scholarly journals FRI0102 SERUM TNFΑ LEVELS AT 24 HOURS AFTER FIRST ADMINISTRATION OF CERTOLIZUMAB PEGOL PREDICT EFFECTIVENESS AT WEEK 12 IN PATIENTS WITH RHEUMATOID ARTHRITIS FROM TSUBAME STUDY (UMIN ID:0002381)

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 630.1-630
Author(s):  
Y. Miyazaki ◽  
K. Nakano ◽  
S. Nakayamada ◽  
S. Kubo ◽  
S. Iwata ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Clinical Response ◽  
Remission Rate ◽  
Certolizumab Pegol ◽  
Univariate Analysis ◽  
Inadequate Response ◽  
Clinical Effects ◽  
Tnf Inhibitor ◽  
Research Support ◽  
Low Serum

Background:To increase the remission rate of rheumatoid arthritis (RA), it is necessary to determine the efficacy of the tumor necrosis factor (TNF) inhibitor as early as possible. Moreover, the response to certolizumab pegol (CZP) at 12 weeks has been reported to predict its long-term efficacy.Objectives:As part of a prospective single-center observational study (TSUBAME study), we prospectively enrolled patients to be treated with CZP in our institution to evaluate its effectiveness and safety starting at 24 hours after the first dose in clinical settings, while recording blood CZP concentrations and biomarkers over time to examine their correlation with clinical effects.Methods:One hundred patients with RA and inadequate response to MTX who received CZP were enrolled in the TSUBAME study. The changes in serum TNFα, IL-6, and CZP levels at 24 hours after first administration of CZP were measured, and the correlation between serum biomarkers and clinical response was determined.Results:At 24 hours after CZP initiation, significant improvement was observed in the disease activity (baseline and 24 h: 5.4 ± 1.3, 5.0 ± 1.3, respectively, p < 0.01), which was maintained until week 12. (baseline and 12 w: 5.4 ± 1.3, 3.3 ± 1.4, respectively, p < 0.01). Serum TNFα and IL-6 levels significantly decreased at 24 hours after first administration of CZP compared to baseline. No correlation was found between TNFα and IL-6 levels at baseline and the clinical response. According to univariate analysis, low serum TNFα and IL-6 levels and high CZP levels at 24 hours were associated with DAS28 (ESR) remission at 12 weeks. According to multivariate analysis, low serum TNFα levels at 24 hours were significantly associated with DAS28 (ESR) remission at 12 weeks (OR 0.05, 95%CI 0.01, 0.75, p = 0.03). Based on these findings, an ROC curve was created using remission according to the DAS28 (ESR) at week 12 as a dependent variable and TNFα concentration at 24 hours as an independent variable, resulting in a cut-off value of 0.76 pg/ml. From this result, the TNFα concentration at 24 hours was divided into 2 groups according to this cut-off, and the rates of remission according to the DAS28 (ESR) at week 12 were compared. In the group with TNFα concentration at 24 hours below the cut-off value, the rate of remission according to the DAS28 (ESR) at week 12 was significantly higher than in the group with TNFα concentration at 24 hours above the cut-off value (below the cut-off: above the cut-off = 56.3%: 21.6%, p < 0.001). Between the group that achieved remission according to the DAS28(ESR) and the group that did not achieve remission at week 12, there was almost no difference in the distribution of TNFα concentrations at baseline; however, the distribution of TNFα concentrations at 24 hours was lower in the group that achieved remission.Conclusion:CZP was effective where serum TNFα was strongly neutralized within 24 hours. These results suggest that low serum TNFα levels at 24 hours after first administration of CZP may predict the effectiveness of CZP. To increase the remission rate in RA, it is necessary to determine the effectiveness of the molecular targeted drugs used at an early point, in addition to how rapid the onset of action is. CZP is extremely fast-acting, and its effectiveness can be predicted as early as 24 hours after the first dose, suggesting that it may be possible to determine the effectiveness early.Acknowledgments:The authors thank Ms. M. Hirahara for providing excellent technical assistance.Disclosure of Interests:Yusuke Miyazaki Grant/research support from: Astellas Pharma Inc and UCB S.A., Kazuhisa Nakano: None declared, Shingo Nakayamada Grant/research support from: Mitsubishi-Tanabe, Takeda, Novartis and MSD, Speakers bureau: Bristol-Myers, Sanofi, Abbvie, Eisai, Eli Lilly, Chugai, Asahi-kasei and Pfizer, Satoshi Kubo: None declared, Shigeru Iwata: None declared, Kentaro Hanami: None declared, Shunsuke Fukuyo: None declared, Ippei Miyagawa: None declared, Ayako Yamaguchi: None declared, Akio Kawabe: None declared, SAITO KAZUYOSHI: None declared, Yoshiya Tanaka Grant/research support from: Asahi-kasei, Astellas, Mitsubishi-Tanabe, Chugai, Takeda, Sanofi, Bristol-Myers, UCB, Daiichi-Sankyo, Eisai, Pfizer, and Ono, Consultant of: Abbvie, Astellas, Bristol-Myers Squibb, Eli Lilly, Pfizer, Speakers bureau: Daiichi-Sankyo, Astellas, Chugai, Eli Lilly, Pfizer, AbbVie, YL Biologics, Bristol-Myers, Takeda, Mitsubishi-Tanabe, Novartis, Eisai, Janssen, Sanofi, UCB, and Teijin

scholarly journals FRI0373 ASSOCIATIONS OF VASCULAR PATHOPHYSIOLOGY AND BONE METABOLISM IN ANTI-TNF- TREATED RHEUMATOID ARTHRITIS AND ANKYLOSING SPONDYLITIS PATIENTS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 783.2-784
Author(s):  
M. Czókolyová ◽  
K. Gulyás ◽  
Á. Horváth ◽  
E. Végh ◽  
Z. Pethö ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Ankylosing Spondylitis ◽  
Bone Loss ◽  
Bone Metabolism ◽  
Certolizumab Pegol ◽  
Univariate Analysis ◽  
Inflammatory Rheumatic Diseases ◽  
Ageing Population ◽  
Research Support ◽  
Vascular Markers

