Data suggest that being female, overweight and mostly obese is associated with a lower rate of success in obtaining response status in axial SpA patients treated with anti-TNF drugs. Body weight could represent a modifiable factor to reach the best outcome in axial SpA patients treated with TNF blockers.

Drug Rash Eosinophilia Systemic Symptoms (DRESS) syndrome is a systemic hypersensitivity reaction characterized by exfoliative dermatitis and maculopapular rash, lymphadenopathy, fever, eosinophilia, leukocytosis, and involvement of internal organs as liver, lung, heart, and kidney; the disorder starts within 2–6 weeks after taking a drug with an incidence that ranges from 1/1000 to 1/10000 exposures. Fatal cases are reported. The exact pathogenesis of DRESS syndrome is not completely understood, while it is reported that amoxicillin could trigger it in patients who are taking allopurinol, sulfasalazine, NSAIDs, carbamazepine, strontium ranelate, lisinopril, lansoprazole, and minocycline. Amoxicillin could act directly, inducing the reactivation of a viral infection (HHV 6 and EBV) with symptoms similar to DRESS syndrome or by reducing the patients' ability to detoxify the body from substances chronically taken. We describe a case of a patient admitted to our hospital for a DRESS syndrome flared after amoxicilline intake during treatment with sulfasalazine; this combination can activate severe reactions often with an insidious onset that can mimic an infectious disease.

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Objectives To compare laboratory and clinical parameters in patients with biopsy proven and not biopsy proven temporal arteritis. To evaluate if the incidence of neurologic complications would be influenced by other clinical factors including the modality of referral to rheumatologist. Methods We retrospectively examined the clinical records of patients who had been diagnosed with giant cell arteritis in our rheumatology unit from February 2007 to December 2012. We recorded data, procedures for referral, time interval between onset of symptoms and diagnosis, clinical features and comorbidities, laboratory exams. Neurologic complications (visual loss, optic and peripheral nerves paralysis) were examined. Biopsy proven and not biopsy proven cases were compared. For the statistical analysis t-Student and Fisher tests were used. Results Thirty six patients (F 27, M 9, age 75.6 yrs) affected by temporal arteritis were included; twenty four 66.6%) had positive arterial biopsy. Fourteen patients (38.8%) were referred to us from other Units: Neurology 6 pts, Ophtftalmology 5 pts, Otorinolaryngology 2 pts, Infectious Disease 1 pt; the other 22 patients (61.2%) went from the General Practitioner (GP). The time interval between onset of symptoms and diagnosis was shorter in the group with not biopsy proven diagnosis (4.0 and 5.7 months respectively). Biological markers of inflammation were more increased in biopsy positive patients, with statistic relevance for C-reactive protein (p=0.0002). No significant differences were found regarding the presence of polymyalgia rheumatica (p=1), temporal/jaw pain (p=0.37), fever (p=0.48), complications (p=0.47). In the biopsy proven group, complications were more frequent in the presence of arterial hypertension (p=0.31), polymyalgia rheumatica (p=0.25) and when diagnosis was later (p=0.11). Rate of complications was higher in patients from ophthalmologist and otorinolaryngologist (100%) than patients from neurologist (50%), GP (13.6%) and infectivologist (none). Among complicated patients, biopsy was performed less frequently in patients referred to us from ophthalmologist (60%), than from neurologist and GP (66.6%). Among uncomplicated patients, however, the majority of biopsies was performed in those sent from GP (86.3%) compared with those sent from neurologist (66.6%). Conclusions In our study, C-reactive protein was the only laboratory test significantly higher in the group of biopsy proven patients. No significant clinical correlations have been found between the two groups regarding to polymyalgia rheumatica, temporal/jaw pain or fever. In biopsy proven patients, late diagnosis seemed to be more predictive of complications than arterial hypertension and polymyalgia rheumatica, but the difference is not significant. Patients referred to rheumatologist by other specialists (mostly ophthalmologists) had the higher rate of complications. Disclosure of Interest None Declared

