Background: Rituximab (RTX) is effective in improving skin affection in patients with diffuse cutaneous systemic sclerosis (DcSSc). However, there are few data on early use of this drug. Objectives: To evaluate RTX effectiveness for skin disease in patients with DcSSc of less than 3 years of evolution. Methods: Multicenter, observational and retrospective study. Patients with DcSSc starting RTX within 3 years since first non-Raynaud symptom were recruited. Demographic variables, time of disease duration at the beginning of RTX, immune pattern and time on RTX treatment were collected. Effectiveness was defined as modified Rodnan skin score (mRSS) improvement. Evaluations were done by the same experienced rheumatologist. Patients subjective perception of skin hardening and/or tightness was evaluated. mRSS changes from baseline to 6 and 12 months after RTX beginning and, later on, to the last available observation were analysed using Wilcoxon test. Statistical analysis was performed with SPSS 20.0. Results: 11 patients (8 women) were recruited from 2 university hospitals. Median age was 48 years (IQR 22). Median time since diagnosis to RTX beginning was 12 months (IQR 8). 5, 3 and 2 patients presented ATA +, RNPIII + and Ro-52 +, respectively. Median duration of RTX treatment was 12 months (IQR 68). Median baseline mRSS was 15.5 (IQR 18). Median mRSS after 6 and 12 months of RTX treatment and at last available mRSS evaluation was 15 (IQR 13), 14.5 (IQR 13) and 11 (IQR 16), respectively. mRSS showed statistically significant improvement at 6 (29%, IQR 37) and 12 months of RTX treatment (35%, IQR 34) and, thereafter, at last available observation (39%, IQR 51), compared to basal mRSS. Most patients reported subjective improvement at 6 (9 of 10 patients) and 12 months (6 of 7), and at last available evaluation (6 of 8); all other patients reported stability. Conclusion: In our experience, patients with DcSSc seem to benefit of early RTX treatment. Improvement may be seen as early as 6 months and seems to reach a plateau at 12 months. Disclosure of Interests: I Vázquez-Gómez: None declared, J. Narváez: None declared, J Lluch Pons: None declared, Marta Aguilar-Zamora: None declared, L Montolio-Chiva: None declared, Ana V Orenes Vera: None declared, Eduardo Flores: None declared, Elia Valls-Pascual Grant/research support from: Roche, Novartis, and AbbVie, Speakers bureau: AbbVie, Lilly, Pfizer, MSD, Novartis, Janssen, Bristol Myers Squibb, UCB Pharma, Desamparados Ybañez: None declared, À Martínez-Ferrer: None declared, A Sendra-García: None declared, Inmaculada Torner Hernández: None declared, V Núñez-Monje: None declared, Juanjo J Alegre-Sancho Consultant of: UCB, Roche, Sanofi, Boehringer, Celltrion, Paid instructor for: GSK, Speakers bureau: MSD, GSK, Lilly, Sanofi, Roche, UCB, Actelion, Pfizer, Abbvie, Novartis
To determine serum trough levels and anti-drug antibodies (Ab) in patients with rheumatoid arthritis (RA) or polyarticular psoriatic arthritis (PsA) in clinical remission (CR) or low disease activity (LDA) on treatment with adalimumab (ADA), etanercept (ETN) and infliximab (IFX) and correlate serum trough levels and Ab with loss of CR o LDA after 1-year of follow-up.
Methods
Prospective, multicenter study of patients diagnosed with RA or PsA attended by 3 hospital outpatient clinics in Catalonia,Spain treated with ADA, ETN or IFX for ≥3 months in CR or with LDA measured by DAS28-ESR at ≥2 consecutive visits. We determined Ab and serum trough levels (commercial ELISA Kit Promonitor®, Progenika SA) at 0,4,8 and 12 months. Variables collected: demographic data; disease activity (different articular indexes), diagnosis; disease duration; biologic drug; reduced dose, and concomitant DMARDs therapy. Study entry data (Visit 0) are presented.