Background:Cardiovascular (CV) disease and osteoporosis (OP) have become increasing challenges in the ageing population, even more in patients with inflammatory rheumatic diseases, such as rheumatoid arthritis (RA) and spondyloarthropathies. Both RA and ankylosing spondylitis (AS) have been associated with generalized and localized bone loss, accelerated atherosclerosis, increased CV morbidity and mortality.Objectives:Bone and vascular biomarkers and parameters along with the effect of one-year anti-TNF therapy on these markers were assessed in order to determine correlations between vascular pathophysiology and bone metabolism in RA and AS.Methods:Fifty-three patients including 36 RA patients treated with etanercept (ETN) or certolizumab pegol (CZP) and 17 AS patients treated with ETN were included in a 12-month follow-up study. Bone and vascular markers were assessed by ELISA. Bone density was assessed by DXA and quantitative CT (QCT). Flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and pulse-wave velocity (PWV) were assessed by ultrasound. The effects of vascular markers on bone and bone effects on vasculature undergone statistical analysis.Results:Serum levels of vascular endothelial growth factor (VEGF), PDGF-BB, angiopoietin 2 (Ang2) and cathepsin K (CathK) decreased, procollagen type 1 N-propeptide (P1NP) and sclerostin (SOST) levels increased, soluble receptor activator nuclear kappa B ligand (sRANKL) and osteoprotegerin (OPG) levels showed no differences. When bone and vascular markers were correlated with each other, at baseline, OPG correlated with Ang2 and adiponectin. SOST correlated positively with ccIMT. DXA L2-4 BMD, DXA L1 BMD and DXA femoral neck (FN) BMD correlated with FMD and CRP. QCT trabecular BMD correlated with ccIMT and PON1. According to the univariate analysis, FMD correlated with OPG, ccIMT correlated with SOST and QCT trabecular BMD. Ang1, Ang2 and PDGF-BB showed correlation with Dickkopf-1 (DKK1). Ang2 also correlated with OPG. As suggested by the multivariate analysis, OPG determined FMD; DKK1 was an independent predictor of Ang1, Ang2 and PDGF-BB. OPG was a predictor of Ang2.Conclusion:In our study of anti-TNF treated RA and AS patients, vascular and bone parameters showed numerous correlations. The therapy was clinically effective, it halted further bone loss over 1 year and reduced the production of angiogenic markers.Acknowledgments:This research was supported by an investigator-initiated research grant from Pfizer.Disclosure of Interests:Monika Czókolyová: None declared, Katalin Gulyás: None declared, Ágnes Horváth: None declared, Edit Végh: None declared, Zsófia Pethö: None declared, Szilvia Szamosi: None declared, Attila Hamar: None declared, Anita Pusztai: None declared, Emese Balogh: None declared, Nóra Bodnár: None declared, Levente Bodoki: None declared, Agnes Szentpetery: None declared, Harjit Pal Bhattoa: None declared, György Kerekes: None declared, Katalin Hodosi: None declared, Andrea Domjan: None declared, Sándor Szántó: None declared, Gabriella Szücs: None declared, Hennie Raterman Grant/research support from: UCB, Consultant of: Abbvie, Amgen, Bristol-Myers Sqibb, Cellgene and Sanofi Genzyme, WIllem Lems Grant/research support from: Pfizer, Consultant of: Lilly, Pfizer, Zoltán Szekanecz Grant/research support from: Pfizer, UCB, Consultant of: Sanofi, MSD, Abbvie, Pfizer, Roche, Novertis, Lilly, Gedeon Richter, Amgen

scholarly journals OP0098 POLYPHARMACY IS ASSOCIATED WITH A POORER TREATMENT RESPONSE AND INCREASED RISK OF ADVERSE EVENTS IN EARLY RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 54.1-54
Author(s):  
S. Benamar ◽  
C. Lukas ◽  
C. Daien ◽  
C. Gaujoux-Viala ◽  
L. Gossec ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Adverse Events ◽  
Treatment Response ◽  
Univariate Analysis ◽  
Group Versus ◽  
Biological Database ◽  
Lower Probability ◽  
Research Support ◽  
Early Ra ◽  
Increased Risk

