Background:Cystoid Macular Edema (CME) is the most important cause of blindness in non-infectious uveitis (NIU) (1). Corticosteroids and conventional and/or biological immunosuppressant may be required (1-6). High-dose intravenous methylprednisolone (IVMP) pulse therapy may induce a rapid improvement.Objectives:To evaluate the efficacy and safety of IVMP pulse therapy in CME of different immune mediated inflammatory diseases (IMID).Methods:Multicentre study of 66 patients with severe ocular inflammation who received IVMP. The underlying diseases were: Vogt Koyanagy Harada disease (VKHD)(n=24), Behçet’s disease (BD) (19) and idiopathic NIU (23). The main outcome variable was macular thickness and macular edema (Optical coherence tomography [OCT] >300 μm); that was assessed at 0 (basal), 2-5, 7, 15 and 30 days after IVMP.The results are expressed as mean ±SD for normally distributed variables, or as median [IQR] when are not. Comparison of continuous variables was performed using the Wilcoxon test.Results:We studied 43♀/ 23♂ patients. The main features are shown in TABLE 1. IVMP dose ranged from 250 to 1000 mg/day administered for 3-5 consecutive days, the dose was established according to the presence or not of other systemic manifestations apart from uveitis. All of them had active intraocular inflammation at the moment of the study.Table 1.Main features of 66 patients with cystoid macular edema.VKHD(n=24)Idiophatic(n=23)Behcet’s disease(n=19)Overall(n=66)Men/Women, n5/199/149/1066Mean age (years)42 ± 1147 ± 1533 ± 10-Unilateral/Bilateral, n (%)2 (8.3) /22 (91.7)10 (43.5) /13 (56.5)4 (21) /15 (79)16/50Inflammatory ocular patterns, n (%) Posterior uveitis6 (25)9 (39.1)3 (15.8)18 Panuveitis18 (75)14 (60.9)16 (84.2)48Laboratory data, n (%) ANA2 (8.34)2 (8.7)0 (0)4 HLA B270 (0)4 (17.4)0 (0)4 HLA B290 (0)1 (4.3)0 (0)1 HLA B510 (0)5 (21.7)8 (42)13A rapid and maintained statistically improvement was observed in OCT values in all underlying diseases (FIGURE 1). No major side effects were observed.Conclusion:High-dose IVMP pulse therapy is useful and safe in the prompt control of CME, regardless of the underlying IMID.References:[1]Vegas-Revenga N, et al. Am J Ophthalmol. 2019; 200:85-94. doi: 10.1016/j.ajo.2018.12.019.[2]Calvo-Río V, et al. Clin Exp Rheumatol. 2014;32(4 Suppl 84): S54-7. PMID: 25005576.[3]Santos-Gómez M, et al. Clin Exp Rheumatol. 2016;34(6 Suppl 102): S34-S40. PMID:27054359.[4]Atienza-Mateo B, et al. Rheumatology (Oxford) 2018;57(5):856-864. doi: 10.1093/rheumatology/kex480.[5]Atienza-Mateo B, et al. Arthritis Rheumatol. 2019; 71(12):2081-2089. doi: 10.1002/art.41026.[6]Martín-Varillas JL, et al. Ophthalmology. 2018;125(9):1444-1451. doi: 10.1016/j.ophtha.2018.02.020.Figure 1.Improvement of OCT in 66 patients with cystoid macular edema.Disclosure of Interests:None declared
BackgroundLarge vessel involvement in Giant Cell Arteritis (GCA), especially the aorta and/or its main branches, is frequent. Tocilizumab (TCZ) has shown efficacy and safety in GCA and other large-vessel vasculitis (1-4).ObjectivesTo assess the efficacy and safety of TCZ in GCA patients with involvement of the aorta and/or its main branches.MethodsMulticenter observational study of 196 patients with GCA and involvement of the aorta and/or its major branches treated with TCZ. GCA was diagnosed by: a) ACR criteria, and/or b) temporal artery biopsy, and/or c) imaging techniques. The presence of aortitis was performed by imaging techniques, mainly PET, and A-MRI.Maintained remission was considered according to EULAR definitions (5).ResultsThe main features of the 196 patients are showed in Table 1. Polymyalgia rheumatica, constitutional syndrome and headache were the most frequent clinical manifestations at TCZ onset. At 6 months after starting TCZ, 20% of the patients reached a sustained remission, that was progressively increasing. (Figure 1). A corticosteroid-sparing effect was observed from month 1 of TCZ onset (Figure 1). Relevant adverse events were observed in 12 per 100 patients-year, documenting serious infections in 4.8 per 100 patients-year (Table 1).Table 1.Main features