, Novartis, Pfizer, SUN and UCB.
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Helliwell, P., F. Van den Bosch, L. C. Coates, D. D. Gladman, C. Tasset, L. Meuleners, L. Gilles et al. « FRI0343 EFFICACY AND SAFETY OF FILGOTINIB, A SELECTIVE JANUS KINASE 1 INHIBITOR, IN PATIENTS WITH ACTIVE PSORIATIC ARTHRITIS : SUBGROUP ANALYSES FROM A RANDOMIZED, PLACEBO-CONTROLLED, PHASE 2 TRIAL (EQUATOR) ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 765.1–766. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2495.

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Background:Treatment with the oral selective Janus kinase 1 inhibitor filgotinib was associated with rapid and significant improvements in multiple domains of active psoriatic arthritis versus placebo in the 16-week Phase 2, multicenter, double-blind, randomized EQUATOR trial (NCT03101670).1A significantly greater proportion of patients receiving filgotinib, versus placebo, achieved the primary endpoint of 20% improvement in American College of Rheumatology (ACR) 20 response at Week 16 (80% vs 33%, respectively).1Objectives:The aim of this predefined analysis was to evaluate the consistency of the response to filgotinib across predefined relevant subpopulations participating in the EQUATOR trial.Methods:In EQUATOR, patients with active psoriatic arthritis were treated with filgotinib 200 mg (n=65) or placebo (n=66) once daily for 16 weeks. Key clinical endpoints, including ACR20 and ACR50 (50% improvement) response rates, Psoriatic Arthritis Disease Activity Score (PASDAS), and Disease Activity Index for Psoriatic Arthritis (DAPSA) were evaluated according to the following baseline characteristics: sex, body mass index, disease duration, baseline disease severity, concurrent use of disease-modifying antirheumatic drug(s), and prior exposure to tumor necrosis factor inhibitor(s). For PASDAS and DAPSA scores, statistical analysis of changes from baseline was performed using analysis of covariance with factors for treatment, randomization stratification, subgroup, and an interaction between treatment and subgroup. Least-squares (LS) mean difference between treatment arms and the corresponding 95% confidence intervals (CI) were calculated. For ACR20 and ACR50 response rates, statistical analysis used the point estimate and corresponding 95% CI, based on the Newcombe method.Results:Sixty patients (92%) in the filgotinib group and 64 (97%) in the placebo group completed the study. The total number of patients in each subpopulation ranged from 18 to 104 (Figure 1). Differences in the proportions of patients achieving ACR20 consistently favored filgotinib, compared with placebo, across all subgroups (Figure 1); all differences reached statistical significance. Similarly, differences in the proportions of ACR50 responders and LS mean treatment differences for PASDAS and DAPSA consistently favored filgotinib, reaching statistical significance in most subgroups. No clinically relevant differences in the effect of filgotinib were observed across subgroups. Filgotinib was generally well tolerated and no new safety signals were identified.Conclusion:In the 16-week EQUATOR trial, the effects of filgotinib on key efficacy endpoints were generally consistent across a range of subgroups based on patient, disease, and treatment characteristics.References:[1]Mease P, et al. Lancet 2018;392:2367–77.Acknowledgments:The EQUATOR trial was sponsored by Galapagos NV and co-funded by Galapagos NV and Gilead Sciences. Medical writing support was provided by Hannah Mace MPharmacol, CMPP (Aspire Scientific Ltd, Bollington, UK) and funded by Galapagos NV (Mechelen, Belgium).Disclosure of Interests:Philip Helliwell: None declared, Filip van den Bosch Consultant of: AbbVie, Celgene Corporation, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Speakers bureau: AbbVie, Celgene Corporation, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Laura C Coates: None declared, Dafna D Gladman Grant/research support from: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – grant/research support, Consultant of: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – consultant, Chantal Tasset Shareholder of: Galapagos (share/warrant holder), Employee of: Galapagos, Luc Meuleners Employee of: Galapagos, Leen Gilles Consultant of: Galapagos, Lien Gheyle Employee of: Galapagos, Mona Trivedi Shareholder of: Amgen and Gilead Sciences, Employee of: Gilead Sciences, Muhsen Alani Employee of: Gilead Sciences, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau
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Juge, P. A., B. Granger, M. P. Debray, E. Ebstein, F. Louis Sidney, J. Kedra, R. Borie et al. « POS0095 DEVELOPPING A SCORE TO PREDICT PRECLINICAL INTERSTITIAL LUNG DISEASE IN PATIENTS WITH RHEUMATOID ARTHRITIS – A CROSS-SECTIONAL STUDY FROM THE ESPOIR COHORT ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 258.1–258. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2817.

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Background:Interstitial lung disease (ILD) is an extra-articular manifestation of rheumatoid arthritis (RA) detected in 20% to 60% of patients with RA on high-resolution computed-tomography (HRCT) chest scan and is clinically significant in near 10%. Despite a high morbi-mortality rate, a definite strategy for preclinical ILD screening in patients with RA remains to be determined. To date, several factors have been reported to increase the risk of RA-ILD occurrence (i.e. older age at RA onset, ACPA positivity, male sex, RA disease activity, the MUC5B rs35705950 promoter variant...). However, none of these risk factors has been validated in a prospective cohort of patients with RA. The ESPOIR prospective cohort includes patients aged 18 to 70 years with recent arthritis (less than 6 months) and a definite or probable diagnosis of RA.Objectives:To identify in the ESPOIR cohort factors associated with ILD after at least 10 years of RA duration in order to develop a predictive score to identify patients with preclinical RA-ILD.Methods:An ILD detection by chest HRCT scan was systematically offered to every patient with definite RA after at least 10 years-follow-up. Chest HRCT scans were centrally reviewed by an experienced radiologist. Potential predictors of ILD were prospectively collected from baseline to the date of the HRCT scan, and all included patients were genotyped for MUC5B rs35705950. To take into account repeated measures, trajectories were determined for disease activity, C reactive protein, smoking, treatment exposure (i.e. prednisone, methotrexate [MTX] and biological disease modifying anti-rheumatic drugs [bDMARDs]). A logistic model was used to identify independent predictors for the occurrence of ILD on HRCT scans. Confidence intervals were estimated using sampling methods. A predictive score for preclinical ILD occurrence was developed based on the identified predictors.Results:163 RA patients according to 2010 ACR/EULAR classification criteria, none of whom had pulmonary symptoms, were investigated with a chest HRCT scan (128 women (78.5%), mean RA duration 13.7 ± 1.1 years, age at inclusion 47.6 y/o ± 10.4, mean disease activity score [DAS]-28 during follow up was 3.1 ± 1.0). ILD was detected in 31 patients (19.0%). The MUC5B rs35705950 minor allele frequency (MAF) was 22.2% and 10.0% in the RA-ILD and RA-noILD populations, respectively (OR univariate=2.6 CI95% [1.2-5.5], P=0.01). After logistic regression, independent predictors for preclinical RA-ILD were male sex (OR=3.9 CI95% [1.4-11.4]), older age at RA onset (OR=1.1 per year CI95% [1.0-1.2]), mean DAS-28 score during the follow-up (OR=2.0 CI95% [1.2-3.4]) and MUC5B rs35705950 T risk allele (OR=3.7 CI95% [1.4-10.4]) (Figure 1). No influence of the use of RA-related drugs (prednisone, MTX or bDMARDs) was identified as risk factor. The logistic model could predict preclinical ILD occurrence after 13 years of RA duration with an AUC=0.82 CI95% (0.72-0.91). A predictive score for preclinical RA-ILD based on the 4 identified predictive risk factors was developed (Sensitivity 80%, Specificity 56%).Figure 1.Factors independently associated with preclinical ILD after 13 years of RA durationConclusion:In this cross-sectional study of the prospective ESPOIR cohort, we identified clinical and genetic predictors for ILD after 13 years of RA duration. We developed a predictive score that could improve risk stratification for preclinical RA-ILD and help physicians identify patients with RA in whom a HRCT scan should be performed.Disclosure of Interests:Pierre-Antoine Juge Consultant of: BMS, Benjamin Granger: None declared, Marie-Pierre Debray: None declared, Esther Ebstein: None declared, Fabienne Louis Sidney: None declared, Joanna KEDRA: None declared, Raphael Borie: None declared, Arnaud Constantin Consultant of: Bristol-Meyers Squibb, Chugai, Roche, Abbvie, MSD, Pfizer, and UCB, Bernard Combe Consultant of: Abbvie, Bristol-Meyers Squibb, Lilly, MSD, Janssen, Pfizer, Roche, Chigai, and Sanofi, Grant/research support from: Abbvie, Bristol-Meyers Squibb, Lilly, MSD, Janssen, Pfizer, Roche, Chugai, and Sanofi, René-Marc Flipo Consultant of: Bristol-Meyers Squibb, Roche, Chugai, Abbvie, and Pfizer, Grant/research support from: Roche, Chugai, Abbvie, and Pfizer, Xavier Mariette Consultant of: Bristol-Meyers Squibb, GSK, Janssen, Pfizer, and UCB, Olivier VITTECOQ Consultant of: Bristol Myers Squibb, Roche, Chugai, MSD, Novartis, Pfizer, Abbvie, and Lilly, Alain Saraux Consultant of: Roche, Chugai, and Bristol-Meyers Squibb, Grant/research support from: Roche, Chugai, and Bristol-Meyers Squibb, Guillermo CARVAJAL ALEGRIA: None declared, Jean Sibilia Consultant of: Roche, Chugai, Bristol-Meyers Squibb, UCB, GSK, LFB, Actelion, Pfizer, MSD, Novartis, Amgen, Hospira, AbbVie, Sandoz, Gilead, Lilly, Sanofi, Janssen, and Mylan, Francis Berenbaum Consultant of: Boehringer, Bone Therapeutics, Expanscience, Galapagos, Gilead, GSK, Elli Lilly, Merck Sereno, MSD, Nordic, Novartis, Pfizer, Regulaxis, Roche, Sandoz, Sanofi, Servier, UCB, Peptinov, TRB Chemedica, 4P Pharma, Caroline Kannengiesser: None declared, Catherine Boileau: None declared, Bruno Crestani Consultant of: Boehringer Ingelheim, Roche, Sanofi, Apellis, Astra-Zeneca, Grant/research support from: MedImmune, Boehringer Ingelheim, Bruno Fautrel Consultant of: AbbVie, Biogen, BMS, Celgene, Janssen, Lilly, Medac, MSD, NORDIC Pharma, Novartis, Pfizer, Roche, Sanofi-Aventis, SOBI, UCB, Grant/research support from: AbbVie, MSD, Pfizer, Philippe Dieudé: None declared
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Coates, L. C., P. J. Mease, P. Helliwell, F. Van den Bosch, M. Trivedi, M. Alani, F. O. Le Brun et al. « POS1049 EFFECT OF FILGOTINIB ON PASDAS : DRIVERS OF LOW AND VERY LOW ACTIVITY UP TO WEEK 100 ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 801.2–802. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1721.