Background:Polypharmacy is steadily increasing in patients with rheumatoid arthritis (RA). They may interfere with treatment response and the occurrence of serious adverse events. Medications taken by a patient may reflect active comorbidities, whereas comorbidity indices usually used include past or current diseases.Objectives:To evaluate whether polypharmarcy is associated with treatment response and adverse events in an early RA cohort and to establish whether polypharmacy could represent a substitute of comorbidities.Methods:We used data from the French cohort ESPOIR, including 813 patients with early onset arthritis. Patients included the current study had to start their first disease modifying anti-rheumatic drug (DMARD) within 24 months of inclusion in the cohort. Disease activity data were collected at one, five and ten years from the initiation of the first DMARD. For each patient, treatments were collected at baseline and at five years. Medications count included all specialties other than background RA therapy, analgesics/NSAIDs and topicals. Polypharmacy was defined as a categorical variable based on the median and tertiles of distribution in the cohort. Treatment response was assessed by achieving DAS28 ESR remission (REM) at 1 year, 5 years and 10 years from the initiation of the first DMARD. The occurrence of severe adverse events (SAE) was measured by the occurrence of severe infection, hospitalization, or death during the 10-year follow-up. The association between patient’s characteristics and achievement of REM and occurrence of SAE were tested in univariate analysis. A logistic regression model was used to evaluate associations between polypharmacy and REM at 1 year, 5 years and 10 years (we used baseline polypharmacy for the 1-year analysis and five years polypharmacy for the 5- and 10-years analyses). Multivariate adjustment was made for age, sex, BMI, duration of disease, initial DAS28 ESR, initial HAQ, smoking status, rheumatic disease comorbidity index (RDCI).Results:The proportion of patients who achieved REM one year after the initiation of the first DMARD was 32.1% in the polypharmacy according to the median group (patients taken ≥2 medication) versus 67.9% in the non-polypharmacy group (p=0.07). At 5 years after the first DMARD, the proportion of patients with REM was 45.0% in the polypharmacy group versus 56.3% in the non-polypharmacy group (p=0.03). At 10 years the proportion of patients with REM was 32.5% in the polypharmacy group versus 67.5% (p=0.06). Patients who take greater or equal to 2 medications had a 40% lower probability of achieving REM (OR = 0.60 [0.38-0.94] p = 0.03) at 5 years from the first DMARD (if RDCI index was not included in the model). At 10 years, patients receiving multiple medications had a 43% lower probability of achieving REM (OR = 0.57 [0.34-0.94] p = 0.02). SAE incidence was 61 per 1000 patient-years. For patients who developed SAE all causes 71.4% where in the polypharmacy group versus 57.8% were in the non-polypharmacy group (p = 0.03; univariate analysis). These results are no longer significant after adjustment for comorbidities indices.Conclusion:In this early RA cohort, polypharmacy is associated with a poorer treatment response and increased risk of adverse events. Polypharmacy may represent a good substitute of comorbidities for epidemiological studies.Acknowledgements:We are grateful to Nathalie Rincheval (Montpellier) who did expert monitoring and data management and all theinvestigators 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).The work reported on in the manuscript did not benefit from any financial support. The ESPOIR cohort is sponsored by the French Society for Rheumatology. An unrestricted grant from Merck Sharp and Dohme (MSD) was allocated for the first 5 years. Two additional grants from INSERM were obtained to support part of the biological database. Pfizer, Abbvie, Lilly and more recently Fresenius and Biogen also supported the ESPOIR cohort.Disclosure of Interests:Soraya Benamar: None declared, Cédric Lukas Speakers bureau: Abbvie, Amgen, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai, UCB, Consultant of: Abbvie, Amgen, Janssen, Lilly, MSD, Novartis, Pfizer, Roche-Chugai, UCB, Grant/research support from: Pfizer, Novartis and Roche-Chugai, Claire Daien Speakers bureau: AbbVie, Abivax, BMS, MSD, Roche, Chugai, Novartis, Pfizer, Sandoz, Lilly, Consultant of: AbbVie, Abivax, BMS, MSD, Roche, Chugai, Novartis, Pfizer, Sandoz, Lilly, Cécile Gaujoux-Viala Speakers bureau: Abbvie, BMS, Celgene, Janssen, Medac, MSD, Nordic Pharma, Novartis, Pfizer, Sanofi, Roche-Chugai, UCB, Consultant of: Abbvie, BMS, Celgene, Janssen, Medac, MSD, Nordic Pharma, Novartis, Pfizer, Sanofi, Roche-Chugai, UCB, Grant/research support from: Pfizer, Laure Gossec Speakers bureau: AbbVie, Amgen, Biogen, Celgene, Janssen, Lilly, Novartis, Pfizer, Sandoz, Sanofi-Aventis et UCB, Consultant of: AbbVie, Amgen, Biogen, Celgene, Janssen, Lilly, Novartis, Pfizer, Sandoz, Sanofi-Aventis et UCB, Anne-Christine Rat Speakers bureau: Pfizer, Lilly, Consultant of: Pfizer, Lilly, 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-Chugai., Jacques Morel Speakers bureau: Abbvie, BMS, Lilly, Médac, MSD, Nordic Pharma, Pfizer, UCB, Consultant of: Abbvie, BMS, Lilly, Médac, MSD, Nordic Pharma, Pfizer, UCB, Grant/research support from: BMS, Pfizer

scholarly journals AB0330 HIGH REMISSION RATES IN RA – REAL LIFE DATA FROM BARITICINIB

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1463.2-1464
Author(s):  
S. Bayat ◽  
K. Tascilar ◽  
V. Kaufmann ◽  
A. Kleyer ◽  
D. Simon ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Disease Activity ◽  
Cox Regression ◽  
Real Life ◽  
Inadequate Response ◽  
Research Support ◽  
Das 28 ◽  
Patient Reported ◽  
One Year

Background:Recent developments of targeted treatments such as targeted synthetic DMARDs (tsDMARDs) increase the chances of a sustained low disease activity (LDA) or remission state for patients suffering rheumatoid arthritis (RA). tsDMARDs such as baricitinib, an oral inhibitor of the Janus Kinases (JAK1/JAK2) was recently approved for the treatment of RA with an inadequate response to conventional (cDMARD) and biological (bDMARD) therapy. (1, 2).Objectives:Aim of this study is to analyze the effect of baricitinb on disease activity (DAS28, LDA) in patients with RA in real life, to analyze drug persistance and associate these effects with various baseline characteristics.Methods:All RA patients were seen in our outpatient clinic. If a patient was switched to a baricitinib due to medical reasons, these patients were included in our prospective, observational study which started in April 2017. Clinical scores (SJC/TJC 76/78), composite scores (DAS28), PROs (HAQ-DI; RAID; FACIT), safety parameters (not reported in this abstract) as well as laboratory biomarkers were collected at each visit every three months. Linear mixed effects models for repeated measurements were used to analyze the time course of disease activity, patient reported outcomes and laboratory results. We estimated the probabilities of continued baricitinib treatment and the probabilities of LDA and remission by DAS-28 as well as Boolean remission up to one year using survival analysis and explored their association with disease characteristics using multivariable Cox regression. All patients gave informed consent. The study is approved by the local ethics.Results:95 patients were included and 85 analyzed with available follow-up data until November 2019. Demographics are shown in table 1. Mean follow-up duration after starting baricitinib was 49.3 (28.9) weeks. 51 patients (60%) were on monotherapy. Baricitinib survival (95%CI) was 82% (73% to 91%) at one year. Cumulative number (%probability, 95%CI) of patients that attained DAS-28 LDA at least once up to one year was 67 (92%, 80% to 97%) and the number of patients attaining DAS-28 and Boolean remission were 31 (50%, 34% to 61%) and 12(20%, 9% to 30%) respectively. Median time to DAS-28 LDA was 16 weeks (Figure 1). Cox regression analyses did not show any sufficiently precise association of remission or LDA with age, gender, seropositivity, disease duration, concomitant DMARD use and number of previous bDMARDs. Increasing number of previous bDMARDs was associated with poor baricitinib survival (HR=1.5, 95%CI 1.1 to 2.2) while this association was not robust to adjustment for baseline disease activity. Favorable changes were observed in tender and swollen joint counts, pain-VAS, patient and physician disease assessment scores, RAID, FACIT and the acute phase response.Conclusion:In this prospective observational study, we observed high rates of LDA and DAS-28 remission and significant improvements in disease activity and patient reported outcome measurements over time.References:[1]Keystone EC, Taylor PC, Drescher E, Schlichting DE, Beattie SD, Berclaz PY, et al. Safety and efficacy of baricitinib at 24 weeks in patients with rheumatoid arthritis who have had an inadequate response to methotrexate. Annals of the rheumatic diseases. 2015 Feb;74(2):333-40.[2]Genovese MC, Kremer J, Zamani O, Ludivico C, Krogulec M, Xie L, et al. Baricitinib in Patients with Refractory Rheumatoid Arthritis. The New England journal of medicine. 2016 Mar 31;374(13):1243-52.Figure 1.Cumulative probability of low disease activity or remission under treatment with baricitinib.Disclosure of Interests:Sara Bayat Speakers bureau: Novartis, Koray Tascilar: None declared, Veronica Kaufmann: None declared, Arnd Kleyer Consultant of: Lilly, Gilead, Novartis,Abbvie, Speakers bureau: Novartis, Lilly, David Simon Grant/research support from: Else Kröner-Memorial Scholarship, Novartis, Consultant of: Novartis, Lilly, Johannes Knitza Grant/research support from: Research Grant: Novartis, Fabian Hartmann: None declared, Susanne Adam: None declared, Axel Hueber Grant/research support from: Novartis, Lilly, Pfizer, EIT Health, EU-IMI, DFG, Universität Erlangen (EFI), Consultant of: Abbvie, BMS, Celgene, Gilead, GSK, Lilly, Novartis, Speakers bureau: GSK, Lilly, Novartis, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Eli Lilly, Novartis, Roche and UCB