Results
165 patients (RA 92 [55.8%], PsA 73 [44.2%]),65.5% female, mean age 57±12 years were included. 121 (73.3%) patients were in CR, 44 (26.7%) with LDA, 63 on ADA, 83 ETN, and 19 IFX. Mean treatment duration was 65.2±40.7 months. 75 patients (45%) were receiving low doses of biologics, and 98 (59.4%) concomitant DMARD (84% methotrexate). In 3 patients (1.8%, 2 in CR and receiving DMARD) significant Ab levels were found, with undetectable serum trough levels (2RA and 1PsA): 2 anti-IFX (10%) and 1 anti-ADA (1.6%). Another patient receiving ADA had low Ab titers and detectable serum drug levels. Mean serum levels of all TNF antagonists were non-significantly different between RA and PsA, monotherapy or combined treatment. Patients with reduced dosage had significantly-lower levels of ADA and ETN than those receiving standard doses. No differences between patients in CR or LDA were observed. According to the ELISA cut-off for appropriate drug serum levels (ADA: >1.274μg/ml, and ETN :>1.242μg/ml) (Chen DY et al. Ann Rheum Dis 2014;0:1-9), 19% and 30.1% of patients treated with ADA and ETA, respectively, had suboptimal levels (30% with ADA and 46.2% with ETA on dose reduction). There were no differences between DAS28-CPR, DAS28-ESR, SDAI, CDAI, ESR or CRP values in patients with suboptimal or appropriate serum levels.
Conclusions
The frequency of anti-drug antibodies is very low in patients with RA and PsA treated with TNF antagonists in CR or with LDA. A significant percentage of patients had suboptimal drug serum trough levels. Prospective follow-up will determine whether these serum levels may predict loss of CR or LDA.
Disclosure of Interest
R. Sanmarti Grant/research support: Unrestricted grant from Pfizer, J. Inciarte Grant/research support: Grant from Hospital Clinic of Barcelona (Premi Emili Letang 2013), P. Estrada Alarcόn: None declared, M. Garcia Manrique: None declared, A. Gonzalez Navarro: None declared, J. Narvaez Grant/research support: Unrestricted grant from Pfizer, J. Rodríguez-Moreno Grant/research support: Unrestricted grant from Pfizer, A. Gomez-Centeno Grant/research support: Unrestricted grant from Pfizer, J. Yagüe Grant/research support: Unrestricted grant from Pfizer
OBJECTIVE: Estimate the frequency of the association of SLE with other autoimmune diseases in a large Spanish cohort of patients with systemic lupus erythematosus (SLE) and investigate the main risk factors for polyatoimmunity.
Methods
Design: RELESSER is a nationwide multicentre, hospital-based registry of SLE patients. This is a cross-sectional study. Patients: Unselected consecutive adult patients with SLE, classified according to the American College of Rheumatology (ACR) 1997 criteria. All patients had been attended upon and followed at Spanish rheumatology departments. The first patient was enrolled in October 2011 and the last in August 2012. Main outcome: Polyautoimmunity was defined as patients who fulfilled criteria for SLE and other autoimmune disease: (1) autoimmune thyroiditis (alteration of thyroid function with the presence of anti-thyroid autoantibodies), (2) other connective tissue disease (rheumatoid arthritis, systemic sclerosis or inflammatory myopathy) and (3) mixed connective tissue disease. Multiple autoimmune syndrome (MAS) was defined as patients who meet SLE criteria and at least two other autoimmune diseases. Other variables: Demographic and clinical variables, Sjogren's syndrome, antiphospholipid syndrome and family history of autoimmune systemic disease were collected. Statistical analysis: Descriptive, Chi-square test and ANOVA or Kruskal-Wallis for comparison between groups of patients. Multiple logistic regression analysis was performed to investigate the possible risk factors for polyautoimmunity in patients with SLE.
Results
From all patients included in the registry, 3679 (91.4%) patients met 4 or more SLE criteria. Of these, 501 (13.6%) patients had Polyautoimmunity. The characteristics of this group are showed in table 1. The most frequent polyautoimmunity types associated with SLE were (in descending order over the total cohort of patients with SLE): autoimmune thyroiditis (7.5%), other connective tissue disorders (4.4%) and mixed connective tissue disease (2.7%). The percentage of patients a family history of SLE was 12.4%. Multiple autoimmune syndrome was observed in 10.2% of patients with Polyautoimmunity. The multivariate analysis identified age (odds ratio [95% confidence interval], 1.01 [1.00–1.02]), sex (3.00 [1.48–6.04]), Raynaud's phenomenon (1.79 [1.34–2.39]), pulmonary fibrosis (2.88 [1.32–6.30]), Ro-La autoantibodies (1.68 [1.20–2.36]), antiRNP (1.79 [1.32–2.42]) and treatment with methotrexate (1.54 [1.08–2.18]) or with antimalarials (0.57 [0.41–0.78]) as factors associated with polyautoimmunity.