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Background:EQUATOR (NCT03101670) was a Phase 2, double-blind, randomised placebo (PBO)- controlled trial of the preferential Janus kinase 1 inhibitor filgotinib (FIL) for the treatment of psoriatic arthritis (PsA); EQUATOR2 (NCT03320876) is the open-label extension (OLE).Objectives:This post-hoc analysis assessed the effect of FIL on individual Psoriatic Arthritis Disease Activity Score (PASDAS) components; and the association between PASDAS disease activity (DA) levels and DA levels achieved for each PASDAS component and patient-reported outcomes (PROs) up to OLE Week (Wk) 100.Methods:In EQUATOR, patients with active moderate-to-severe PsA were randomised 1:1 to oral FIL 200 mg or PBO once daily (QD) for 16 wks.1 At Wk 16, patients could continue into the 304-wk OLE, in which all patients received FIL 200 mg QD. The proportions of patients with PASDAS of very low DA (VLDA; ≤1.9), LDA (>1.9–<3.2), moderate DA (MoDA; ≥3.2–<5.4), and high DA (HDA; ≥5.4) at core Wk 16 and OLE Wk 52 and 100 were assessed. The proportion with improved PASDAS status vs baseline (BL) at OLE Wk 52 and 100 was calculated. Percent change from BL in PASDAS components and PROs were assessed at core Wk 16 and OLE Wk 52 and 100 by PASDAS status (VLDA, LDA, other). Multivariate logistic regression analyses performed cross-sectionally identified PASDAS components and PROs associated with not achieving VLDA or LDA at core Wk 16 and OLE Wk 52 and 100; all analyses were observed cases.Results:At OLE Wk 52, LDA and VLDA were achieved by 27.5% and 16.8% of randomised patients, respectively (44.3% combined). At OLE Wk 100, LDA and VLDA were achieved by 26.0% and 17.6% of patients (43.6% combined; Figure 1). Of patients with HDA at BL, 69% improved to MoDA/LDA/VLDA, <4% remained in HDA and 27% did not reach Wk 100; of those in MoDA at BL, 63% improved to VLDA/LDA, 11% remained stable, <4% worsened and 22% did not reach Wk 100. Patient Global Assessment of Disease Activity (PtGDA), Short Form-36 physical component scale (SF-36 PCS), Functional Assessment of Chronic Illness Therapy, and Health Assessment Questionnaire Disability Index were found to be important components/PRO measures in achieving VLDA vs LDA (Table 1). Logistic regression indicated that factors associated with not achieving LDA at Wk 52 were PtGDA (odds ratio [OR]: 1.20, 95% confidence interval [CI]: 1.07–1.35), physician GDA (PhGDA; OR: 1.58, 95% CI: 1.18–2.12), and SF-36 PCS (OR: 0.79, 95% CI: 0.67–0.95); PtGDA was associated with not achieving VLDA (OR: 1.30, 95% CI: 1.15–1.47).Conclusion:The proportion of patients achieving PASDAS VLDA or LDA increased over time and remained stable between OLE Wk 52 and 100. Important factors in determining whether VLDA/LDA was met were PtGDA, PhGDA, and SF-36 PCS, although the low patient numbers is a limitation.References:[1]Mease P, et al. Lancet. 2018;392:2367–77Table 1.Mean % change from baseline in PASDAS components and PROs (observed cases)Core Wk 16 (FIL + PBO groups combined)n=122OLE Wk 52n=110OLE Wk 100n=97VLDAn=8(7%)LDAn=22(18%)Othersn=92(75%)VLDAn=22(20%)LDAn=36(33%)Othersn=52(47%)VLDA n=23(24%)LDAn=34(35%)Othersn=40(41%)PhGDA−93−75−44−94−82−56−96−84−54PtGDA−87−69−13−86−58−24−90−57−13Tender joint count 68−94−80−42−99−84−64−98−87−61Swollen joint count 66−99−80−64−99−96−78−99−94−80LEI−100−86−32−96−100−78−100−99−78Dactylitis−100−100−73−100−100−97−100−100−98C-reactive protein−66−2217138*−32−25−12−1324SF-36 PCS53261133239472316FACIT1195032975134994636HAQ-DI−84−68−18−85−51−18−88−45−19PASI−84−66−29−54−59−56−49−76−42Components or PRO measures in bold are those for which numerical differences between VLDA and LDA are greatest across timepoints*Due to outlier (3784)FACIT, Functional Assessment of Chronic Illness Therapy; HAQ-DI, Health Assessment Questionnaire Disability Index; LEI, Leeds Enthesitis Index; PASI, Psoriasis Area Severity Index; PhGDA, Physician Global Assessment of Disease Activity; PtGDA, Patient Global Assessment of Disease Activity; SF-36 PCS, Short Form-36 physical component summary; (V)LDA, (very) low disease activityAcknowledgements:EQUATOR and EQUATOR2 were sponsored by Galapagos NV Mechelen, Belgium) and co-funded by Galapagos NV and Gilead Sciences, Inc (Foster City, CA, USA). Benjamin Pett and his team, employees of Galapagos, provided assistance with statistical analyses. Medical writing/editorial support was provided by Debbie Sherwood, BSc, CMPP (Aspire Scientific, Bollington, UK), and was funded by Galapagos NV.Disclosure of Interests:Laura C Coates Speakers bureau: AbbVie, Amgen, Biogen, Celgene, Eli Lilly, Gilead, Janssen, Medac, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Novartis, and Pfizer, Philip J Mease Speakers bureau: AbbVie, Amgen, Eli Lilly, Janssen, Novartis, Pfizer, and UCB, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead Sciences, GlaxoSmithKline, Janssen, Novartis, Pfizer, SUN, and UCB, Grant/research support from: AbbVie, Amgen, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead Sciences, Janssen, Novartis, Pfizer, SUN, and UCB, Philip Helliwell Paid instructor for: Janssen, Novartis, and Pfizer, Consultant of: Eli Lilly, Filip van den Bosch Consultant of: AbbVie, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Pfizer, and UCB, Grant/research support from: AbbVie, Merck, and UCB, Mona Trivedi Shareholder of: Gilead Sciences, Amgen, Employee of: Gilead Sciences, Muhsen Alani Shareholder of: Gilead Sciences, Employee of: Gilead Sciences, Franck Olivier Le Brun Shareholder of: Galapagos, Employee of: Galapagos, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Lien Gheyle Shareholder of: Galapagos, Employee of: Galapagos, Emilia Gvozdenovic Employee of: Galapagos, Dafna D Gladman Consultant of: AbbVie, Amgen, Bristol Myers Squibb, Celgene, Eli Lilly, Galapagos, Gilead, Janssen, Novartis, Pfizer, and UCB., Grant/research support from: AbbVie, Amgen, Celgene, Eli Lilly, Janssen, Novartis, Pfizer, and UCB.
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Husni, M. E., D. D. Gladman, P. Helliwell, F. Van den Bosch, C. Tasset, L. Meuleners, L. Gilles et al. « FRI0344 THE LONG-TERM EFFECT OF TREATING PSORIATIC ARTHRITIS WITH THE JANUS KINASE 1-SELECTIVE INHIBITOR FILGOTINIB ON LIPID PROFILES : AN ANALYSIS OF THE EQUATOR AND EQUATOR2 TRIALS ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 766. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2494.

