Background:The presence or absence of marrow bone edema (MBE) in the sacroiliac joints (SIJ) is very important in the diagnosis of axial Spondyloarthritis (axSpA). The quantification of this lesion and its extension may be important to analyze responsiveness of the treatment. Several scoring systems have been proposed for MRI images of SIJ, some of them being observer dependent (Berlin, SPARCC). Others, works in a semi-automatically way, such as the s-SCAISS[1], which makes it possible to quantify the size of the lesion, based on the indication of the expert. Recently, methods like the KITs4R[2], based on a deep patch-based classification network. allow a fully automated detection and quantification of the MBE lesions.Objectives:To analyze responsiveness of several scores (observer independent, semiautomatic and full automatic) for quantify MBE in SIJ of axSpA patients.Methods:Two rheumatologists independently quantified SIJ images from axSpA patients by visual inspection methods (Berlin and SPARCC indexes) and a semiautomatic system (s-SCAISS) on a single semi-coronal MRI slide (STIR). Full semi-coronal MRI images (15 to 18 slices) were used for an automatic detection algorithm (KITs4R), where total MBE was calculated as sum of areas of MBE in each slice. Patients were assessed before TNF-α therapy (PRE) and 3 months later (POST). Spearman correlations was used to analyze relationship between variables, Wilcoxon signed-rank test for significant differences and Cohen’s d for calculating the effect size of improvement. Figure 1 shows processing of the MRI images: A) Area of MBE selected by the SCAISS, when the rheumatologist “click” on each MBE; B) Lesions detected automatically by KITs4R; C) Automated deep segmentation of bones and subchondral regions (with split into quadrants with central axes of joints also shown. D) Superposed A, B and C images.Results:12 axSpA patients were recruited from the CASTRO cohort (42% female, age 46±11 years, disease duration 16±13 years, BMI 28±5). Results PRE and POST are shown in Table 1: mean values (sd), statistical significance (NS, not significant; *, p<0.05; **, p<0.01), and effect size. Activity indexes and CRP were lower. ASDAS and CRP shown significant differences and a large effect size. All MRI scores showed good responsiveness (ES medium-large, p<0.01), specially KITs4R. Agreement between all MRI scores were high (r>0.8;p<0.01). Between semiautomatic and automatic methods, this agreement was also excellent (r=0.92;p<0.001). Correlation in improvements (reductions in scores) were also significant between all MRI scores (r>0.7;p<0.05).PREPOSTSignESBASDAI6.12 (2.45)4.96 (2.74)N.S.0.44-SmallASDAS3.61 (1.04)2.58 (1.25)*0.89-LargeCRP11.26 (8.93)4.81 (4.08)**0.84-LargeBERLIN2.58 (1.98)1.17 (1.85)**0.74-MediumSPARCC3.92 (3.42)1.58 (2.43)**0.69-MediumSCAISS295 (332)95 (163)**0.68-MediumKITs4R1671 (1596)258 (421)**1.04-LargeNS, not significant; *, p<0.05; **, p<0.01Conclusion:All MRI scores have good level of agreement between them and good responsiveness. Berlin and SPARCC are observer dependent, and do not quantify the extension of the MBE area. s-SCAIS helps to this quantification. KITs4R is not observer dependent but clinimetric validation, analizing agreement level with human expert, is necessary. New advanced tools are improving quantitative and objective measurement of BME which is important to analyze responsiveness.References:[1]Development and validation of SCAISS, a tool for semi-automated quantification of sacroilitis by magnetic resonance in spondyloarthritis. Rheumatol Int. 2018 Oct;38(10):1919-1926.[2]The semi-automated algorithm for the detection of bone marrow oedema lesions in patients with axial spondyloarthritis. Rheumatol Int. 2020 Apr;40(4):625-633.Disclosure of Interests:None declared.