of 196 GCA patients with involvement of the aorta and/or its main branches treated with TCZ.GCA (n=196)Features at TCZ onsetAge(years), mean±SD71.3±9.5Sex, female/male (% female)148/48 (75)Time from GCA diagnosis to TCZ onset (months), median [IQR]7 [2-18.25]Systemic manifestations, n (%)Fever, n (%)24 (12)Constitutional syndrome, n (%)87 (44)PmR, n (%)131 (67)Ischaemic manifestations, n (%)Visual involvement, n (%)16 (8)Headache, n (%)74 (38)Jaw claudication, n (%)27 (14)Laboratory dataESR, mm 1st hour, median [IQR]32 [14-54]CRP, mg/dL, median [IQR]1.5 [0.6-3.2]Prednisone dose, mg/day, median [IQR]15 [10-30]Safety after TCZ onsetRelevant adverse events, per 100 patients-year12Serious infections, per 100 patients-year4.8Figure 1.A) Sustained remission, and B) median prednisone dose required in GCA patients with aortitis treated with tocilizumabConclusionTCZ seems to be effective and relatively safe in GCA patients with involvement of the aorta and/or its main branches.References[1]Calderón-Goercke M, et al. Semin Arthritis Rheum. 2019; 49: 126-135. PMID: 30655091[2]Loricera J, et al. Clin Exp Rheumatol. 2016; 34: S44-53. PMID: 27050507[3]Loricera J, et al. Clin Exp Rheumatol. 2015; 33: S19-31. PMID: 25437450[4]Prieto-Peña D, et al. Ther Adv Musculoskelet Dis. 2021; 13: 1759720X211020917. PMID: 34211589[5]Hellmich B, et al. Ann Rheum Dis. 2020; 79: 19-30. PMID: 31270110Disclosure of InterestsLara Sanchez-Bilbao: None declared, Javier Loricera Speakers bureau: from Roche, Novartis, UCB Pharma, Celgene, and Grünenthal., Rafael Melero: None declared, Santos Castañeda Speakers bureau: UAM-Roche, EPID- Future chair, Department of Medicine, Universidad Autónoma de Madrid, Madrid, Spain., Clara Moriano: None declared, Iván Ferraz-Amaro: None declared, J. Narváez: None declared, Vicente Aldasoro: None declared, Olga Maiz: None declared, Ignacio Villa-Blanco: None declared, Paloma Vela-Casasempere: None declared, Susana Romero-Yuste: None declared, Jose Luis Callejas-Rubio: None declared, Eugenio de Miguel: None declared, E. Galíndez-Agirregoikoa: None declared, Francisca Sivera: None declared, Carlos Fernández-López: None declared, Carles Galisteo: None declared, Julio Sanchez-Martin: None declared, Monica Calderón-Goercke: None declared, J. Luis Hernández: None declared, Miguel A González-Gay Speakers bureau: Abbvie, Pfizer, Roche, Sanofi, Lilly, Celgene, and MSD., Grant/research support from: AbbVie, MSD, Jansen, and Roche,, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Lilly, Janssen, and MSD., Grant/research support from: Abbvie, MSD, and Roche
patients with ankylosing spondylitis (AS), and to look for correlations with clinical findings, plain radiography and pulmonary function testing. Methods 28 patients with AS meeting the modified New York criteria and without history of respiratory symptoms were enrolled prospectively: 25 men (89.2%) and 3 women with mean age of 37.8 (9.1) years and mean disease duration of 7. 8 (4.6) years [0.4-19]. All patients underwent posteroanterior plain chest radiography, HRCT and pulmonary function tests.Results HRCT revealed abnormalities in 17 patients (60.7%): these included interstitial lung disease (n = 2), paraseptal emphysema (n = 2), apical fibrosis (n = 2), bronchiectasis (n = 1), and non-specific interstitial lung disease (n = 11). Plain radiography was abnormal in only 2 cases. Comparison between patients with and without defined thoracic HRCT abnormalities showed no differences in age, sex, disease duration, history of smoking, radiological scores (syndesmophytes score, BASRI) or ESR but showed significant statistical difference in symptomatic severity parameters (Schöber, BASMI, BASDAI). Pulmonary function tests showed a restrictive process in four patients in whom three had an abnormal chest HRCT and an obstructive process in two patients in whom one had emphysema and apical fibrosis on chest HRCT. Conclusion This study, which describes thoracic HRCT findings in patients with AS and without respiratory symptoms, confirms the high prevalence of a spectrum of abnormalities undetectable on standard plain radiography.