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Background:Cardiovascular (CV) comorbidities are common in psoriatic arthritis (PsA); patients are at high risk for major adverse cardiovascular events (MACE).1In the Phase 2, double-blind, randomized EQUATOR trial, significant improvements across multiple PsA domains were observed with the oral selective Janus kinase (JAK) 1 inhibitor filgotinib compared with placebo.2Inhibition of JAK signal transducer and activator of transcription signaling is associated with raised serum lipids.3Objectives:To evaluate the effects of filgotinib on the lipid profile of PsA patients and determine if those with higher MACE risk show similar changes in lipid profile compared with the overall population.Methods:In EQUATOR, 131 patients with active PsA received filgotinib 200 mg (n=65) or placebo (n=66) once daily for 16 weeks. Patients completing EQUATOR could enter the ongoing EQUATOR2 open-label extension (OLE;NCT03320876), in which patients receive filgotinib 200 mg for up to 148 weeks. Effects of filgotinib on total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and TC/HDL-C ratio at OLE Week 52 (68 weeks after EQUATOR initiation) were analyzed. In a post hoc analysis, patients were classified into subgroups according to presence/absence of obesity (baseline body mass index [BMI]; ≥30 vs <30 kg/m2, respectively), diabetes mellitus, arterial hypertension (≥130/80 mmHg), hyperlipidemia, and metabolic syndrome. Changes in lipid levels were explored graphically.Results:124 patients (95%) completed EQUATOR; 122 (93%) enrolled in the OLE. Of these, 11 patients (9%) discontinued treatment by OLE Week 52. Median (range) exposure to filgotinib was 66.0 (0.4–104.1) weeks. In the OLE, TC, LDL-C, and HDL-C levels increased versus baseline with filgotinib, resulting in a decreased TC/HDL-C ratio. Changes in lipid levels were consistent irrespective of presence of obesity (n=56;Fig), diabetes (n=53), arterial hypertension (n=80), hyperlipidemia (n=108), or metabolic syndrome (n=36); baseline lipid values were greater in the higher risk groups. In patients who were assigned placebo in the randomized controlled trial (RCT), HDL-C increased on switching to filgotinib in the OLE (in a manner similar to that seen in filgotinib-treated patients during the RCT), and remained elevated compared with baseline (Fig). Triglyceride levels remained stable throughout, across all subgroups. Seventeen patients (13%) were taking lipid-lowering drugs (LLDs) prior to the start of the trial (and continued to do so); the effect of filgotinib on the lipid profile in these patients was similar to that in the overall population. During the RCT phase, another six patients in the filgotinib group and one in the placebo group began taking LLDs.Conclusion:In patients exposed to filgotinib for ≥52 weeks, the effects on lipid profile were consistent regardless of baseline CV risk. Lipid changes included an elevation in TC and HDL-C, with a decrease in TC/HDL-C ratio.References:[1]Haddad A & Zisman D. Rambam Maimonides Med J 2017;8:e0004[2]Mease P, et al. Lancet 2018;392:2367–77[3]Sands B, et al. Clin Gastroenterol Hepatol 2020;18:123–32Acknowledgments:Studies were sponsored by Galapagos NV; co-funded by Galapagos NV and Gilead Sciences. Writing support from Hannah Mace MPharmacol, CMPP (Aspire Scientific Ltd, Bollington, UK) was funded by Galapagos NV (Mechelen, Belgium).Disclosure of Interests:M Elaine Husni Grant/research support from: Pfizer, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, Janssen, Novartis, Regeneron, and UCB, Dafna D Gladman Grant/research support from: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – grant/research support, Consultant of: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – consultant, Philip Helliwell: None declared, Filip van den Bosch Consultant of: AbbVie, Celgene Corporation, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Speakers bureau: AbbVie, Celgene Corporation, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Chantal Tasset Shareholder of: Galapagos (share/warrant holder), Employee of: Galapagos, Luc Meuleners Employee of: Galapagos, Leen Gilles Consultant of: Galapagos, Lien Gheyle Employee of: Galapagos, Mona Trivedi Shareholder of: Amgen and Gilead Sciences, Employee of: Gilead Sciences, Muhsen Alani Employee of: Gilead Sciences, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau
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Gladman, D. D., L. C. Coates, F. Van den Bosch, P. Helliwell, C. Tasset, L. Meuleners, L. Gilles et al. « FRI0339 LONG-TERM EFFICACY OF THE ORAL SELECTIVE JANUS KINASE 1 INHIBITOR FILGOTINIB IN PSORIATIC ARTHRITIS : WEEK 52 RESPONSE PATTERNS IN INDIVIDUAL PATIENTS FROM AN OPEN-LABEL EXTENSION (OLE) STUDY (EQUATOR2) ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 763.1–763. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2624.

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Background:EQUATOR (NCT03101670) was a 16-week, Phase 2, multicenter, double-blind, placebo-controlled, randomized controlled trial (RCT) of filgotinib in patients with active psoriatic arthritis.1Filgotinib demonstrated rapid efficacy compared with placebo across multiple domains, including the primary endpoint of Week 16 American College of Rheumatology (ACR) 20 response.1Patients completing the RCT could join an ongoing 148-week OLE (EQUATOR2;NCT03320876).Objectives:In this prespecified interim analysis at Week 52 of the OLE, individual patient responses with respect to disease activity were evaluated.Methods:Placebo-treated RCT patients switched to filgotinib (200 mg once daily) at Week 16 and entered the OLE; patients previously assigned to filgotinib continued. Individual response patterns at Week 52 of the OLE were evaluated for ACR20/50/70, Psoriatic Arthritis Disease Activity Score (PASDAS) low disease activity (LDA), minimal disease activity (MDA), and MDA/very low disease activity (VLDA).Results:124 patients (95%) completed EQUATOR; 122 (93%) enrolled in the OLE. At Week 52, 11 patients (9%) had discontinued treatment in the OLE. Median (range) exposure to filgotinib was 66.0 (0.4–104.1) weeks. In patients originally assigned to filgotinib, sustained efficacy was seen through to OLE Week 52 for ACR20, 50, and 70; PASDAS LDA; MDA (Table;Figure 1a); and MDA/VLDA. In total, 77% and 93% of those achieving MDA and ACR50 response in the RCT period maintained this at Week 52 (Table). A substantial proportion of RCT non-responders also achieved a treatment response in the OLE, meeting MDA and ACR50 criteria (22% and 37%, respectively;Table). Response patterns in the OLE were similar regardless of prior RCT treatment. In total, at Week 52 of the OLE, 33.6% of patients achieved MDA response (Figure 1a); 55.0% achieved ACR50 response. Figure 1bshows individual patient response over time for MDA.Conclusion:Data from this 52-week OLE interim analysis suggest that further improvement in disease activity can be expected with filgotinib beyond 16 weeks in patients with active psoriatic arthritis. Sustained efficacy was demonstrated across several measures of disease activity, including MDA and ACR50.References:[1]Mease P, et al. Lancet 2018;392:2367–77.Table.Responders at Week 52 of the OLE, by treatment and previous RCT responder status (observed cases).TreatmentFilgotinib (N=59) → Filgotinib (N=54)aPlacebo (N=63) → Filgotinib (N=57)an/N, %OLE responders/RCT respondersOLE responders/RCT non-respondersOLE responders/RCT respondersOLE responders/RCT non-respondersACR2040/47 (85.1)5/7 (71.4)17/18 (94.4)27/38 (71.1)ACR5025/27 (92.6)10/27 (37.0)5/8 (62.5)21/49 (42.9)ACR7010/13 (76.9)12/41 (29.3)3/4 (75.0)12/53 (22.6)PASDAS LDAb19/21 (90.5)12/32 (37.5)5/6 (83.3)21/48 (43.8)MDA10/13 (76.9)9/41 (22.0)4/5 (80.0)14/51 (27.5)aIndicates number remaining at OLE Week 52 interim analysis, after dropoutsbPASDAS information was not available for one patient at Week 16 of the RCTAcknowledgments:EQUATOR and EQUATOR2 were sponsored by Galapagos NV and co-funded by Galapagos NV and Gilead Sciences. Medical writing support was provided by Hannah Mace MPharmacol, CMPP (Aspire Scientific Ltd, Bollington, UK) and funded by Galapagos NV.Disclosure of Interests:Dafna D Gladman Grant/research support from: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – grant/research support, Consultant of: AbbVie, Amgen Inc., BMS, Celgene Corporation, Janssen, Novartis, Pfizer, UCB – consultant, Laura C Coates: None declared, Filip van den Bosch Consultant of: AbbVie, Celgene Corporation, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Speakers bureau: AbbVie, Celgene Corporation, Eli Lilly, Galapagos, Janssen, Novartis, Pfizer, and UCB, Philip Helliwell: None declared, Chantal Tasset Shareholder of: Galapagos (share/warrant holder), Employee of: Galapagos, Luc Meuleners Employee of: Galapagos, Leen Gilles Consultant of: Galapagos, Lien Gheyle Employee of: Galapagos, Mona Trivedi Shareholder of: Amgen and Gilead Sciences, Employee of: Gilead Sciences, Muhsen Alani Employee of: Gilead Sciences, Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Philip J Mease Grant/research support from: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – grant/research support, Consultant of: Abbott, Amgen, Biogen Idec, BMS, Celgene Corporation, Eli Lilly, Novartis, Pfizer, Sun Pharmaceutical, UCB – consultant, Speakers bureau: Abbott, Amgen, Biogen Idec, BMS, Eli Lilly, Genentech, Janssen, Pfizer, UCB – speakers bureau
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Taylor, P. C., C. Charles-Schoeman, M. Alani, M. Trivedi, V. Castellano, I. Tiamiyu, D. Jiang et al. « POS0660 CONCOMITANT USE OF STATINS IN FILGOTINIB-TREATED PATIENTS WITH RHEUMATOID ARTHRITIS ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 572–73. http://dx.doi.org/10.1136/annrheumdis-2021-eular.933.