Background:The presence of inflammatory signals in sacroiliac joints (SIJ), using MRI, is used for early diagnosis of axial spondyloarthritis (axSpA)[1]. Some studies also demonstrate that this inflammation can be suppressed quite dramatically by TNF-α blockers. Different scoring methods to quantify inflammatory changes in SIJ using MRI have been defined and validated: SPARCC, Leeds, Berlin, and ASSpiMRI-a. However, its use is complex and subjective. Recently Zarco et al[2] developed a method to measure bone marrow edema (BME) in MRI images from SIJ. This method, in a semiautomatic procedure, allows to measure the area affected by inflammation and the signal intensity to produce an index: the SCAISS. A simplified version, the s-SCAISS, using only a semi-coronal slide, has been proposed with good validity and reliability results.Objectives:To assess responsiveness of inflammation in SIJ of axSpA patients, treated with TNF-α inhibitors, using a novel score method: the s-SCAISS.Methods:Two rheumatologists independently quantified SIJ images from axSpA patients by three methods (s-SCAISS, SPARCC and Berlin) on a single semi-coronal MRI slide (STIR). Patients were assessed before TNF-α therapy (PRE) and 3 months later (POST). Spearman correlations was used to analyze relationship between variables, Wilcoxon signed-rank test for significant differences and Cohen’s d for calculating the effect size of improvement. Figure shows MRI images of a patient before and after treatment.Results:9 axSpA patients were recruited from the COSPAR cohort (44% female, age 47±13 years, disease duration 18±14 years, BMI 29±4). Results PRE and POST are shown in Table: mean values (sd), statistical significance (NS, not significant; *, p<0.05; **, p<0.01), and Effect Size. In the first rows, different scoring system for MRI inflammation appears: Area analyzed by s-SCAISS, s-SCAISS, Berlin and SPARCC (using only a semi-coronal slide). Activity and functional indexes were lower with significant differences and a large effect size. Correlations of s-SCAISS with Berlin (rho=0.78;p<0.05) and SPARCC (rho=0.96;p<0.001) were good; with clinical disease activity outcomes were poor, except with BASDAS (rho=0.70;p<0.05). The best correlation according improvements appeared comparing reduction of ASDAS with reduction of s-SCAISS (rho=0.57) but this difference was not significant. Although improvements in BASMI was not significant, a good correlation was found between improvement in s-SCAISS and BASMI (rho=-0.72;p<0.05).PREPOSTSignE.S.Area71.33 (66.71)20.89 (39.02)**0.86-Larges-SCAISS118.67 (114.6)27.78 (51.09)**0.98-LargeBERLIN2.33 (1.66)0.67 (1.12)**1.14-LargeSPARCC3.11 (2.26)0.78 (1.39)**1.18-LargeCRP13.1 (9.4)4.1 (3.2)**0.90-LargeBASDAI6.5 (1.7)4.4 (2.7)*0.84-LargeBASFI6.3 (2.6)4.1 (3.4)*0.69-MediumASDAS3.6 (1.0)2.3 (1.2)**1.15-LargeBASDAS3.7 (1.1)2.6 (1.3)*0.96-LargeBASMI3.6 (1.5)3.3 (1.3)NSConclusion:Different methods exist for quantifying inflammation in MRI images of SIJ in axSpA patients. According to our preliminary results, all of them had significant improvements in axSpA patients treated with anti tnf-α. The s-SCAISS index show good responsiveness, with similar features to validated indexes, but with an accuracy assessment of the BME area.References:[1]Defining active sacroiliitis on MRI for classification of axial spondyloarthritis: update by the ASAS MRI working group. Annals of the Rheumatic Diseases 2016;75:1958-1963.[2]Development and validation of SCAISS, a tool for semi-automated quantification of sacroilitis by magnetic resonance in spondyloarthritis. Rheumatol Int. 2018 Oct;38(10):1919-1926.Disclosure of Interests:Cristina Garrido-González: None declared, María del Carmen Castro Villegas: None declared, MLourdes Ladehesa Pineda: None declared, Juan L. Garrido-Castro: None declared, Rafaela Ortega Castro: None declared, Cristina Gonzalez-Navas: None declared, Pedro Zarco-Montejo Speakers bureau: Abbvie, MSD, Novartis, Pfizer., RAQUEL ALMODOVAR Speakers bureau: Abbvie, Celgene, Janssen, Lilly, Novartis, Pfizer., Angel Bueno: None declared, Luis Miguel Molinero: None declared, Eduardo Collantes Estevez Grant/research support from: ROCHE and Pfizer, Speakers bureau: ROCHE, Lilly, Bristol and Celgene