BackgroundPatients with Rheumatoid Arthritis (RA) present an increased risk of mortality. In the last decades, mortality rates tended to decrease but cardiovascular (CV) events remained as the leading cause of death in most series (1).ObjectivesTo assess mortality rates and leading causes of death, as well as predictors of mortality related to disease activity in a prospectively followed-up cohort of RA patients.MethodsWe conducted a prospective longitudinal study that included 673 RA patients from a single tertiary center. Univariate and multivariate Cox proportional hazards regression were used to identify predictors of mortality.ResultsWe studied 673 patients with RA (75% women), mean age 61±13 years. The main general characteristics, CV risk factors, RA disease activity data and current treatment are summarized in the Table 1.Table 1.Baseline characteristics of 673 RA patientsAge, years, (mean±sd)61 ± 13Female/Male, n (%)505 (75) /168 (25)Past or Current smoker, n (%)338 (50)Obesity, n (%)226 (34)Hypertension, n (%)310 (46)Diabetes Mellitus, n (%)85 (13)Dyslipidemia, n (%)310 (46)BMI, kg/m2 (mean±sd)28 ± 6Abdominal circumference, cm (mean±sd)97 ± 15Total/HDL/LDL cholesterol, mg/dl (mean±sd)204±38/62±18/120 ± 31Disease duration, years (median, [IQR])13 [10-20]CRP, mg/l (median, [IQR])3.0 [0.8-7.0]ESR, mm/ 1º hour (median, [IQR])12 [5-21]Rheumatoid factor/ ACPA, n (%)376 (56) / 314 (48)DAS28-ESR/ DAS28-PCR (mean±sd)3.18 ± 1.41/3.00 ± 1.23NSAIDs / Prednisone, n (%)265 (39) /341 (51)Prednisone dose, mg/day (median, [IQR])5 (2.5-5)c-DMARDS: Metotrexate/ Leflunomide/ Hydroxychloroquine/ Salazopyrin, n (%)406 (60) /52 (8) / 178 (26) / 10 (1)b-DMARDS: TNFi/ Tocilizumab/ Rituximab/ Abatacept, n (%)88 (13) / 43 (6) / 13 (2) / 8 (1)JAK inhibitors, n (%)12 (2)After a follow-up of 4,367 person-years (mean 6.4±1.4), 67 deaths were recorded. Considering all causes of mortality, the cumulative incidence was 14% (95% CI 11-18) with a mortality incidence rate of 0.015 (95% CI 0.012-0.020) patient/year. The main causes of mortality in decreasing order of frequency were infections (N=23) (34%), incidence rate-IR: 0.005 [95% CI 0.003-0.008]), cancer (N=18) (27%), IR: 0.004 [95% CI 0.002-0.007]), CV events (N= 12) (18%), IR: 0.003 [95% CI 0.001-0.005]), respiratory diseases (N=2) (3%), IR: 0.0005 [95% CI 0.00007-0.002] and other causes (N=12) (18%), IR: 0.003 [95% CI 0.001-0.005I].The statistically significant predictive factors of mortality in the univariate analysis were male gender (HR 1.97[95%CI 1.20-3.21, p=0.007), abdominal circumference (HR 1.03 [95% CI 1.01-1.05], p=0,0006), diabetes (HR 2.85 [95%CI 1.68-4.86], p<0.001) and hypertension (HR 2.92 [95%CI 1.73-4.94], p<0.001). Also, baseline data of variables associated with disease activity such as increased CRP, ESR, DAS28-CRP, DAS28-ESR were predictors of mortality (Figure 1). Disease related parameters were adjusted by CV risk factors in a multivariate analysis. Following this procedure, the predictive factors that reached statistical significance; (Hazard Ratio [95%CI]), were an increased in DAS28-VSG (1.40 [1.07-1.83], p=0.016), DAS- 28-PCR (1.40 [1.07-1.83], p=0.016), CRP (1.02 [1.01-1.05] p=0.002), and ESR (1.03 [1.01- 1.05], p=<0.001) (Figure 1).Figure 1.Forest Plot of mortality (Univariate and multivariate analysis).Results expressed in logarithmic scale. Multivariate analysis: Disease activity related parameters adjusted by age, gender, disease duration, smoker, diabetes, hypertension and abdominal circumference. CDAI, ESR and CPR expressed value/10. (*) p<0.05.ConclusionIn a cohort of patients with RA followed prospectively in a tertiary hospital, infections and malignancies are the main cause of mortality rather than CV events. Disease activity parameters are associated with an increased risk of mortality in these patients with RA.References[1]Avina-Zubieta JA et al. Risk of cardiovascular mortality in patients with rheumatoid arthritis: a meta-analysis of observational studies. Arthritis Rheum 2008,59:1690–97.Disclosure of InterestsNone declared.
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