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Background:The Janus kinase-1 preferential inhibitor filgotinib (FIL) improved rheumatoid arthritis (RA) signs and symptoms in phase (P)3 trials.1–3 RA elevates cardiovascular disease risk; statins are used to reduce risk.Objectives:To assess safety of statin and filgotinib coadministration across the clinical program.Methods:Patients (pts) meeting 2010 ACR/EULAR RA criteria in P2 DARWIN 1–2 (D1–2; NCT01888874, NCT01894516), P3 FINCH 1–3 (F1–3; NCT02889796, NCT02873936, NCT02886728), and long-term extensions DARWIN 3 and FINCH 4 (D3, F4; NCT02065700, NCT03025308) receiving FIL 100 mg (FIL100) QD, FIL 200 mg QD (FIL200), adalimumab (ADA), methotrexate (MTX), or placebo (PBO) were included. Events related to statin use were analysed as exposed by treatment received. N and % were provided.Week (W)12 PBO-controlled safety analysis included pts receiving FIL100, FIL200, or PBO for ≤12W (D1–2, F1–2); as-treated safety analysis included pts receiving long-term FIL100 QD (n=1647), FIL200 QD (n=2267), ADA (n=325), MTX (n=416), or PBO (n=781) (D1–3, F1–4); P3 as-randomised analysis included data up to W52 (F1–3) per assigned treatment.Results:In each arm, similar proportions of pts took statins at baseline (9.4%–11.9%); initiation during study was low (1.2%–6.8%). Through W12 in PBO-controlled analysis, mean creatine phosphokinase (CPK; Figure 1), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were similar regardless of statin use and remained within normal levels across all arms.Mean baseline ALT and AST levels were 20–23 and 20–22 U/L, respectively; at W12, ALT and AST ranged from 22–24 and 20–25 U/L, respectively. Graded CPK, ALT, and AST elevations are in Table 1.Table 1.Graded laboratory abnormalities at week 12 by baseline statin use in PBO-controlled analysisConcomitantNoneFIL200(n=68)FIL100(n=95)PBO(n=93)FIL200 (n=709)FIL100(n=693)PBO(n=688)CPK increased*598281562549537G1 (≤2.5×ULN)10 (16.9)13 (15.9)6 (7.4)71 (12.6)47 (8.6)18 (3.4)G2 (>2.5 to 5×ULN)3 (5.1)006 (1.1)2 (0.4)3 (0.6)G3 (>5 to 10×ULN)0001 (0.2)03 (0.6)G4 (>10×ULN)0001 (0.2)2 (0.4)0AST increased**689492708692684G1 (≤3.0×ULN)9 (13.2)11 (11.7)7 (7.6)97 (13.7)79 (11.4)60 (8.8)G2 (>3.0 to 5.0×ULN)0003 (0.4)2 (0.3)3 (0.4)G3 (>5.0 to 20.0×ULN)01 (1.1)02 (0.3)00G4 (>20.0×ULN)000000ALT increased**689492708692684G1 (≤3.0×ULN)13 (19.1)14 (14.9)13 (14.1)98 (13.8)92 (13.3)72 (10.5)G2 (>3.0 to 5.0×ULN)02 (2.1)010 (1.4)5 (0.7)6 (0.9)G3 (>5.0 to 20.0×ULN)0001 (0.1)01 (0.1)G4 (>20.0×ULN)000000Data are n (%). Grading per Common Terminology Criteria for Adverse Events v4.03*FINCH 1–2**DARWIN 1–2, FINCH 1–2ALT, alanine aminotransferase; AST, aspartate aminotransferase; CPK, creatine phosphokinase; csDMARD, conventional synthetic disease-modifying antirheumatic drug; FIL200/100, filgotinib 200/100 mg + csDMARDs; Grade, G; PBO, placebo; ULN, upper limit of normal.In the long-term as-treated analysis, 1 (0.5%)/6 (3.2%)/0/0/0 treatment-emergent adverse events (AE) of myalgia occurred in pts on statins at baseline receiving FIL200/FIL100/ADA/MTX/PBO and in 12 (0.6%)/8 (0.5%)/3 (1.0%)/2 (0.5%)/1 (0.1%) pts not on statins. Muscle spasms occurred in 2 (0.9%)/3 (1.6%)/1 (3.2%)/0/1 (1.1%) pts on statins at baseline receiving FIL200/FIL100/ADA/MTX/PBO and 21 (1.0%)/8 (0.5%)/0/3 (0.8%)/1 (0.1%) pts not on statins at baseline. One patient not on statins receiving FIL200 reported rhabdomyolysis. For all treatment arms in P3 as-randomised analysis, mean LDL and HDL increased similarly from baseline (108–110 and 56–59 mg/dL, respectively) to W52 (119–130 and 59–71 mg/dL, respectively).Conclusion:No increases in statin-induced AEs such as muscle or liver toxicities occurred with statins and filgotinib coadministration; results are supported by a drug-drug interaction study.4 Mean LDL and HDL increased at W52 in all treatment arms.References:[1]Genovese et al. JAMA. 2019;322:315–25.[2]Westhovens et al. Ann Rheum Dis. 2021; online first.[3]Combe et al. Ann Rheum Dis. 2021; online first.[4]Anderson et al. EULAR 2021 abstract.Disclosure of Interests:Peter C. Taylor Consultant of: AbbVie, Biogen, Eli Lilly, Fresenius, Galapagos, Gilead, GlaxoSmithKline, Janssen, Nordic Pharma, Pfizer, Roche, BMS, Sanofi, Celltrion, and UCB, Grant/research support from: Celgene, Eli Lilly, Galapagos, and Gilead, Christina Charles-Schoeman Consultant of: Gilead, Pfizer, and Regeneron-Sanofi, Grant/research support from: AbbVie, Bristol-Myers Squibb and Pfizer Inc, Muhsen Alani Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Mona Trivedi Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Vanessa Castellano Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Iyabode Tiamiyu Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Deyuan Jiang Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Lei Ye Shareholder of: Gilead Sciences, Inc., Employee of: Gilead Sciences, Inc., Sander Strengholt Shareholder of: Galapagos BV, Employee of: Galapagos BV, Michael Nurmohamed Speakers bureau: AbbVie, Bristol-Myers Squibb, Eli Lilly, Roche, and Sanofi, Consultant of: AbbVie, Celgene, Celltrion, Eli Lilly, Janssen, and Sanofi, Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, MSD, Mundipharma, Novartis, Pfizer, Roche, and Sanofi, Gerd Rüdiger Burmester Speakers bureau: AbbVie, Eli Lilly, Pfizer, and Gilead Sciences, Inc., Consultant of: AbbVie, Eli Lilly, Pfizer, and Gilead Sciences, Inc.
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Dougados, M., J. Lucas, E. Desfleurs, P. Claudepierre, P. Goupille, A. Ruyssen-Witrand, A. Saraux, A. Tournadre, D. Wendling et C. Lukas. « POS0300 FACTORS ASSOCIATED WITH SECUKINUMAB (SEC) RETENTION IN AXIAL SPONDYLOARTHRITIS (axSpA) : RESULTS OF THE FRENCH RETROSPECTIVE STUDY FORSYA ». Annals of the Rheumatic Diseases 81, Suppl 1 (23 mai 2022) : 398. http://dx.doi.org/10.1136/annrheumdis-2022-eular.1933.