BackgroundThe prevalence of late-onset psoriatic arthritis (PsA) is increasing in parallel with the progressive aging of the population. The elderly population presents a greater functional deterioration and a greater number of comorbidities than the young people. With this study we aim to find clinically relevant differences to predict the evolution and prognosis of the disease depending on the onset of the symptoms to carry out a more exhaustive follow-up.ObjectivesTo evaluate the association of the age at onset of PsA symptoms with the characteristics and burden of the disease.MethodsObservational study that includes a subgroup of 231 patients with Psoriatic Arthritis (PsA) from the REGISPONSER study (Registry of Spondyloarthritis of Spanish Rheumatology) and the RESPONDIA study (Ibero-American Registry of Spondyloarthropathies). Patients with less than 10 years of disease duration (since the first symptom) were selected so that the sample was homogeneous. Patients were divided into two groups according to the age of PsA onset (early-onset: ≤40 years old and late-onset: ≥60 years old). The characteristics and burden of the disease were compared using the Student’s t-test/Mann-Whitney U test for quantitative variables or using the chi-square/Fisher test for qualitative variables.Results411 patients were included [early-onset 179 (77.5%); late-onset 52 (22.5%)]. There was a higher percentage of men in the late-onset group compared to the early-onset group [94 (62.3%) vs. 38 (86.4%), p = 0.003]. The diagnostic delay was shorter in those whose onset of the disease was late [1.5 (2.7) vs 4 (7.7), p=0.036], as well as the duration of the disease [2.9 (2.4) vs 4.2 (2.7), p= 0.012]. A lower presence of sacroiliitis was found in patients with late-onset PsA [6 (12.2%) vs 58 (32.6%), p=0.005] as well as enthesitis [5 (9.8%) vs 44 (24.6%), p =0.023]. Regarding the comorbidities, there was a higher frequency of heart disease among patients with late-onset PsA [4 (7.8) vs 0 (0), p=0.000]. No statistically significant differences were found between kidney and lung disease. Regarding the outcome measures, the BASFI score was higher in the late-onset group [3.3 (2.5) vs. 2.2 (2.2), p=0.002]. The late-onset group had a lower FSF12 component [34.6 (8.7) vs. 38.7 (10.5), p = 0.001]. The radiographic indices measured by BASRI showed worse results in those patients with late-onset disease both in the spine [2.9 (3) vs 1.6 (2), p=0.020] and in the total BASRI [3.4 (3 .4) vs 1.9 (2.4), p=0.012].ConclusionOur study suggests that the age of onset of PsA was associated with the different characteristics of the disease. Patients with late-onset PsA were more frequently males, showed worse functionality and more structural damage in comparison with early-onset PsA. Sacroiliitis and enthesitis were found less frequently in the late-onset group. Quality of life, disease activity and treatments taken were not associated significantly with age of onset.Table 1.Description of different characteristics across two groups: early and late onsetEarly-onset N=179 n (%)=77.5Late-onset N=52 n (%)=22.5p-valueSex (male)94 (62.3)38 (86.4)0.003Age (SD)38.7 (9.3)71.3 (7.5)0.000Enthesitis44 (24.6)5 (9.8)0.023Dactilytis36 (20.1)9 (17.6)0.695Sacroiliitis58 (32.6)6 (12.2)0.005Diagnostic Delay, mean (SD)4 (7.7)1.5 (2.7)0.036Disease Duration, mean (SD)4.2 (2.7)2.9 (2.4)0.012Arthritis (lower limbs)118 (65.9)33 (64.7)0.872Arthritis (upper limbs)82 (45.8)31 (60.8)0.059BASDAI, mean (SD)3.9 (2.5)3.8 (2.4)0.932BASFI, mean (SD)2.2 (2.2)3.3 (2.5)0.002ASDAS, mean (SD)2.3 (1.1)2.3 (0.9)0.894FSF12, mean (SD)38.7 (10.5)34.6 (8.7)0.001MSF12, mean (SD)47.7 (10.6)49.3 (9.2)0.341BASRI spine1.6 (2)2.9 (3)0.020BASRI total1.9 (2.4)3.4 (3.4)0.012ESR mm/h, mean (SD)17.2 (14.2)23.9 (19.1)0.005csDMARDs (ever)111 (62.7)31 (63.3)0.943bDMARDs (ever)21 (11.9)3 (6)0.234Disclosure of InterestsNone declared