Conclusions
SLE patients frequently associate other autoimmune diseases, detecting poliautoimmunity in 14%, MAS in 2%, family history of SLE in 12.4% and others such as Sjogren's syndrome and secondary SAF in 12.8% and 12.7% respectively. More studies are needed to better understand the increase of polyautoimmunity that seems to be observed in SLE.
The mortality in Systemic Lupus Erythematosus (SLE) varies largely across different countries most probably due to social, healthcare and ethnic differences. The contemporary cohorts continue to show higher mortality rates in SLE patients as compared with the general population 1,2. We need to identify demographic, clinical and serological predictors of mortality in SLE in our country, to improve the prognosis of SLE patients.
Objectives
To analyze the causes and identify predictive factors of mortality of SLE, and to assess the time evolution and chronological changes in Spain.
Methods
We performed a cross-sectional and retrospective study analyzing data from the RELESSER cohort (Spanish Registry of SLE of the Spanish Society of Rheumatology). Sociodemographic, clinical and serological variables, comorbidities and treatments, as well as indicators of disease activity, damage and severity were recorded. We excluded patients with lost information about the death variable and analyzed the differential features of deceased patients in comparisons with survivors through different time stages according to the date of diagnosis: until the 1980's; the 1990's and the first decade of the 21st century. Variables associated with mortality in univariate analysis were entered into different multivariate models to determine which ones were independently associated with the outcome of the disease in each decade.
Results
A total of 3665 patients were included, mostly caucasian female with similar general features regardless of the different time stages analyzed. The 18.4% until the 1980´s, the 5.97% in the 1990´s and up to 2.84% of the individuals in the first decade of the 21st century, had died. The main age of death was similar in the different groups, around 55-58 years old (Table 1). The vascular events were the leading cause of death until the 1980´s, while in the last two decades, were infections. The older age at diagnosis was predictor of mortality in our cohort. Neither gender nor delay in diagnosis was independently associated with mortality, with the exception of the female sex, which behaved as a protective factor until the 1980's. The mortality predictors in our cohort were the presence of hypocomplementemia and organ damage until the 1980´s; thrombocytopenia, antiphospholipid syndrome and valve disease in the 1990´s; serositis, organ damage and depression in the first decade of the 21st century. Conversely, skin involvement was related to greater survival over the last two decades and comorbidities were associated with mortality in all periods of the study. The use of high doses of corticosteroids (>30mg/day) was predictor of mortality in each time stage, as well as the use of cyclophosphamide and rituximab from the year 2000. Antimalarial treatment was linked to improved survival in all the decades analyzed.
Conclusion
In the RELESSER cohort, the main cause of death in the last decades were infections. However, until the 1980´s, vascular events were predominant. Older age at diagnosis, the use of corticosteroids and comorbidities were associated with a significant increase in mortality in SLE, while antimalarial treatment was linked to improved survival. Data indicate that organ damage is a risk factor and skin involvement is a protective factor against mortality. Differentially, female sex until the 1980´s was independently associated with improved survival, and depression at the beginning of the 21st century was linked to mortality. Our results must be confirmed in prospective studies that minimize methodological limitations.
References
[1]Rees F, et al. Rheumatology (Oxford) 2016;55:854–60. [2]Jorge AM, et al. Rheumatology (Oxford) 2018;57:337–44
Acknowledgements
Thank you to RELESSER researchers and collaborators, especially to profesor Jaime Calvo-Alén for having helped to develop this study.
Aortitis related to Giant Cell Arteritis (GCA-aortitis) is a frequent and potential severe complication. Tocilizumab (TCZ) was approved in GCA, but the efficacy in GCA- aortitis has not been specifically studied in randomized clinical trials.
Objectives:
To assess the effectiveness and safety of TCZ in monotheraphy compared with combined in a wide series of GCA-aortitis.
Methods:
Multicentre observational study with GCA-aortitis treated with TCZ. GCA was diagnosed by: a) ACR criteria, b) temporal artery biopsy, and/or c) imaging techniques. Aortitis was diagnosed mainly by PET/CT. Main outcomes were EULAR and imaging remission (considered when vascular FDG uptake was less than liver uptake in 18 F-FDG PET/CT). Others were clinical remission, corticosteroid-sparing effect, TCZ optimization and adverse effects.
Results:
We studied 196 patients with GCA-aortitis treated with TCZ (136 in monotheraphy/60 combined with others DMARDs). Figure 1. After 24 months, there were statistical differences in imaging and complete remission (17.2% vs 42.1%) Figure 2. Nevertheless, there were no differences in clinical and EULAR remission.