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BackgroundWhile data on real-life SEC retention rate in patients (pts) with axSpA is accumulating, there are no data on predictive factors for this retention. Presence of objective sign of inflammation (OSI) are known to be predictive of efficacy of anti-TNFs and their retention in axSpA.ObjectivesTo assess whether OSI were predictive of SEC retention at 1 year in axSpA.MethodsFrench retrospective study collecting between October 2019 and September 2020 data from axSpA pts a) having initiated and received at least one dose of SEC between August 11th 2016 and August 31st 2018, b)with at least a one year follow-up period. Retention of SEC at 1 year was estimated by the Kaplan Meier (KM) method. OSI were defined by at least one of the following: CRP> N, MRI-inflammation at the sacroiliac or spine level. Preselected factors of SEC retention at 1 year (≥1 OSI, age, sex, BMI, smoking, HLA B27, non-radiographic vs radiographic axSpA, past or present uveitis / Inflammatory Bowel Disease (IBD) / psoriasis / arthritis or synovitis, diagnostic delay, disease duration, SEC line of biologic therapy, SEC maintenance dose, concomitant csDMARD / oral corticosteroids / proton pomp inhibitor, history of depression / fibromyalgia) were analyzed by multivariate cox model regression. Only variables with <20% missing data were included in the model after imputation and stepwise selection (significance level for entering variables = 20%; for removing variables = 10%). OSI was forced into the model whatever its significance level or rate of missing data.ResultsIn total, 906 pts from 47 centers (male: 42.2%, mean age: 46.2 ± 11.7 years, mean disease duration: 9,3 ± 9.1 years), were included in the analysis. At initiation of SEC, 86.3% of pts had ≥ 1 OSI and respectively 8.0%, 14.9% and 77.1% were in 1st, 2nd and ≥ 3rd line (L) of biologic/targeted synthetic DMARD. The 1 year KM survival rate for SEC was 59% [95%CI:55%-62%] overall, 58% [54%-62%] and 63% [53%-73%] for pts with or without OSI, and was numerically greater in 1st L vs 2nd and ≥3rd L (70% [59%-81%], 62% [54%-70%], 57% [53%-61%] respectively). In multivariate analysis absence of OSI, lack of prior exposure to anti-TNF inhibitors, absence of IBD, and absence of history of depression were associated with a better SEC retention at 1 year (Table 1).Table 1.Predictive factors of SEC 1 year retention identified by multivariate cox regression analysis (multiple imputation + stepwise selection)Predictive factors (* reference)Still on SEC at 1 Year (%)#HR [95% CI]p vs refp type III≥ 1 objective sign of inflammationNo (N=165)*65.3%yes (N=711)58.8%1.44 [1.08; 1.93]0.014SEC treatment line1st L (N=68)*72.2%0.0842nd L (N=132)62.7%1.53 [0.91; 2.57]0.107≥ 3rd L (N=676)57.6%1.67 [1.06; 2.62]0.028Past or present history of IBDNo (N=854)*59.8%Yes (N=22)40.9%1.76 [1.01; 3.07]0.047History of depression or anti-depressive concomitant treatmentNo (N=716)*60.8%Yes (N=160)54.5%1.25 [0.97; 1.60]0.090# without imputation for missing dataInterpretation HR > 1: the hazard of discontinuation at 1 year is X times higher vs referenceConclusionThe overall retention of SEC at 1 year in daily practice at the time of its launch in France was 59% for axSpA patients and OSI, prior exposure to TNF inhibitors, IBD and history of depression were identified as predictive factors of SEC retention.AcknowledgementsAuthors thank the participating investigators, centers and patients. NOVARTIS Pharma France financially supported this study.Disclosure of InterestsMaxime Dougados Consultant of: Honorarium from Novartis Pharma France, Julien Lucas: None declared, Emilie Desfleurs Employee of: Novartis employee, Pascal Claudepierre Consultant of: Honorarium from Novartis Pharma France, Philippe Goupille Consultant of: Honorarium from Novartis Pharma France, Adeline Ruyssen-Witrand Consultant of: Honorarium from Novartis Pharma France, Alain Saraux Consultant of: Honorarium from Novartis Pharma France, Anne Tournadre Speakers bureau: AbbVie, Fresenius-Kabi, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai, Sanofi, Consultant of: AbbVie, Fresenius-Kabi, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai, Sanofi, Grant/research support from: AbbVie, Fresenius-Kabi, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai, Sanofi, Daniel Wendling Consultant of: Honorarium from Novartis Pharma France, Cédric Lukas Consultant of: Honorarium from Novartis Pharma France
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Pina Vegas, L., E. Sbidian, D. Wendling, P. Goupille, S. Ferkal, P. Le Corvoisier, B. Ghaleh, A. Luciani et P. Claudepierre. « OP0052 FACTORS ASSOCIATED WITH REMISSION AT 5 YEARS OF FOLLOW-UP IN EARLY ONSET AXIAL SPONDYLOARTHRITIS : RESULTS FROM THE DESIR COHORT ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 27.1–28. http://dx.doi.org/10.1136/annrheumdis-2021-eular.305.

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Background:The disease course of axial SpA (axSpA) is highly variable and can be characterized by ongoing axial inflammation and radiographic progression associated with restricted mobility of the spine, reduced function and disability leading to impairment in quality of life. Control of disease activity is a primary aim in axSpA management. To assess disease activity the Ankylosing Spondylitis Disease Activity Score-C-reactive protein (ASDAS-CRP) is often considered as a reference tool. The data on remission are spare in axSpA and the identification of long-term remission factors, enabling the patient’s management to be adapted, seems necessary but remains unclear.Objectives:To evaluate the proportion of patients in remission according to ASDAS-CRP at 5 years of follow-up, to describe their characteristics in comparison with patients with active disease at that time, and to identify baseline factors associated with remission at 5 years of follow-up.Methods:We included all patients from the DESIR (Devenir des Spondylarthropathies Indifférenciées Récentes) cohort with available data on ASDAS-CRP at 5-year follow-up and TNFα inhibitors exposure. Patients in remission, defined as an ASDAS-CRP<1.3, and with active disease were compared according to their main demographic, clinical, biological and radiological characteristics. A logistic model stratified on TNFα inhibitors exposure was used in the main analysis. Sensitivity analyses among patients with axSpA diagnosis confirmed by rheumatologist at 5-years were performed.Results:A total of 614 patients were followed in the DESIR cohort at M60. After excluding those with missing data on ASDAS score (n= 163) and TNFα inhibitors exposure (n= 2), analyzed patients were 449 (73%). Excluded patients had similar baseline characteristics to those included in the analysis. Among patients unexposed to TNFα inhibitors (n=247), 77 (31%) were in remission (37,8±8,3 years; 55% men, 58% NSAID users), 170 (69%) weren’t (39,8±8,6 years; 42% men, 81% NSAID users). Among exposed patients (n=202), 34 (17%) were in remission (36,1±8,1 years; 71% men, 29% NSAID users), 168 (83%) weren’t (39,5±9,0 years; 41% men, 63% NSAID users) (Figure 1). Overall, patients in remission were more frequently men, HLA-B27+, with high education and lower BMI at 5-year of follow-up. The baseline factors associated with remission at 5 years of follow-up from the multivariate analysis are presented in Table 1.Table 1.Baseline factors associated with remission at 5-year follow-up (multivariate analysis)TNFα: Tumor Necrosis Factor alpha; ORa: adjusted Odd Ratio; 95%IC: 95% confidence interval; BASDAI: Bath Ankylosing Spondylitis Disease Activity Index; BMI: Body Mass Index.Conclusion:The overall remission rate at 5 years was 25%, 31% among patients unexposed to TNFα inhibitors and 17% among those exposed. This study reveals the difficulty in achieving 5-year remission in recent axSpA, especially in the most active forms at baseline; socio-educational factors and overweight also appear to be related.Acknowledgements:L Pina Vegas received a Master 2 grant from the French Society of Rheumatology (Bourse Master 2ème Année 2019)Disclosure of Interests:Laura Pina Vegas: None declared, Emilie Sbidian: None declared, Daniel Wendling: None declared, Philippe Goupille: None declared, Salah Ferkal: None declared, Philippe Le Corvoisier: None declared, Bijan Ghaleh: None declared, Alain Luciani: None declared, Pascal Claudepierre Speakers bureau: Abbvie, Janssen, Lilly, MSD, Novartis, Pfizer, Consultant of: Abbvie, Pfizer, Roche-Chugai, Bristol-Myers Squibb, MSD, UCB, Novartis, Janssen, Lilly, Celgene (consulting fees, less than 10,000 $ each)., Employee of: Roche Chugai, Sanofi Aventis, Celgene, Pfizer, MSD, Novartis and BMS (investigator).
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Warner, Nicholas O. « Dostoevsky and Suicide. By N. N. Schneidman. Oakville, Ontario, New York, and London : Mosaic Press, 1984. 124 pp. $19.95, cloth. $9.95, paper. - Dostoïevski et L'Autre. By Louis Allain. Bibliothèque russe de I'lnstitute d'Études Slaves, vol. 70. Paris : Institut d'Études Slaves and Presses universitaires de Lille, 1984. 202 pp. 85 F, paper. » Slavic Review 45, no 2 (1986) : 402–4. http://dx.doi.org/10.2307/2499277.

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Levy, D., B. Nespola, M. Giannini, R. Felten, C. Varoquier, M. Rinagel, A. S. Korganow et al. « FRI0249 IN MYOSITIS PATIENTS, SJÖGREN’S SYNDROME IS ASSOCIATED WITH INCLUSION BODY MYOSITIS AND WITH ANTI-CN1A ANTIBODIES INDEPENDENTLY OF THE MYOSITIS SUBTYPE ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 708.3–709. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5766.