Background:The prevalence of inflammatory bowel disease (IBD) in ankylosing spondylitis (AS) has been reported to range between 6%-15%. As occurs with axial spondyloarthrtitis (axSpA), patients with IBD have an increased risk of cardiovascular (CV) events because of a process of accelerated atherosclerosis1. However, it is unknown whether the presence of IBD confers an increased cardiovascular CV risk in patients with axSpA.Objectives:To compare the atherosclerotic burden, CV events, CV risk factors and disease related factors including structural damage in axSpA patients with and without IBD.Methods:Cross-sectional analysis of the AtheSpAin cohort, a Spanish multicenter cohort designed for the study of atherosclerosis in axSpA, comparing axSpA patients with and without concomitant IBD. Background information on CV and disease-related factors was reviewed. Data on CV risk and disease status at the time of the study were also obtained, including the structural damage assessed by the presence of syndesmophytes, the severity of the sacroiliitis (defined as grade 3 or 4 according to New York criteria), and the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS). Carotid ultrasound (US) was performed in all patients at the time of the study, including measurement of carotid intima-media wall thickness (cIMT) and plaque detection according to the Mannhein consensus criteria.Results:A set of 886 axSpA patients were included. 829 (93.6%) of them had no concomitant IBD, which was present in 57 (6.4%) patients. Age, sex and AS/nr-axSpA ratio were comparable in both groups (Table 1. next page). Patients with IBD were characterised by a lower prevalence of HLA B27 (46% vs 72%, p=0.01) and a higher presence of concomitant psoriasis (21% vs 10%, p=0.01)Regarding peripheral disease (history of synovitis, enthesitis, dactylitis) and hip involvement, no differences were found between both groups. There were either no differences in the structural damage found in patients with and without IBD (Table 1. next page).With respect to the management of the disease, prednisone (21% vs 13%, p = 0.03), DMARDs (54% vs 35%, p = 0.01) and anti-TNFα therapy (54% vs 31%, p = 0.00) were more commonly used in the group with IBD, while treatment with NSAIDs was more frequent in patients without IBD (81% vs 70%, p = 0.04).Regarding CV risk features, smoking was more frequent in patients without IBD (34% vs 21%, p = 0.045) (Table 1. next page). No differences were observed neither in the lipid profile or blood pressure at the time of the study, nor in the prevalence of CV events (5% vs 4%, p=0.99) (Table 1) and the subclinical atherogenic burden assessed both by the presence of carotid plaques (31% vs 37%, p=0.45) and the cIMT (645 ± 147 mm vs 636 ± 112 mm, p = 0.64) (Table 1. next page).Conclusion:The presence of IBD does not confer additional CV risk to axSpA. In our series, patients with axSpA and IBD showed a lower frequency of HLA B27 and a higher prevalence of psoriasis.Table 1.axSpA without IBD (n=829)axSpA with IBD (n=57)pMen/Women, n272/55715/420.33Mean age (years) ±SD at the time of study49 ± 1349 ± 100.99AS/nr-AxSpa656/17345/120.97History of CV risk factors Current smoker285 (34)12 (21)0.045 Obesitty Dyslipemia280 (34)16 (28)0.42 Hypertension223 (27)16 (28)0.79 Diabetes Mellitus60 (7)4 (7)0.99 Chronic Kidney Disease20 (2)2 (4)0.65History of cardiovascular events, n (%)40 (5)2 (4)0.99Structural damage at the time of studyPresence of syndesmophytes, n (%)307 (37%)23 (49%)0.66mSASSS5 (1-15)6 (3-23)0.64Severe sacroiliitis (grade 3,4), n (%)436 (53)34 (60)0.42CV data at the time of studyCarotid plaques261 (31)21 (37)0.45IMT (mm)645 ± 147636 ± 1120.64IMT >= 0.9 mm46 (6)0 (0)0.066Abbreviations: AS = ankylosing spondylitis. AxSpA= axial spondylitis. CV = cardiovascular. IBD = Inflammatory bowel disease. IMT = intima-media wall thickness. Nr-axSpA = no-radiographic axial spondylitis.Disclosure of Interests:None declared