scholarly journals SAT0084 SERUM ADIPOKINES PROFILE IN PATIENTS WITH RHEUMATOID ARTHRITIS TREATED WITH TNF-INHIBITORS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 976.2-976
Author(s):  
M. Novella-Navarro ◽  
B. Hernández-Breijo ◽  
F. Genre ◽  
L. Lera-Gómez ◽  
V. Pulito-Cueto ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Remission Rate ◽  
Binary Logistic Regression ◽  
Negative Influence ◽  
Normal Weight ◽  
The Body ◽  
Response To Treatment ◽  
Bivariate Analysis ◽  
Tnf Inhibitor ◽  
Serum Leptin

Background:In recent years, the relationship between obesity and autoimmune diseases has taken interest, since adipose tissue has been identified as an endocrine organ that secretes cytokines (adipokines), among which leptin stands out as a soluble pro-inflammatory mediator associated with the body mass index (BMI).Objectives:The main objectives of this study are: i) to analyse the influence of BMI on clinical response in Rheumatoid Arthritis (RA) patients who initiate TNF-inhibitor (TNFi) therapy; ii) to analyse the differences in the serum profile of adipokines (leptin and adiponectin) according to BMI and their association with response to treatment.Methods:Observational study of a prospective cohort of 73 RA patients who initiated biological treatment with TNFi from the Complex Therapy Unit (CTU) of our Hospital. Patients were classified according to their BMI in normal-weight (BMI<25) and overweight/obesity (O/O) (IMC≥25). Demographic, clinical and laboratory variables were collected at baseline and at 6 months. Our outcome measures were DAS28-VSG remission (DAS28<2.6) at 6 months after TNFi initiation. Serum leptin and adiponectin levels were measured by Enzyme-Linked Immuno Sorbent Assay (ELISA) at baseline and 6 months. A descriptive sample analysis comparing the characteristics of both patient subgroups was performed using Chi-square, T-test for independent samples and U-Mann Whitney. Likewise, a bivariate analysis was carried out by means of binary logistic regression to assess the probable association of the parameters studied with remission.Results:Of the 73 patients studied, 51% were classified in O/O group. The O/O patients presented higher levels of baseline CRP (16.69±6.16 vs 8.74±3.81, p=0.01). No statistically significant differences were observed in the remaining variables (sex, age at the beginning of the TNFi, disease duration, baseline DAS-28), as well as therapeutic variables (use of previous DMARDs and doses of methotrexate and/or steroids). Patients with overweight/obesity presented higher DAS28-ESR values at 6 months of treatment (3.59±1.14 vs 2.93±1.27, p=0.02) and achieved remission less frequently (18.9% vs 48.6%, p=0.007). Serum leptin levels were significantly higher in O/O patients, both baseline (29.39±21.50 vs 13.49±8.78, p<0.001) and 6 months (33.06±22.03 vs 14.77±9.50, p<0.001) after TNFi initiation. In addition, O/O patients were less likely to reach remission at 6 months than normal-weight patients. [OR= 4.04 IC95% (1.40-11.64); p=0.009]. Lower frequency of remission was associated to greater leptin levels at 6 months [OR=0.94 CI95% (0.90-098); p=0.012]. No differences in serum adiponectin were found between both subgroups of patients.Conclusion:In this RA patient cohort, overweight/obesity is associated with i) a reduced response to TNFi therapy and ii) a lower short-term remission rate. Within the adipokine profile, leptin seems to play a relevant role in the maintenance of pro-inflammatory activity with a negative influence on the response to TNFi therapy in O/O patients.References:[1] Versini M. et al. Autoimmun Rev. 2014; 13, 981-1000[2] Toussirot E et al. Life Sci. 2015;140: 29-36.Disclosure of Interests:Marta Novella-Navarro: None declared, Borja Hernández-Breijo: None declared, Fernanda Genre: None declared, Leticia Lera-Gómez: None declared, Verónica Pulito-Cueto: None declared, Laura Nuño: None declared, Alejandro Villalba: None declared, Alejandro Balsa Grant/research support from: BMS, Roche, Consultant of: AbbVie, Gilead, Lilly, Pfizer, UCB, Sanofi, Sandoz, Speakers bureau: AbbVie, Lilly, Sanofi, Novartis, Pfizer, UCB, Roche, Nordic, Sandoz, Chamaida Plasencia: None declared

scholarly journals POS0407 PROTEOMICS ANALYSIS COMPARING THE MODE OF ACTION OF UPADACITINIB BETWEEN NON-BIOLOGIC-DMARD-IR AND BIOLOGIC-DMARD-IR PsA PATIENTS IDENTIFIES DISTINCT PATHOGENIC PATHWAYS IN THE SELECT-PsA 1 AND SELECT-PsA 2 PHASE 3 STUDIES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 433.1-433
Author(s):  
T. Sornasse ◽  
J. Anderson ◽  
K. Kato ◽  
A. Lertratanakul ◽  
I. McInnes ◽  
...  
Keyword(s):  
Disease Activity ◽  
Clinical Response ◽  
Rheumatic Diseases ◽  
Inadequate Response ◽  
Protein Biomarkers ◽  
Research Support ◽  
Positive Correlation ◽  
Disease Biology ◽  
Biologic Dmard ◽  
Favorable Clinical Response