Conclusion:
In GCA-aortitis, TCZ therapy combined with DMARDs could be more effective than in monotherapy in imaging and complete remission.
REFERENCES:
NIL.
Acknowledgements:
NIL.
Disclosure of Interests:
Adrián Martín-Gutiérrez: None declared, Javier Loricera Roche, Galápagos, Novartis, UCB Pharma, MSD, Celgene, Astra Zeneca, and Grünenthal, Janssen, Abbvie, Roche, Novartis, MSD, UCB Pharma, Celgene, Lilly, Pfizer, Galápagos, Carmen Secada-Gómez: None declared, Javier Narváez: None declared, Olga Maiz: None declared, Iñigo Hernández-Rodríguez AbbVie, Amgen, Janssen, Merck Sharp & Dohme, Novartis, Sanofi, Pfizer, UCB y Galápagos, AbbVie, Amgen, Janssen, Merck Sharp & Dohme, Novartis, Sanofi, Pfizer, UCB y Galápagos, Susana Romero-Yuste Abbvie, Astra-Zeneca, Bristol, Janssen, Lilly, Roche, Sandoz, Sanofi, UCB, Eugenio De Miguel Abbvie, Novartis, Pfizer, Roche, Janssen, Lilly, MSD, BMS, UCB, Grunental and Sanofi, Abbvie, Novartis, Pfizer, Roche, Janssen, Lilly, MSD, BMS, UCB, Grunental and Sanofi, Eva Galíndez-Agirregoikoa: None declared, Iván Ferraz-Amaro Abbvie, Pfizer, Roche, Sanofi, Celgene, and MSD, Abbvie, MSD, Janssen, and Roche, Julio Sanchez-Martin: None declared, Patricia Moya: None declared, Cristina Campos Fernández: None declared, Fernando López-Gutiérrez Janssen, Abbvie, Roche, Novartis, MSD, UCB Pharma, Celgene, Lilly, Pfizer, Galápagos, Santos Castañeda assistant professor of the cátedra EPID-Future, funded by UAM-Roche, Universidad Autónoma de Madrid (UAM), Spain, BMS, Eli-Lilly, Roche, Gedeon-Richter, Grünenthal Pharma and UCB, MSD and Pfizer, Ricardo Blanco AbbVie, Pfizer, Roche, GSK, Lilly, UCB, Bristol-Myers, Novartis, Janssen, UCB and MSD, AbbVie, MSD, and Roche.
The aims of this study were to investigate the prevalence of dose reduction in patients with SLE treated with belimumab (BEL) in Spain, analyze treatment modalities, and determine impact on control of disease activity.
Mucocutaneous lesions are the most frequent symptoms of Behçet’s disease (BD). Recently, new therapies are being used to treat refractory cases, but the effect of these treatments on mucocutaneous manifestations has been scarcely reported. Our objective was to describe the mucocutaneous response to the different therapies used to treat BD in routine clinical practice. We retrospectively reviewed the clinical records of all patients diagnosed with BD seen at our institution between January 2010 and January 2022. Patients with BD without mucocutaneous manifestations were excluded. We included 109 patients diagnosed with BD: 51 males (46.8%) and 58 females (53.2%). The mean age at diagnosis was 31.58 years (standard deviation (SD) 12.110) and the mean time of disease evolution was 14.94 years (SD 11.094). Oral ulcers were the most frequent symptom present in 100% of patients, followed by genital ulcers (GU) in 76.1% of patients. Twenty‐four patients (22%) had severe mucocutaneous symptoms (>12 lesions/year) before treatment. We found that among patients with GU there was a higher prevalence of episodes of posterior uveitis and venous thrombosis ( p = 0.011 and p = 0.045, respectively). In our series, we observed a lower complete cutaneous response to colchicine in patients with GU, pathergy or severe mucocutaneous symptoms ( p < 0.05). Regarding the choice of a TNF‐ α inhibitor, we observed a lower prevalence of complete cutaneous response to adalimumab among patients with GU (53.3% complete response in patients with GU vs. 100% in patients without GU, p = 0.022), whereas no differences were found between clinical characteristics in the response to infliximab.
Immunoglobulin A Vasculitis (IgAV) is an inflammatory disease caused by the accumulation of immune complexes of IgA in the walls of small blood vessels [1]. It has been shown that these immunocomplexes activate the mannan-binding lectin and the alternative complement pathway [2]. Moreover, the presence of complement system components has been observed in skin and kidney biopsies in IgAV patients [3]. In this context, C5a (a protein fragment cleaved from C5 complement factor), together with its receptor, C5aR1, have been proposed as therapeutic targets in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) [4], another small-vessel vasculitis [1]. Nevertheless, the molecular mechanisms by which the complement is involved in IgAV are poorly understood.