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Background:Myositis are characterized by weakness and muscle inflammation. They encompass heterogeneous conditions, which include dermatomyositis (DM), inclusion body myositis (IBM) and polymyositis (PM) according to the EULAR/ACR 2017 criteria. We recently recorded a high prevalence of IBM in a cohort of primary Sjögren’s syndrome (SS) (1). The signification of SS in the setting of myositis is unanswered.Objectives:To refine the signification of SS in the setting of myositis.Methods:Among a monocentric myositis cohort (according to the EULAR/ACR 2017 criteria), SS patients (according to the ACR/EULAR 2016 criteria) were identified (myositis/SS+ group) and compared to myositis patients without SS (myositis/SS- group).Results:Among 414 myositis patients, SS criteria were available for 96 patients. Thirty two (33%) presented SS. Patients with SS tended to be more frequently women (F/M ratio 9.7 vs 3.0, p = 0.07). Age at diagnosis of myositis was similar in both groups (53 years [range 21-74] vs 53 years [range 16-77], p = 0.51).Myositis subtypes repartition (as defined by EULAR/ACR 2017 criteria) was different in myositis/SS+ and myositis/SS- groups (p = 0.021), IBM being four-fold more prevalent in myositis/SS+ group (25% vs 6%, p = 0.018). Accordingly, the delay between the first muscle symptoms and myositis diagnosis was longer in myositis/SS+ group (7 months [0-336] vs 4 months [0-122], p = 0.041). Moreover, aside anti-cN1A antibodies, myositis-specific antibodies were less frequently found in myositis/SS+ patients than in myositis/SS- ones (16/32 [50%] vs 46/64 [72%], p = 0.035).Anti-cN1A antibodies were more prevalent in myositis/SS+ patients (33% vs 5.8%, p = 0.0032). However, in myositis/SS+ group, anti-cN1A were frequent in each of the EULAR/ACR 2017 myositis subtypes and the association between SS and anti-cN1A positivity was maintained in a multivariate analysis adjusted with the diagnosis of IBM (p = 0.023).Seven of the myositis/SS+ patients (22%) had systemic involvement typical of SS (vs 6 [9%] of the myositis/SS- patients, p = 0.12) including polyneuropathy (6 [20%] vs 6 [10%]) and type 2 cryoglobulinaemic vasculitis (1 [3%] vs 1 [1.6%]). In addition, 2 (6%) myositis/SS+ patients developed a lymphoma (one B diffuse large cell lymphoma of the parotid and one non-Hodgkin lymphoma), vs none of the myositis/SS- patients (p = 0.11). Only one (3%) of the myositis/SS+ patients developed myositis-associated cancer (diagnosed within 3 years of myositis diagnosis) versus 6 (9%) of the myositis/SS- patients (p = 0.66).Aside hydroxychloroquine, more frequently used in myositis/SS+ group (38% vs 16%, p = 0.018), no significant difference was found in the management of the patients (taking into account the myositis subtype).Conclusion:Myositis patients with SS have more frequently IBM than myositis patients without SS. They also have more frequently anti-cN1A antibodies, independently of the myositis subtype. They might develop systemic complications of SS.References:[1]Felten R, Seror R, Vittecoq O, Hachulla E, Perdriger A, Dieude P, et al. SAT0470 Myositis, often suspected, is actually rare in primary Sjögren’s syndrome: data from the French cohort ASSESS. In BMJ Publishing Group Ltd and European League Against Rheumatism; 2018. p. 1093.1–1093. Available from:http://ard.bmj.com/lookup/doi/10.1136/annrheumdis-2018-eular.2945Disclosure of Interests:Dan LEVY: None declared, Benoit Nespola: None declared, Margherita Giannini: None declared, Renaud FELTEN: None declared, Coralie Varoquier: None declared, Marina Rinagel: None declared, Anne-Sophie Korganow: None declared, Vincent Poindron: None declared, Thierry Martin: None declared, Francois Maurier: None declared, Hassam Chereih: None declared, Bastien Bouldoires: None declared, Baptiste Hervier: None declared, Cédric Lenormand: None declared, Laurent Arnaud: None declared, Bernard Geny: None declared, Jean Sibilia: None declared, Jacques-Eric Gottenberg Grant/research support from: BMS, Pfizer, Consultant of: BMS, Sanofi-Genzyme, UCB, Speakers bureau: Abbvie, Eli Lilly and Co., Roche, Sanofi-Genzyme, UCB, alain meyer: None declared
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Villon, C., L. Orgeolet, A. M. Roguedas-Contios, L. Misery, J. E. Gottenberg, D. Cornec, S. Jousse-Joulin et al. « THU0282 EPIDEMIOLOGY OF CUTANEOUS INVOLVEMENT IN SJÖGREN’S SYNDROME : DATA FROM THREE FRENCH POPULATIONS OF PSS (TEARS, ASSESS, DIAPSS) ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 368.1–368. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1847.

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Background:Cutaneous involvement is common during primary Sjogren’s Syndrome (pSS) but prevalence and characteristics are difficult to establish precisely because of the limited number of patients studied in most cohorts, the variability of the disorders evaluated in each cohort, the rarity of some of them, and the heterogeneity of evaluations from previous studies (1).Objectives:To determine the prevalence and significance of dermatological disorders in primary Sjogren Syndrome.Methods:We use 2 French cohorts (ASSESS, in which prevalence of skin disorders in 395 pSS patients was evaluated, and diapSS in which 91 consecutive pSS patients had an examination by a dermatologist) and baseline data of the TEARS randomized trial (110 patients with recent or active pSS, treated with rituximab or placebo, and evaluated for skin dryness using a visual analogue scale out of 100).Results:Skin manifestations included in the ESSDAI were rare in the ASSESS cohort (n=16/395, 4.1%, mainly purpuras; only 3 had high activity) but associated with activity in the other ESSDAI domains (peripheral neurological (p<0.001), muscular (p=0.01), hematological (p=0.017) and biological (p=0.017)), history of arthritis (p=0.008), splenomegaly (p=0.024) and higher gamma globulin level (p=0.008)) (Table). Compared to pSS patients not receiving a dermatological consultation, the pSS patients who had a dermatological consultation had significantly more dermatological involvement outside ESSDAI score [42% (29/69) versus 19.6% (11/56); p=0.008]. The TEARS study showed a high prevalence of cutaneous dryness (VAS>50; 48.2%) and that these dry skin patients had higher pain VAS (61.5+/-28.2 vs 46.8+/-27.0; p=0.003) and drought (79.4+/-15.2 vs 62.5+/-21.7; p<0.0001).Cutaneous involvementNo Cutaneous involvementTotalp values*Muscular3/16 (18.8)10/373 (2.7)13/389 (3.3)0.001Peripheral nervous system PNS4/16 (25)34/373 (9.1)38/389 (9.8)0.00001Biological8/16 (50)138/371 (37.2)146/387 (37.7)0.017Hematologic7/16 (43.8)55/373 (14.7)62/389 (15.9)0.017History of arthritis12/16 (75)154/374 (41.2)166/390 (42.6)0.008History of splenomegaly2/16 (12.5)10/3762.7)12/392 (3.1)0.024History of lymphoma0/16 (0)18/379 (4.7)18/395 (4.6)0.372Mean (SD) ESSDAI score14.5 (6.8)4.4 (5.1)0.00001Mean (SD) ESSDAI score after excluding the points awarded by skin manifestations8.1 (6.2)4.4 (5.1)0.014Gammaglobulin levels (mean +/- SD)23.1 +/-7.318.5 +/-8.1-0.006Conclusion:The most common skin disorder is dryness, which is associated with a higher level of pain and overall subjective dryness. ESSDAI skin activity is rare, associated with hypergammaglobulinemia and ESSDAI activity. Systematic dermatological examination is informative for non-specific pSS lesionsReferences:[1]Orgeolet L, Foulquier N, Misery L, Redou P, Pers J-O, Devauchelle-Pensec V, et al. Can artificial intelligence replace manual search for systematic literature? Review on cutaneous manifestations in primary Sjögren’s syndrome. Rheumatol Oxf Engl. 2019 Aug 31;Disclosure of Interests:Camille Villon: None declared, Laure Orgeolet: None declared, Anne-Marie Roguedas-Contios: None declared, Laurent Misery: None declared, Jacques-Eric Gottenberg Grant/research support from: BMS, Pfizer, Consultant of: BMS, Sanofi-Genzyme, UCB, Speakers bureau: Abbvie, Eli Lilly and Co., Roche, Sanofi-Genzyme, UCB, Divi Cornec: None declared, Sandrine Jousse-Joulin: None declared, Raphaèle Seror Consultant of: BMS UCB Pfizer Roche, Jean-Marie Berthelot: None declared, Philippe Dieudé: None declared, Jean-Jacques Dubost: None declared, anne-laure Fauchais: None declared, Vincent Goeb: None declared, Eric Hachlla: None declared, Pierre-Yves Hatron: None declared, Claire Larroche: None declared, Gilles Hayem: None declared, Véronique LE GUERN Grant/research support from: UCB for GR2 study (to our institution), Aleth Perdriger: None declared, Jacques Morel: None declared, Olivier VITTECOQ: None declared, Xavier Mariette Consultant of: BMS, Gilead, Medimmune, Novartis, Pfizer, Servier, UCB, Valerie Devauchelle-Pensec: None declared, alain saraux: None declared
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Seror, R., G. Baron, M. Camus, D. Cornec, E. Perrodeau, S. J. Bowman, M. Bombardieri et al. « OP0286 DEVELOPMENT AND PRELIMINARY VALIDATION OF THE SJÖGREN’S TOOL FOR ASSESSING RESPONSE (STAR) : A CONSENSUAL COMPOSITE SCORE FOR ASSESSING TREATMENT EFFECT IN PRIMARY SJÖGREN’S SYNDROME ». Annals of the Rheumatic Diseases 81, Suppl 1 (23 mai 2022) : 189.2–190. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2583.