Background:Treatment of non-biologic-DMARD-IR1 (DMARD-IR) and biologic-DMARD-IR2 (bio-IR) PsA patients with upadacitinib (UPA) at 15 mg QD, an oral JAK1 selective inhibitor, resulted in significant improvement in signs and symptoms compared to placebo.Objectives:Using a pre-defined set of inflammation-related plasma protein biomarkers (pBM), to explore immunological pathway modulation by UPA 15 mg QD in PsA patients with active disease despite treatment with non-biologic or biologic DMARDs in the context of clinical response vs. non-response to treatment.Methods:Patients from the SELECT-PsA 1 (DMARD-IR) and the SELECT-PsA 2 (bio-IR) studies were randomly selected (PBO, n=100; UPA 15 mg QD, n=100 for each study). The levels of 92 inflammation related protein biomarkers (pBM) were analyzed using a multiplexed Proximity Extension Assay platform in plasma samples collected at baseline, week 2, and 12; change from baseline in protein levels was expressed as Log2 Fold Change; a Repeated Measure Mixed Linear Model was used to identify pBM modulated by UPA compared to Baseline, and those differentially modulated between responders (R) and non-responders (NR) according to ACR50, PASDAS Minimal Disease Activity, and PASI75 at week 12. Correlation of disease activity measures with relative levels of pBM were derived using Pearson’s correlation; PASI score was transformed as Log10 (x+1) prior to the analysis. Functional pathway prediction was performed in silico with a commercial distributed software.Results:At baseline, the relative levels of 37 pBM correlated with at least one baseline disease activity measure, with a marked positive correlation of IL6 with musculoskeletal end points (PASDAS and DAS28CRP), and a strong positive correlation of IL20, IL17A, IL17C, and TGFA with baseline PASI.At the single pBM-level, treatment with UPA 15 mg QD resulted in a down modulation of pBM associated with T cells, myeloid cells, and IFN-, IL6-, and TNF-related pathways in both DMARD-IR and bio-IR PsA patients. Overall effects of UPA on single pBMs were broadly similar between DMARD-IR and bio-IR patients. However, analysis of pBMs differentially modulated by UPA in R vs NR indicated that favorable clinical response (achievement of ACR50, PASDAS MDA, and PASI75) in DMARD-IR patients was associated with the down modulation of pBMs predicted to be linked to IFN, IL10, IL17, IL22, and IL27 pathways; while favorable clinical response in bio-IR patients was associated with the down modulation of multiple pBM predicted to be linked to the IL17, IL23, and IL1 pathways.Conclusion:UPA effects in both DMARD-IR and bio-IR PsA patients likely stem from the direct and indirect inhibition of multiple biological pathways belonging to the adaptive and innate immune systems. Responder/Non-Responder analysis suggests a possible shift from a TH1 biased biology in DMARD-IR PsA patients to a more TH17 biased biology in bio-IR PsA patients. This apparent change in the disease biology of PsA patients after inadequate response to prior therapy could be attributed to the actual alteration of the disease biology, treatment outcome-based patient selection, or both. Considering the clinical efficacy of UPA in both DMARD-IR and bio-IR PsA patients, this observation highlights the importance of targeting multiple pathways with drugs such as UPA for the treatment of a broad range of PsA patients.References:[1]McInnes, I. et al. Annals of the Rheumatic Diseases 79, 16-17 (2020).[2]Mease, P.J. et al.Annals of the Rheumatic Diseases, annrheumdis-2020-218870 (2020).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.Disclosure of Interests:Thierry Sornasse Shareholder of: AbbVie, Employee of: AbbVie, Jaclyn Anderson Shareholder of: AbbVie, Employee of: AbbVie, Koji Kato Shareholder of: AbbVie, Employee of: AbbVie, Apinya Lertratanakul Shareholder of: AbbVie, Employee of: AbbVie, Iain McInnes Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, Sanofi Regeneron, UCB Pharma, Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Novartis, Pfizer, Sanofi Regeneron, UCB Pharma, Christopher T. Ritchlin Consultant of: AbbVie, Amgen, Celgene, Janssen, Lilly, Novartis, Pfizer, Sun, UCB Pharma, Grant/research support from: AbbVie, Amgen, UCB

scholarly journals THU0207 SUSTAINABILITY OF RESPONSE TO UPADACITINIB AS MONOTHERAPY OR IN COMBINATION AMONG PATIENTS WITH RHEUMATOID ARTHRITIS AND PRIOR INADEQUATE RESPONSE TO CONVENTIONAL SYNTHETIC DMARDS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 327.1-328
Author(s):  
A. Kavanaugh ◽  
M. H. Buch ◽  
B. Combe ◽  
L. Bessette ◽  
I. H. Song ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Disease Activity ◽  
Inadequate Response ◽  
Research Support ◽  
Two Phase ◽  
First Occurrence ◽  
Activity Measures ◽  
Disease Activity Measures