Background:Psoriatic arthritis (PsA) is a chronic inflammatory disease associated with an increased prevalence of cardiovascular (CV) events. Traditional CV risk factors do not account for the increased CV disease mortality in PsA. Inflammation seems to have a key role in the development of this comorbidity, however the specific molecular mechanisms involved are not defined yet.Objectives:To evaluate clinical CV risk factors and surrogate markers and their relationship with inflammation, disease activity and metabolic comorbidities in PsA patientsMethods:This is a cross-sectional study including 100 PsA patients without CV disease recruited in the routine clinical practice at the Rheumatology Department, Reina Sofia Hospital of Cordoba and 100 age-matched healthy donors (HDs). Different parameters related to the cardiometabolic risk were analyzed. Clinical and analytical parameters were collected: lipid profile (cholesterol, HDL, LDL, TG, ApoA and ApoB), glucose and insulin, body surface area (BSA) affected by psoriasis, number of tender and swollen joints, DAPSA, VAS, CRP and ESR. To measure the persistence of inflammation, CRP levels were recorded retrospectively once, twice, or three times during the 5 years prior to study and at the moment of the study. Increased levels of CRP in at least 50% of the determinations was considered as persistent inflammation. Plasma and peripheral blood mononuclear cells (PBMCs) were isolated from peripheral blood of patients and HDs. A panel of 92 proteins involved in CV disease and an adipocytokine profile was measured in plasma and PBMCs. In addition, activation of 18 intracellular pathways involved in cell activation was also measured in PBMCs. In vitro experiments in adipocytes treated with serum from PsA patients were also carried out.Results:Traditional CV risk factors including atherogenic risk, insulin resistance (IR), metabolic syndrome, smoking, obesity, arterial hypertension, apolipoprotein B/A risk, type 2 diabetes mellitus and the levels of SCORE were significantly increased in PsA patients. The presence of IR was associated with disease activity markers (DAPSA, ESR and CRP). In fact, the HOMA-IR index was related to the CRP persistence. PsA patients with obesity had significantly increased the number of tender and swollen joints, the levels of DAPSA and CRP. Twenty-eight proteins involved in CV disease and six adipocytokines were significantly elevated in the plasma of PsA patients. Several of these cardiovascular molecules were associated with higher levels of DAPSA (CTSD, GAL3, CD163, FABP4, IL6 and IL1RT2), acute phase reactants (GAL3, TNFα, Adiponectin, TNFR1 and IL6), affected body surface area (IL2RA, GAL3, CCL15, TRAP, CSTB, CD163, OPG and CNTN1) and onychopaty (TRAP, VWF, MCP-1, GAL3, LTBR, TFPI, CHI3L1, CTSZ and JAM-A). In addition, the mRNA expression of most of those 28 CV molecules were significantly increased in PBMCs from PsA patients. At intracellular level, the activation of 11 kinases (ERK1/2, AKT, S6 Ribosomal, mTOR, HSP27, Bad, p70 S6 kinase, PRAS40, p53 and caspase-3) involved in insulin signaling, inflammation, cell survival and apoptosis were altered in PBMCs. Finally, serum from PsA patients was able to modify the expression of these molecules in adipocytes.Conclusion:1) Disease activity and inflammatory burden are closely associated with the presence of metabolic alterations, specifically obesity and IR in patients with PsA. 2) The development of IR is extremely related to the persistence of CRP levels in the previous 5 years. 3) Inflammation is closely associated to the adipose tissue dysfunction in PsA and 4) FABP4, CD163 and GAL3 are surrogate CV markers commonly associated with clinical features of PsA, suggesting the role of these molecules linking CVD and PsA pathogenesis.Funded by ISCIII (PI17/01316 and RIER RD16/0012/0015) co-funded with FEDER.Disclosure of Interests:None declared.
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