Objectives:
The aim of this work was to determine whether C5 and C5AR1 represent novel genetic risk factors for IgAV.
Methods:
346 patients with IgAV, the largest series of Caucasian patients with IgAV ever assessed for genetic studies, and 723 healthy ethnically matched controls, were recruited for this study. Among the IgAV patients, 117 presented nephritis (IgAVN). Eight tag single nucleotide polymorphisms (SNPs) within C5 (rs10760128, rs74971050, rs4310279, rs7868761, rs10818495, rs10156396, rs3815467, and rs16910280) and 3 C5AR1 tag SNPs (rs10853784, rs11673071, and rs11670789) were genotyped using TaqMan Probes. p values < 0.05 after Benjamini-Hochberg correction for an FDR of 5% were considered statistically significant.
Results:
No statistically significant difference was found in C5 and C5AR1 genotype and allele frequencies between patients with IgAV and healthy controls (HC) (Table 1). Likewise, no statistically significant differences were observed in genotype and allele frequencies of C5 and C5AR1 when IgAV patients were stratified according to the severity of the disease, represented by the presence or absence of renal manifestations (Table 1). In addition, no statistically significant differences were shown among IgAV patients stratified according to other clinical aspects, such as the age at disease onset or the presence/absence of articular and gastrointestinal manifestation in C5 and C5AR1 (Data not shown). Furthermore, no differences in the haplotype frequencies of C5 and C5AR1 were observed between IgAV patients and HC (Table 2), and between stratified IgAV patients according to the severity of the disease (Table 2) as well as to other clinical manifestations (Data not shown).
Conclusion:
Our results suggest that C5 and C5AR1 do not seem to be involved in the pathogenesis of IgAV.
REFERENCES:
[1] Arthritis Rheum. 2013 Jan;65(1):1-11. [2] Front Immunol. 2022 Oct 3:13:921864. [3] Autoimmun Rev. 2017 Dec;16(12):1246-1253. [4] Immunobiology. 2023 Sep;228(5):152413.
Acknowledgements:
This research was funded by European Union FEDER funds and "Fondo de Investigaciones Sanitarias" from "Instituto de Salud Carlos III" (ISCIII, Health Ministry, Spain), grant number PI18/00042 and PI21/00042. JCB-L is a recipient of a PFIS programme fellowship from the ISCIII, co-funded by the European Social Fund ("Investing in your future"), grant number FI22/00020.VC-R is a recipient of a grant for research activity intensification provided by the Spanish Rhemathology Foundation. MSM-G is supported by funds of "Fondo de Investigaciones Sanitarias" from ISCIII, grant number PI18/00042.VP-C is supported by funds of IDIVAL, grant number NVAL23/02. RL-M is a recipient of a Miguel Servet type II program fellowship from the ISCIII, co-funded by ESF ("Investing in your future"), grant number CPII21/00004.
Disclosure of Interests:
Joao Carlos Batista-Liz: None declared, Vanesa Calvo-Río Abbvie, Lilly, Grünenthal, AMGEN. MSD, Novartis, Galapagos, Vifor, GSK, and Otsuka, María Sebastián Mora-Gil: None declared, Belén Sevilla-Pérez: None declared, José Luis Callejas: None declared, María Teresa Leonardo: None declared, Ana Peñalba: None declared, María Jesús Cabero: None declared, Javier Narváez: None declared, Luis Martín-Penagos: None declared, Lara Belmar-Vega: None declared, Cristina Gomez-Fernandez: None declared, Luis Caminal-Montero: None declared, Paz Collado: None declared, Patricia Quiroga Colina: None declared, Esther Vicente-Rabaneda: None declared, Esteban Rubio-Romero: None declared, Manuel León Luque: None declared, Juan María Blanco-Madrigal: None declared, Eva Galíndez-Agirregoikoa: None declared, Santos Castañeda: None declared, Ricardo Blanco Abbvie, Pfizer, Roche, Bristol-Myers, Lilly, Janssen, and MSD, Abbvie, Pfizer, Roche, Bristol-Myers, Lilly, Janssen, and MSD, Abbvie, MSD, and Roche, Verónica Pulito-Cueto: None declared, Raquel López-Mejías: None declared.
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