Background:The primary treatment goal for patients (pts) with rheumatoid arthritis (RA) is a state of sustained clinical remission (REM) or low disease activity (LDA).1,2Objectives:To assess the long-term sustainability of responses to upadacitinib (UPA), a JAK inhibitor, with or without background csDMARD(s) in pts with RA.Methods:Data are from two phase 3 randomized, controlled trials of UPA in RA pts with roughly similar baseline disease characteristics: SELECT-NEXT enrolled pts with an inadequate response (IR) to csDMARD(s) on background stable csDMARD(s) receiving UPA 15 mg or 30 mg once daily or placebo for 12 weeks (wks); SELECT-MONOTHERAPY enrolled methotrexate (MTX)-IR pts receiving UPA 15 mg or 30 mg monotherapy or blinded MTX for 14 wks. After 12/14 wks, pts could enter a blinded long-term extension and receive UPA 15 mg or 30 mg for up to 5 years. This post hoc analysis evaluated clinical REM (CDAI ≤2.8; SDAI ≤3.3), LDA (CDAI≤10; SDAI≤11), and DAS28(CRP) <2.6/≤3.2 at first occurrence before Wk 84; additionally, these measures were evaluated at 3, 6, and 12 months after the first occurrence for the total number of pts randomized to UPA 15 mg. Sustainability of response was evaluated by Kaplan-Meier only for those pts who achieved REM/LDA and was defined as time to the earliest date of losing response at two consecutive visits or discontinuation of study drug. The predictive ability of time to clinical REM/LDA was assessed using Harrell’s concordance (c)-index (for reference, an index ~ 0.5, indicates no ability to predict; an index of 1 or -1 would be a perfect prediction). The last follow up dates were 22 March, 2018 (SELECT-NEXT) and 25 May, 2019 (SELECT-MONOTHERAPY), when all pts had reached the Wk 84 visit.Results:Through Wk 84, the percent of treated pts achieving CDAI REM/LDA was 43%/79% for those receiving UPA 15 mg with background csDMARD(s) (SELECT-NEXT) and 37%/76% for those receiving UPA 15 mg without background csDMARD(s) (SELECT-MONOTHERAPY). 35%/25% of pts randomized to UPA 15 mg with background csDMARD(s) and 27%/23% of pts randomized to UPA 15 mg without background csDMARD(s) achieved sustained CDAI REM through 6/12 months after the first occurrence. 64%/56% of pts randomized to UPA 15 mg with background csDMARD(s) and 61%/56% of pts randomized to UPA 15 mg without background csDMARD(s) achieved sustained CDAI LDA through 6/12 months after the first occurrence (Figure 1). Time to initial clinical REM/LDA did not appear to be associated with sustained disease control. The c-indices (95%CI) for CDAI REM in the UPA 15 mg with background csDMARD(s) and UPA 15 mg without background csDMARD(s) groups were 0.541 (0.47, 0.62) and 0.568 (0.49, 0.65) and that of LDA were 0.521 (0.46, 0.58) and 0.498 (0.43, 0.56), respectively. Through last follow-up visit, 55% of pts receiving UPA 15 mg with background csDMARD(s) and 62% of pts receiving UPA 15 mg without background csDMARD(s) remained in CDAI REM while 72% and 70% of pts remained in CDAI LDA, respectively (Figure 2). Similar results were observed across other disease activity measures (SDAI REM/LDA and DAS28(CRP) <2.6/≤3.2).Conclusion:More than a quarter and more than a half of pts with RA and prior IR to csDMARD(s) receiving UPA with or without background csDMARD therapy achieved sustained clinical REM and LDA, respectively, across disease activity measures. Sustainability of responses appeared comparable among pts receiving UPA with or without background csDMARDs through up to 84 wks.References:[1]EULAR: Smolen JS, et al. Ann Rheum Dis 2017;76:960–977.[2]ACR: Singh et al. Arthritis & Rheumatology Vol. 68, No. 1, January 2016, pp 1–26.Disclosure of Interests: :Arthur Kavanaugh Grant/research support from: Abbott, Amgen, AstraZeneca, BMS, Celgene Corporation, Centocor-Janssen, Pfizer, Roche, UCB – grant/research support, Maya H Buch Grant/research support from: Pfizer, Roche, and UCB, Consultant of: Pfizer; AbbVie; Eli Lilly; Gilead Sciences, Inc.; Merck-Serono; Sandoz; and Sanofi, Bernard Combe Grant/research support from: Novartis, Pfizer, Roche-Chugai, Consultant of: AbbVie; Gilead Sciences, Inc.; Janssen; Eli Lilly and Company; Pfizer; Roche-Chugai; Sanofi, Speakers bureau: Bristol-Myers Squibb; Gilead Sciences, Inc.; Eli Lilly and Company; Merck Sharp & Dohme; Pfizer; Roche-Chugai; UCB, Louis Bessette Grant/research support from: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi, UCB Pharma, Consultant of: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Roche, Sanofi, UCB Pharma, Speakers bureau: AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Sanofi, In-Ho Song Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Yanna Song Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Jessica Suboticki Shareholder of: AbbVie Inc., Employee of: AbbVie Inc., Peter Nash Grant/research support from: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Gilead, Janssen, MSD, Novartis, Pfizer Inc, Roche, Sanofi, UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, MSD, Novartis, Pfizer Inc, Roche, Sanofi, UCB, Speakers bureau: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, MSD, Novartis, Pfizer Inc, Roche, Sanofi, UCB

scholarly journals AB0138 A MOLECULAR SIGNATURE RESPONSE CLASSIFIER STRATIFIES SEROPOSITIVE RHEUMATOID ARTHRITIS PATIENTS BASED ON THEIR LIKELIHOOD OF INADEQUATE RESPONSE TO TNF INHIBITOR THERAPIES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1096.3-1097
Author(s):  
S. Cohen ◽  
V. Strand ◽  
E. Connolly-Strong ◽  
J. Withers ◽  
L. Zhang ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Targeted Therapy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Molecular Signature ◽  
Inadequate Response ◽  
Tnf Inhibitor ◽  
Odds Ratios ◽  
Selection For ◽  
Necrosis Factor