BackgroundThe recent EULAR recommendations [1,2] suggest using JAK-inhibitors (JAKis) for treating RA patients. These drugs include both selective (upadactinib and filgotinib) and unselective (tofacitinib and baricitinib) JAKis.ObjectivesTo describe JAKis’ discontinuation rate and to determine predictors of JAKIs’ discontinuation in a real life setting.MethodsAll patients with RA treated with JAKis were prospectively followed up for at least 12 months in this multicentric study carried out on 23 Italian centres. For each patient, the following variables were collected: sex, age, disease duration, smoking, BMI, comorbidities (diabetes, hypertension, hypercholesterolemia, cancer, major cardiovascular events), positive RF/ACPA, cDMARDs at baseline, prednisone at baseline, previous use of JAKis, discontinuation, time to discontinuation, JAKis line of treatment, DAS28-ESR at baseline, 6 and 12 months. Statistical analyses were performed using R (2022.12.0).Results864 patients were included (Table 1). 487 (55.2%) received baricitinib, 213 (24.6%) tofacitinib, 111 (12.8%) upadacitinib and 62 (7.2%) filgotinib. 192 (22.2%) patients discontinued JAKis after a median time of 334 days (IQR 154.5-879.5). Among them, a statistical difference was found between selective-JAKis and other JAKis (p=0.03, 14.6% of selective JAKis vs 85.4% of other JAKis); finally unselective JAKis were discontinued later than selective JAKis (p<0.001, median 401.5 days, IQR 197.5-976 for unselective JAKis vs median 74 days, IQR 129-212 for selective JAKis). Discontinuation’s causes are reported inFigure 1. Notably, VZV infection determined JAKis withdrawal in 4 patients and pulmonary embolism/deep venous thrombosis in 6 patients (both with baricitinib). Regarding discontinuations’ causes, no differences between selective JAKis and other JAKis were found with factor logistic regression model. At multivariate analysis, predictors of discontinuation were prednisone at baseline (OR 1.48, p=0.03), treatment with unselective JAKis (OR 1.79, p=0.01), and line of treatment (OR 1.29 p<0.001).ConclusionOur study showed that only a minority of patients discontinued JAKis. Among discontinuation‘s causes, no differences between selective JAKis and other JAKis were found. Predictors of JAKis discontinuation were prednisone at baseline, treatment with unselective JAKis and line of treatment (with more advanced lines of treatment associated with a higher risk of discontinuation).References[1] Smolen JS, et al. Ann Rheum Dis 2020.[2] Smolen JS, et al. Ann Rheum Dis 2023.Table 1.General features of 864 RA patientsVariableN (%)Mean age at baseline (SD) (N=863)58.79 (12.84)Females678 (78.47)Mean BMI (Kg/cm2) at baseline (SD) (N=626)25.19 (3.79)Smoking (N=799)Yes151 (18.89)No504 (63.01)Former144 (18.02)Positive RF (N=809)533 (65.88)Positive ACPA (N=796)498 (61.56)Diabetes (N=770)70 (9.09)Hypertension (N=771)302 (39.17)Hypercholesterolemia (N=769)196 (25.49)Previous MACE (N=768)47 (6.12)Previous cancer (N=770)42 (5.45)Disease duration (months), (median, IQR) (N=855)77 (30-157)Mean DAS28-ESR at baseline (SD) (N=746)5.29 (1.06)cDMARDs at baseline (N=781)287 (36.75)PDN at baseline (N=780)444 (56.92)Median dosage (IQR) of PDN (mg/day)5.00 (4.00-5.00)JAKis naïve (N=853)731 (85.70)Line of JAKis treatment  1^247 (26.59) 2^211 (24.42) 3^181 (20.64) 4^111 (12.84) 5^65 (7.52) 6^29 (3.35) 7^12 (1.39) 8^3 (0.35) 9^2 (0.23) 10^3 (0.35)Patients who discontinued JAKis192 (22.2)Time to discontinuation (days), (median, IQR) (N=863)334 (154.5-879.5)Legends to Table 1:RA: rheumatoid arthritis; SD: standard deviation; BMI: Body Mass Index; RF: Rheumatoid Factor; ACPA: Autoantibodies against citrullinated peptides/proteins; MACE: Major cardiovascular events; PDN: prednisone; IQR: interquartile range; DAS28-ESR: Disease Activity Score-28 for Rheumatoid Arthritis with ESR; cDMARDs: conventional Disease-modifying antirheumatic agents; JAKis: JAK inhibitors.Acknowledgements:NIL.Disclosure of InterestsMaddalena Larosa: None declared, Alarico Ariani: None declared, Dario Camellino Speakers bureau: Abiogen, GSK, Paid instructor for: Mylan, Andrea Becciolini: None declared, Gerolamo Bianchi: None declared, Eleonora Di Donato: None declared, Giuditta Adorni: None declared, Daniele Santilli: None declared, Gianluca Lucchini: None declared, Massimo Reta: None declared, Olga Addimanda: None declared, Alberto Lo Gullo: None declared, elisa visalli: None declared, Rosario Foti: None declared, Giorgio Amato: None declared, Francesco De Lucia: None declared, antonella farina: None declared, Francesco Girelli: None declared, Simone Bernardi: None declared, Giulio Ferrero: None declared, Romina Andracco: None declared, Marino Paroli: None declared, Natalia Mansueto: None declared, rosalba caccavale: None declared, Patrizia Del Medico: None declared, Aldo Molica Colella: None declared, Veronica Franchina: None declared, Francesco Molica Colella: None declared, Federica Lumetti: None declared, Gilda Sandri: None declared, Carlo Salvarani: None declared, Marta Priora: None declared, Aurora Ianniello: None declared, Valeria Nucera: None declared, Francesca Ometto: None declared, Ilaria Platé: None declared, eugenio arrigoni: None declared, Alessandra Bezzi: None declared, Maria Cristina Focherini: None declared, Fabio Mascella: None declared, Vincenzo Bruzzese: None declared, Palma Scolieri: None declared, Simone Parisi: None declared, Maria Chiara Ditto: None declared, Enrico Fusaro: None declared, Viviana Ravagnani: None declared, Rosetta Vitetta: None declared, Alessia Fiorenza: None declared, Guido Rovera: None declared, Alessandro Volpe: None declared, Antonio Marchetta: None declared, Matteo Colina: None declared, Elena Bravi: None declared.