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BackgroundToday, there are still no DMARDs licensed for primary Sjögren Syndrome (pSS) patients. Among the explanations, are the limitations of current outcome measures used as primary endpoints: e.g; high placebo response rate, evaluation of either symptoms or systemic activity, and important features not being assessed. The NECESSITY consortium (https://www.necessity-h2020.eu/), including pSS experts from academia, pharmaceutical industry and patient groups formed to develop a new composite responder index, the Sjögren’s Tool for Assessing Response (STAR) that solve the issues of current outcome measures in pSS and is intended for use in clinical trials as an efficacy endpoint.ObjectivesTo develop a composite responder index in primary Sjögren’s syndrome (pSS): the STAR.MethodsTo develop the STAR, the NECESSITY consortium used data-driven methods, based on 9 randomized controlled trials (RCTs), and consensus techniques, involving 78 experts and 20 patients. Based on reanalysis of rituximab trials (TRACTISS and TEARS) and literature review, the Delphi panel identified a core set of domains to include in the STAR, with their respective outcome measures. STAR options combining these domains were designed and proposed to the panel to select and improve them. For each STAR option, sensitivity to change was estimated by the C-index (derived from Effect size) in all 9 RCTs. Delphi rounds were run for selecting STAR among these options. The Delphi panel also voted to classify trials as positive, negative or “in between” in regards to primary but also key secondary endpoints. For the options remaining before the final vote, meta-analyses of the RCTs were performed separately for positive and “in between” trials together, and for negative trials.ResultsThe Delphi panel identified 5 core domains (systemic activity, patient symptoms, lachrymal gland function, salivary gland function and biological parameters), and 227 STAR options, combining these domains, were selected to be tested for sensitivity to change. After two Delphi rounds, meta-analyses of the 20 remaining options were performed. The candidate STAR was selected by a final vote based on metrological properties and clinical relevance. In positive/in between trials, candidate STAR detected a difference between arms (OR 3.29, 95%-CI [2.07;5.22], whereas it did not in negative trials (OR 1.53, 95%-CI [0.81;2.91]).ConclusionThe candidate STAR is a composite responder index, including in a single tool all main disease features, and is designed for use as a primary endpoint in pSS RCTs. Its rigorous and consensual development process ensures its face and content validity. The candidate STAR showed good sensitivity and specificity to change. The candidate STAR will be prospectively validated in a dedicated three arms RCT of the NECESSITY consortium that will evaluate combination of synthetic DMARDs (hydroxychloroquine + lefunomide or hydroxychloroquine + mycophenolate vs placebo). We encourage the use of STAR in any ongoing and future trials.Table 1.Candidate STARDomainPointDefinition of responseSystemic activity3Decrease of clinESSDAI ≥ 3Patient reported outcome3Decrease of ESSPRI ≥ 1 point or ≥ 15%Lachrymal gland function1Schirmer:If abnormal score at baseline: increase ≥ 5 mm from baselineIf normal score at baseline: no change to abnormalOrOcular Staining Score:If abnormal score at baseline: decrease ≥ 2 points from baselineIf normal score at baseline: no change to abnormalSalivary gland function1Unstimulated Whole Salivary Flow:If score > 0 at baseline: increase ≥ 25% from baselineIf score is 0 at baseline: any increase from baselineorUltrasound:Decrease ≥ 25% in total Hocevar score from baselineBiological1Serum IgG levels: decrease ≥ 10%orRheumatoid Factor levels: decrease ≥ 25%Candidate STAR responder≥ 5 pointsESSDAI: EULAR Sjögren syndrome disease activity index; ESSPRI: EULAR Sjögren syndrome patient reported index; IgG: Immunoglobulin G;AcknowledgementsNECESSITY WP5 STAR development participants: Suzanne Arends (University Medical Center Groningen, Department of Rheumatology and Clinical Immunology, Groningen 9700 RB, Netherlands), Francesca Barone (Centre for Translational Inflammation Research, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK), Albin Björk (Division of Rheumatology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden), Coralie Bouillot (Association Française du Gougerot Sjögren et des Syndromes Secs, France), Guillermo Carvajal Alegria (University of Brest, Inserm, CHU de Brest, LBAI, UMR1227, Brest, France; Service de Rhumatologie, Centre de Référence Maladies Autoimmunes Rares CERAINO, CHU Cavale Blanche, Brest, France), Wen-Hung Chen (GlaxoSmithKline, Research Triangle Park, North Carolina, USA), Kenneth Clark (GlaxoSmithKline Medicines Research Centre, Gunnels Wood Road, Stevenage, Hertfordshire SG1 2NY, United Kingdom), Konstantina Delli (Department of Oral and Maxillofacial Surgery, University Medical Center Groningen (UMCG), University of Groningen, The Netherlands), Salvatore de Vita (Rheumatology Clinic, University Hospital of Udine, Italy), Liseth de Wolff (University Medical Center Groningen, Department of Rheumatology and Clinical Immunology, Groningen 9700 RB, Netherlands), Jennifer Evans (Novartis Pharmaceuticals corporation USA), Stéphanie Galtier (Institut de Recherches Internationales Servier (IRIS), Suresnes Cedex, France), Saviana Gandolfo (Rheumatology Clinic, Department of Medical area, University of Udine, ASUFC, 33100 Udine, Italy), Mickael Guedj (Institut de Recherches Internationales Servier (IRIS), Suresnes Cedex, France), Dewi Guellec (CHU de Brest, Service de Rhumatologie, Inserm, CIC 1412, Brest, France), Safae Hamkour (Center of Translational Immunology, Department of Immunology, University Medical Center Utrecht, Utrecht 3584 GA, Netherlands), Dominik Hartl (Novartis Institutes for BioMedical Research, Basel, Switzerland), Malin Jonsson (Section for Oral and Maxillofacial Radiology, Department of Clinical Dentistry, Faculty of Medicine and Dentistry, University of Bergen, Norway), Roland Jonsson (Broegelmann Research Laboratory, Department of Clinical Science, University of Bergen, Department of Rheumatology, Haukeland University Hospital, Bergen, Norway), Frans Kroese (University Medical Center Groningen, Department of Rheumatology and Clinical Immunology, Groningen 9700 RB, Netherlands), Aike Albert Kruize (University Medical Center Utrecht, Department Rheumatology and Clinical Immunology, Utrecht, Netherlands), Laurence Laigle (Institut de Recherches Internationales Servier (IRIS), Suresnes Cedex, France), Véronique Le Guern (AP-HP, Hôpital Cochin, Centre de référence maladies auto-immunes et systémiques rares, service de médecine interne, Paris, France), Wen-Lin Luo (Department of Biometrics and Statistical Science, Novartis Pharmaceuticals, East Hanover, New Jersey), Esther Mossel (University Medical Center Groningen, Department of Rheumatology and Clinical Immunology, Groningen 9700 RB, Netherlands), Wan-Fai Ng (Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK), Gaëtane Nocturne (Department of Rheumatology, Université Paris-Saclay, INSERM U1184: Centre for Immunology of Viral Infections and Autoimmune Diseases, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre, Le Kremlin Bicêtre, Paris, France), Marleen Nys (Global Biometric Sciences, Bristol Myers Squibb, Braine L’Alleud, Belgium), Roald Omdal (Clinical Immunology Unit, Department of Internal Medicine, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway), Jacques-Olivier Pers (LBAI, UMR1227, University of Brest, Inserm, Brest, France and CHU de Brest, Brest, France), Maggy Pincemin (Association Française du Gougerot Sjögren et des Syndromes Secs, France), Manel Ramos-Casals (Department of Autoimmune Diseases, Hospital Clinic de Barcelona Institut Clinic de Medicinai Dermatologia, Barcelona, Catalunya, Spain), Philippe Ravaud (Centre d’Epidémiologie Clinique, Hôpital Hôtel-Dieu, Assistance Publique-Hôpitaux de Paris, Paris, France), Neelanjana Ray (Global Drug Development - Immunology, Bristol Myers Squibb Company, Princeton, New Jersey, USA), Alain Saraux (HU de Brest, Service de Rhumatologie, Univ Brest, Inserm, UMR1227, Lymphocytes B et Autoimmunité, Univ Brest, Inserm, LabEx IGO, Brest, France), Athanasios Tzioufas (Rheumatology Clinic, Department of Medical area, University of Udine, ASUFC, 33100 Udine, Italy), Gwenny Verstappen (University Medical Center Groningen, Department of Rheumatology and Clinical Immunology, Groningen 9700 RB, Netherlands), Arjan Vissink, Marie Wahren-Herlenius (Division of Rheumatology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden). We thank the following experts: Esen Karamursel Akpek, Alan Baer, Chiara Baldini, Elena Bartoloni, Marí-Alfonso Begona, Johan Brun, Vatinee Bunya, Laurent Chiche, Troy Daniels, Paul Emery, Robert Fox, Roberto Giacomelli, John Gonzales, John Greenspan, Robert Moots, Susumu Nishiyama, Elizabeth Price, Christophe Richez, Caroline Shiboski, Roser Solans Laque, Muthiah Srinivasan, Peter Olsson, Tsutomu Takeuchi, Frederick Vivino, Paraskevi Voulgari, Daniel Wallace, Ava Wu, Wen Zhang. We thank the anonymous patients from the NECESSITY Patient Advisory Group and the Sjögren Foundation for their valuable contribution to the Delphi process. We thank EW StClair and AN Baer who generated the baminercept data and made them publicly available.Disclosure of InterestsRaphaèle Seror Consultant of: GlaxoSmithKline, Boehringer, Janssen and Novartis, Grant/research support from: GlaxoSmithKline and Amgen, Gabriel Baron: None declared, Marine Camus: None declared, Divi Cornec Consultant of: GlaxoSmithKline, Bristol Myers Squibb, Janssen, Amgen, Pfizer and Roche, Elodie Perrodeau: None declared, Simon J. Bowman Consultant of: Abbvie, Astra Zeneca, Galapagos and Novartis Pharmaceuticals, Michele Bombardieri Consultant of: UCB, Amgen/Medimmune, Janssen, and GlaxoSmithKline, Grant/research support from: Amgen/Medimmune, Janssen, and GlaxoSmithKline, Hendrika Bootsma: None declared, Jacques-Eric Gottenberg Consultant of: AbbVie, Bristol Myers Squibb, Eli Lilly, Galapagos, Gilead, Pfizer, Roche, Sanofi, Novartis, MSD, CSL-Behring and Genzyme, Grant/research support from: Bristol Myers Squibb, Benjamin Fisher Speakers bureau: Bristol Myers Squibb and Novartis, Consultant of: Novartis, Bristol Myers Squibb, Janssen and Servier, Grant/research support from: Servier, Galapagos and Janssen, Wolfgang Hueber Shareholder of: Novartis Pharma, Employee of: Novartis Pharma, Joel van Roon: None declared, Valerie Devauchelle-Pensec: None declared, Peter Gergely Shareholder of: Novartis Pharma, Employee of: Novartis Pharma, Xavier Mariette Consultant of: Bristol Myers Squibb, Galapagos, GlaxoSmithKline, Janssen, Novartis, Pfizer and UCB, Grant/research support from: Ose Pharmaceuticals, Raphaël Porcher: None declared
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Alonso Veloso, María José. « Quevedo, lector del "Anticlaudiano" de Alain de Lille. Noticia sobre nuevas anotaciones autógrafas ». La Perinola, 11 mars 2016, 277–303. http://dx.doi.org/10.15581/017.14.4533.