Background:There is an urgent need for precision medicine in targeted therapy selection for the treatment of rheumatoid arthritis (RA). TNF inhibitor (TNFi) therapies are the most prescribed targeted therapy for RA patients, yet the majority of patients fail to achieve a clinically meaningful response using this medication class. A blood-based molecular signature test evaluates RNA and clinical metrics to stratify RA patients based on their likelihood of having an inadequate response to TNFi therapies.1 Patients unlikely to respond to TNFi therapies can be directed to a different treatment option such as a JAK inhibitor, thus reducing the time needed to identify an effective therapy, improving confidence in and adherence to treatment, and increasing the patients’ chance of reaching treat-to-target goals.Objectives:High-titers of anti-cyclic citrillunated protein (anti-CCP) have been independently associated with reduced response to TNFi therapy;2 thus, we evaluated the ability of a blood-based molecular signature response classifier (MSRC) test to stratify RA patients by their likelihood of inadequate response to TNFi therapies – regardless of their positive or negative anti-CCP status.Methods:A subset of patients enrolled in the Network-04 prospective observational trial evaluating the ability of a molecular signature response classifier to stratify patients were subdivided into two groups based upon whether they were positive (N = 72) or negative (N = 74) for anti-CCP. The odds of inadequate response to TNFi therapies were calculated based on whether or not a patient had a molecular signature of non-response to TNFi therapy at baseline before the start of treatment. Odds ratios and confidence intervals were calculated3,4 to represent the strength of association between detecting the molecular signature of non-response and the patient’s failure to achieve ACR50 at 6 months.Results:The odds that a patient with a molecular signature of non-response failed to meet ACR50 criteria at 6 months was approximately three times greater than among those patients who lacked the signal (Table 1). No significant difference in odds ratios was observed between patients who were positive or negative for anti-CCP.Table 1.The odds of patients with a molecular signature of non-response failing to achieve an ACR50 response 6 months after TNF inhibitor therapy initiationOdds ratio (95% confidence interval)Anti-CCP positive3.5 (1.3-9.7)Anti-CCP negative3.1 (1.2-8.3)Conclusion:The MSRC test evaluates RA disease biology and accurately stratifies patients based on their likelihood of having an inadequate response to TNFi therapies, regardless of being negative or positive for anti-CCP autoantibodies. Rheumatologists can use the results of the MSRC test to inform targeted therapy selection for RA patients, instead of their anti-CCP serostatus, eliminating the variability inherent to the anti-CCP measurement and its inability to consistently predict TNFi therapy incompatibility. With the MSRC test, providers can rely on a more predictable and accurate assessment of TNFi therapy success or failure when coordinating patient management.References:[1]Mellors, T. et al. Clinical Validation of a Blood-Based Predictive Test for Stratification of Response to Tumor Necrosis Factor Inhibitor Therapies in Rheumatoid Arthritis Patients. Network and Systems Medicine3, 91-104, doi:10.1089/nsm.2020.0007 (2020).[2]Braun-Moscovici, Y. et al. Anti-cyclic citrullinated protein antibodies as a predictor of response to anti-tumor necrosis factor-alpha therapy in patients with rheumatoid arthritis. J Rheumatol33, 497-500 (2006).[3]Szumilas, M. Explaining odds ratios. J Can Acad Child Adolesc Psychiatry19, 227-229 (2010).[4]Sperandei, S. Understanding logistic regression analysis. Biochem Med (Zagreb) 24, 12-18, doi:10.11613/BM.2014.003 (2014).Disclosure of Interests:Stanley Cohen: None declared, Vibeke Strand Consultant of: Abbvie, Amgen, Arena, BMS, Boehringer Ingelheim, Celltrion, Galapagos, Genentech/Roche, Gilead, GSK, Ichnos, Inmedix, Janssen,Kiniksa, Lilly,Merck, Novartis, Pfizer, Regeneron, Samsung, Sandoz, Sanofi, Setpoint, UCB, Erin Connolly-Strong Shareholder of: Scipher Medicine Corporation, Employee of: Scipher Medicine Corporation, Johanna Withers Shareholder of: Scipher Medicine Corporation, Employee of: Scipher Medicine Corporation, Lixia Zhang Shareholder of: Scipher Medicine Corporation, Employee of: Scipher Medicine Corporation, Ted Mellors Shareholder of: Scipher Medicine Corporation, Employee of: Scipher Medicine Corporation, Viatcheslav Akmaev Shareholder of: Scipher Medicine Corporation, Employee of: Scipher Medicine Corporation

scholarly journals FRI0128 FILGOTINIB PROVIDED RAPID AND SUSTAINED IMPROVEMENTS IN FUNCTIONAL STATUS, PAIN, HEALTH-RELATED QUALITY OF LIFE, AND FATIGUE IN PATIENTS WITH RHEUMATOID ARTHRITIS AND INADEQUATE RESPONSE TO METHOTREXATE: RESULTS FROM THE FINCH 1 STUDY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 645.2-646
Author(s):  
A. Kivitz ◽  
Y. Tanaka ◽  
S. Lee ◽  
L. Ye ◽  
H. Hu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Pain Scale ◽  
Inadequate Response ◽  
Health Related Quality ◽  
Research Support ◽  
Sf 36 ◽  
Related Quality ◽  
Health Related ◽  
Time Point

Background:In the FINCH 1 study, filgotinib (FIL)—an oral, potent, selective Janus kinase 1 inhibitor—in combination with methotrexate (MTX) provided significant improvements in the signs and symptoms of rheumatoid arthritis (RA) in patients (pts) with inadequate response to MTX.1While EULAR guidelines recommend a treat-to-target approach focusing on reducing inflammation to prevent joint damage, physical disability, and mortality, pts consider control of pain and fatigue, along with maintenance of physical function and health-related quality of life (HRQoL), to be important aspects for their care.2,3Objectives:To evaluate the rate and magnitude of change in patient-reported outcomes (PROs) from FINCH 1.Methods:In the FINCH 1 study (NCT02889796), pts with active RA received oral FIL 200 mg + MTX, FIL 100 mg + MTX, PBO + MTX, or subcutaneous adalimumab (ADA) 40 mg + MTX for up to 52 weeks (W); pts receiving PBO at W24 were rerandomised 1:1 to FIL 100 or 200 mg. PROs included the HAQ-DI and VAS pain scale, SF-36, and FACIT-Fatigue questionnaire. The change from baseline (CFB) at each time point was assessed up to W52 for each treatment group. The mixed-effects model for repeated measures was used to compare each FIL group with PBO for the CFB at each time point through W24. The logistic regression model was used to compare each FIL group with PBO for the proportion of pts achieving the minimum clinically important difference (MCID) of ≥0.22 reduction in CFB in HAQ-DI at each time point through W24.Results:Of 1755 pts randomised and treated (475 FIL 200 mg + MTX; 480 FIL 100 mg + MTX; 325 ADA + MTX; and 475 PBO + MTX), 1417 (80.7%) received study drug through W52. As early as W2 through W24, pts receiving either dose of FIL experienced nominally significantly greater (p <0.001) CFB in HAQ-DI and VAS pain scale than those receiving PBO; CFB improvements were maintained through W52 (Fig 1A, B). At W2, compared with PBO (40.2%), a nominally significantly greater proportion of pts achieved the HAQ-DI MCID in both the FIL 200 (52.5%; p <0.001) and 100 mg (46.7%; p = 0.043) groups. This benefit vs PBO was maintained up to W24 and the proportion of pts who achieved a HAQ-DI reduction of ≥0.22 remained ≥75.8% in the FIL 200 mg group and ≥71.5% in the FIL 100 mg group from W12 through W52. FIL provided nominally significantly greater improvement in HRQoL vs PBO at W4 and W12 for both the CFB of the SF-36 Physical Component Summary (PCS) (p <0.001) and Mental Component Summary (MCS) (p ≤0.006); nominal significance was also seen at W24 for CFB of SF-36 PCS (Fig 2A, B). By W4, pts receiving either dose of FIL reported a nominally significantly greater mean CFB in FACIT-Fatigue scores vs PBO (p <0.001); significance was maintained through W24 and improvement in reported fatigue continued through W52 in the FIL groups (Fig 2C). In general, CFB for HAQ-DI, VAS pain scale, and FACIT-Fatigue observed for the FIL groups was higher or comparable to ADA at various time points (Fig 1, 2).Conclusion:Both doses of FIL provided rapid and sustained improvements in functional status, pain, HRQoL, and fatigue compared with PBO for pts with RA and inadequate response to MTX throughout the 52-week period.References:[1]Combe BG, et al.Ann Rheum Dis.2019;78 (Suppl 2):A77.[2]Fautrel B, et al.Rheumatol Int.2018;38:935–47.[3]Smolen JS, et al.Ann Rheum Dis.2017;76:960–77.Disclosure of Interests:Alan Kivitz Shareholder of: AbbVie, Amgen, Gilead, GSK, Pfizer Inc, Sanofi, Consultant of: AbbVie, Boehringer Ingelheim,,Flexion, Genzyme, Gilead, Janssen, Novartis, Pfizer Inc, Regeneron, Sanofi, SUN Pharma Advanced Research, UCB, Paid instructor for: Celgene, Genzyme, Horizon, Merck, Novartis, Pfizer, Regeneron, Sanofi, Speakers bureau: AbbVie, Celgene, Flexion, Genzyme, Horizon, Merck, Novartis, Pfizer Inc, Regeneron, Sanofi, Yoshiya Tanaka Grant/research support from: Asahi-kasei, Astellas, Mitsubishi-Tanabe, Chugai, Takeda, Sanofi, Bristol-Myers, UCB, Daiichi-Sankyo, Eisai, Pfizer, and Ono, Consultant of: Abbvie, Astellas, Bristol-Myers Squibb, Eli Lilly, Pfizer, Speakers bureau: Daiichi-Sankyo, Astellas, Chugai, Eli Lilly, Pfizer, AbbVie, YL Biologics, Bristol-Myers, Takeda, Mitsubishi-Tanabe, Novartis, Eisai, Janssen, Sanofi, UCB, and Teijin, Susan Lee Shareholder of: Gilead Sciences Inc., Employee of: Gilead Sciences Inc., Lei Ye Shareholder of: Gilead Sciences Inc., Employee of: Gilead Sciences Inc., Hao Hu Shareholder of: Gilead Sciences Inc., Employee of: Gilead Sciences Inc., Robin Besuyen Shareholder of: Galapagos, Employee of: Galapagos, Bernard Combe Grant/research support from: Novartis, Pfizer, Roche-Chugai, Consultant of: AbbVie; Gilead Sciences, Inc.; Janssen; Eli Lilly and Company; Pfizer; Roche-Chugai; Sanofi, Speakers bureau: Bristol-Myers Squibb; Gilead Sciences, Inc.; Eli Lilly and Company; Merck Sharp & Dohme; Pfizer; Roche-Chugai; UCB

scholarly journals AB0237 INFECTIONS IN PATIENTS WITH RHEUMATOID ARTHRITIS TREATED WITH RITUXIMAB AND ANTI-TNF INHIBITOR

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1144.2-1144
Author(s):  
N. Zehraoui ◽  
R. Benaziez.Boutaleb ◽  
H. Hafirassou ◽  
F. Mechid ◽  
N. Bahaz ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Best Practice ◽  
Biological Therapy ◽  
Patient Characteristics ◽  
Inadequate Response ◽  
Tnf Inhibitor ◽  
Clinical Rheumatology ◽  
Number Of Patients ◽  
Serious Infections ◽  
Comparative Risk

Background:Biological therapies have significantly improved the management of rheumatoid arthritis (RA). These molecules are very effective, but are known for their specific risks, especially infectious. It depends on several factors including the type of molecule used.Objectives:The objective of our study is to compare the rate of infection in RA patients treated with rituximab and anti-TNFα.Methods:Prospective, observational, monocentric study. Were included RA patients (ACR / EULAR 2010 criteria) treated with rituximab and anti-TNFα (adalimumab, infliximab and Etanercept) after inadequate response to DMARDs.Demographic characteristics, comorbidities, association with methotrexate and corticosteroids were collected and compared for each group.The number, type and severity of the infections in both cases were noted.SPSS (Statistical Package for Social Science) was used for data analysis.Results:40 RA patients treated with rituximab and 31 patients who received anti-TNFα were included.Patient characteristics and Comparison of rate of infection in RA patients between the two groups are summarized in Table 1Table 1.ParametersRituximabAnti-TNFαpNumber of patients4031Average age (years)56,2846,060,01Sexratio0,140,110,7Average duration of evolution (years)15,8313,740,3Patients under corticosteroid (%)97,587,10,08Average corticosteroid dose6,415,480,3patients under methotrexate (%)37,545,20,5Diabetes (%)2016,10,7Patients with infection (%)32,551,60,1Number of infections18240,4Number of serious infections500,04Conclusion:The rate of infections in patients with RA treated with rituximab or anti-TNF was similar. However, the infections observed were more serious in patients with RA treated with rituximabReferences:[1]Fabiola Atzeni MD PhD and al. Infections and Biological Therapy in Patients with Rheumatic Diseases. IMAJ . VOL 18. march-APRIL 2016.[2]Huifeng Yun and al. Comparative Risk of Hospitalized Infection Associated with Biologic Agents in Rheumatoid Arthritis Patients Enrolled in Medicare. ARTHRITIS & RHEUMATOLOGY. Vol. 68, No. 1, January 2016, pp 56–66.[3]Manjari Lahiri and al. Risk of infection with biologic antirheumatic therapies in patients with rheumatoid arthritis. Best Practice & Research Clinical Rheumatology (2015) 1-16.Disclosure of Interests:None declared

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