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Quevedo poseyó, leyó y anotó el Anticlaudiano de Alain de Lille. Tal es la conclusión que se infiere del examen del ejemplar custodiado en la Biblioteca de Menéndez Pelayo en Santander, con signatura (466), perteneciente a una edición de Basilea, 1536. Además de su firma autó- grafa en la portada, el libro contiene abundantes anotaciones marginales de su puño y letra. Además de dar noticia de tal hallazgo, este artículo pretende deslindar la autoría de cada una de ellas, habida cuenta de que el libro tuvo al menos dos poseedores. Presentan la peculiar caligrafía quevediana 53 notas, en tanto que 2 plantean dudas y 8 deben atribuirse a otra mano. A estas anotaciones, de contenido heterogéneo y extensión variable, se suman abundantes subrayados, muchos de ellos localizados en lugares anotados.
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Júnior, Carlile Lanzieri. « O lugar da infância medieval nos escritos dos mestres Alain de Lille (1128-1203), João de Salisbury (c.1115-1180) e Adelardo de Bath (1080-1152) ». BRATHAIR - REVISTA DE ESTUDOS CELTAS E GERMÂNICOS 20, no 1 (31 décembre 2020). http://dx.doi.org/10.18817/brathair.v20i1.2312.

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Não houve lugar para a infância na Idade Média. Uma afirmação que se enraizou na historiografia ao longo da segunda metade do século passado. Pretendemos aqui analisá-la e apontar novos caminhos analíticos. Caminhos que têm como referências os testemunhos deixados por personagens como Alain de Lille, João de Salisbury e Adelardo de Bath. A partir da importância que deram à Gramática, a primeira das Sete Artes Liberais, confiamos ter elementos suficientes para afirmar que o medievo, e em específico os séculos XI e XII, voltou seus olhos para as crianças e os adolescentes.
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Varela Gestoso, Mónica Inés. « Algunas fuentes de la "inventio" en la poesía religiosa de Quevedo ». La Perinola, 19 juin 2018, 337–54. http://dx.doi.org/10.15581/017.3.28185.

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Atendiendo a la delimitación de las fuentes de la inventio en la poesía religiosa de Quevedo se señala la importancia del género desarrollado para establecer el corpus de autores a que el poeta puede recurrir en cada caso. Sirven de muestra algunos ejemplos en el caso de la poesía épica del Poema heroico a Cristo resucitado, donde cabe destacar la imitación de unos pasajes del De raptu Proserpinae de Claudiano y del Anticlaudiano de Alain de Lille, la poesía meditativa del Heráclito cristiano y Lágrimas de un penitente y la poesía doctrinal de los Sonetos sacros.
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Benedetto, Luana C. « Alegoria medieval : onde se situa a poesia de Charles d’orléans ? » Revista Conexão Letras 1, no 1 (14 mai 2015). http://dx.doi.org/10.22456/2594-8962.55664.

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Este estudo tem o objetivo de analisar brevemente a alegoria, a personificação e a metáfora, do modo como se apresentam na obra de Charles d’Orléans, poeta francês do século XV. Para tanto, consideram-se a atitude alegórica desde sua origem na antiguidade clássica, os diversos tipos de alegoria e a tradição alegórica medieval na qual Charles d’Orléans se insere. Trata-se de uma tradição iniciada pelo Romance da Rosa, cujas raízes mergulham na obra de Alain de Lille. Além disso, faz-se um estudo sucinto do símbolo e da sinédoque, discutindo as visões de Curtius, Huizinga, Hansen, Eco, Greimas, Dubois, Lausberg e Ricoeur, entre outros.Palavras-chave: Idade Média, alegoria, personificação, metáfora, poesia.
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48

Puente, O. P., P. Mauricio Beuchot. « La analogía en algunos medievales ». Albertus Magnus 3, no 3 (2 janvier 2012). http://dx.doi.org/10.15332/s2011-9771.2012.0003.08.

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<p align="justify">Al rehacer la historia de la analogía a lo largo de los siglos, se constata la riqueza de significado y cómo la utilizaron algunos pensadores en el contexto filosófico-teológico. También se hizo uso de ella en el conocimiento de las cosas creadas y su aplicación sobre todo en la antropología filosófica y en la ética. Los primeros en utilizar la analogía de atribución fueron los padres de la Iglesia y los primeros medievales a través de los neoplatónicos. en autores como Boecio, el Pseudo Dionisio y Juan escoto eriúgena se encuentran verdaderos avances en la implementación de la analogía, que va más allá de lo unívoco o equívoco, siendo una analogía propiamente analógica.</p><p align="justify">en esta tradición analógica se cuentan también Pedro Lombardo, Bernardo Silvestris, Alain de Lille, la escuela de san Víctor, san Alberto Magno, san Buenaventura, santo Tomás de Aquino, Juan eckhart y Raymundo Lulio, entre otros. A partir de lo ante- rior, se muestra la importancia de la analogía y sus aplicaciones a la hermenéutica analógica.</p>
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« Jean-Luc Solère, Anca Vasiliu, and Alain Galonnier, eds., Alain de Lille, le docteur universel : Philosophie, théologie et littérature au XIIe siècle. Actes du XIe Colloque international de la Société Internationale pour l'Étude de la Philosophie Médiévale, Paris, 23–25 October 2003. (Rencontres de Philosophie Médiévale, 12.) Turnhout : Brepols, 2005. Paper. Pp. xiv, 495 ; 1 black-and-white figure and tables. €55. » Speculum 82, no 03 (juillet 2007) : 793. http://dx.doi.org/10.1017/s0038713400011209.

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« Alain Lottin, Jean-Claude Hocquet, and Stéphanie Lebecq, eds., with Françoise Lottin-Triquet and Nadein Malle-Grain, Les hommes et la met dans l'Europe du nord-ouest de l'antiquité à nos jours. Special issue of Revue du Nord. Proceedings of a conference at Boulogne-sur-Mer, 15–17 June 1984. (Collection Histoire, Special Hors-Série, 1.) Villeneuve d'Ascq, 1986. Paper. Pp. xxvi, 520 ; illustrated. F 150. May be ordered from Revue du Nord, Univ. de Lille III, B.P. 149, 59653 Villeneuve d'Ascq, France. » Speculum 63, no 01 (janvier 1988) : 252–53. http://dx.doi.org/10.1017/s0038713400117403.

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