Abstract: Patients with immune-mediated inflammatory diseases (IMID), particularly if treated with B-cell depleting therapies, show reduced humoral responses to SARS-CoV-2 vaccines and increased risk of severe COVID-19 (1,2). Since pre-exposure prophylaxis (PrEP) with monoclonal antibodies against SARS-CoV-2 proved effective in preventing infection and COVID-19 (3) in the general population, PrEP could be used for passive immunization of vaccine-refractory patients with IMIDs. Objectives To evaluate the persistence of serum and salivary anti-SARS-CoV-2 IgG antibodies in vaccine-refractory patients with IMID after PrEP with casirivimab/imdevimab. Secondary outcomes were safety, SARS-CoV-2 infection, and adverse COVID-19 outcomes. Methods We performed a longitudinal analysis on anti-SARS-CoV-2 IgG titers in IMID patients who received a PrEP with 1200 mg of subcutaneous casirivimab/imdevimab due to high infection risk, as they had not developed an adequate humoral response at least 21 days after three COVID-19 vaccinations (Table 1). Serum and salivary anti-SARS-CoV-2 Spike IgG were quantified by ELISA (EUROIMMUN, Lübeck, Germany) before PrEP and after 1, 14, and 30 days. IgG levels are given as antibody ratios by dividing the optical density of the sample by that of the calibrator. A cutoff of ≥1.1 was considered positive. Safety as well as polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infection and adverse COVID-19 outcomes (hospitalization, mechanical ventilation, death) after PrEP were recorded. Table 1. Baseline characteristics. N 26 Age, mean (SD) 54 (14) Sex, n (%) Female 15 (57.7) Male 39 (42.3) Diagnosis, n (%) ANCA-associated vasculitis 10 (38.5) Rheumatoid arthritis 6 (23.1) Immunoglobulin deficiency 4 (15.4) Systemic sclerosis 2 (7.7) Psoriatic arthritis 1 (3.8) Systemic Lupus Erythematosus 1 (3.8) Non-infectious Uveitis 1 (3.8) Multiple sclerosis 1 (3.8) IgG4-related disease 1 (3.8) Autoinflammatory syndrome 1 (3.8) CD20-depletion Rituximab, n (%) 22 (84.6) Other therapies, n (%) Methotrexate 6 (23.1) Immunoglobulins 4 (15.4) Mycophenolate 1 (3.8) Infliximab 1 (3.8) CD19+ lymphocytes/mm 3 , median (IQR) 0 (0-9) Serum total IgG, median (IQR) 894 (745-987) SD, standard deviation; IQR, interquartile range; ANCA, anti-neutrophil cytoplasmic antibodies. Results We obtained 92 serum and 75 saliva samples from 26 participants at four consecutive timepoints (Figure 1). Anti-SARS-CoV-2 IgG titers were observed in serum and saliva samples of all participants from day 1 and throughout 30 days after PrEP independently of diagnosis, therapy, total IgG, and peripheral CD19+ B-cells. Serum IgG increased rapidly at day 1 and plateaued from day 14 to 30 (Figure 1A), reaching similar levels as seen in healthy subjects after full vaccination (1), while saliva IgG increased steadily from administration up to day 14 and plateaued at day 30 (Figure 1B). No side effects were reported. Five patients (19.2%) had a close contact with a SARS-CoV-2-infected person, after which all but one remained asymptomatic and with a negative PCR test. The patient who tested positive developed mild COVID-19 with fever and cough. Figure 1. Temporal pattern and distribution of serum (A) and salivary (B) anti-SARS-CoV-2 IgG levels. Results from individual participants are represented as line (top) and scatter plots (bottom). Horizontal lines represent median values, the dotted horizontal line represents the positivity cutoff of 1.1. ** p =0.0082; *** p 〈 0.001; **** p 〈 0.0001. mAbs: monoclonal antibodies. Conclusion SARS-CoV-2 PrEP induces stable serum and salivary antibody levels in IMID patients who did not respond to COVID-19 vaccination, regardless of pre-existing clinical and serological features. In IMID, PrEP with casirivimab/imdevimab is safe and has the potential to prevent infection and severe COVID-19. References [1]Simon D, et al. Ann rheum dis. 2021;80:1312-1316. [2]Fagni F et al, et al. Lancet Rheumatol. 2021; e724-e736. [3]Flonza I, et al . MedRxiv . 2021. doi: 10.1101/2021.11.10.21265889 Disclosure of Interests None declared

Abstract: Due to better treatment strategies and higher remission rates the management of rheumatoid arthritis (RA) patients in sustained remission is of increasing interest (1). The Rheumatoid Arthritis in Ongoing Remission (RETRO) study investigated the possibility to taper and stop disease modifying anti-rheumatic drugs (DMARDs). Objectives: To compare one-year remission and relapse rates in rheumatoid arthritis patients randomized to continued treatment, reduced treatment or gradual treatment withdrawal after stable remission under routine care. Methods: Primary data of the phase III, randomized, controlled RETRO trial in RA patients with stable conventional synthetic and/or biologic DMARD treatment in sustained ( 〉 6 months) DAS28-ESR remission ( 〈 2.6 units). Patients were randomized 1:1:1 into three strategy arms (continuation of 100% DMARD dose, CONT; tapering to 50% DMARD dose, TAP; 50% tapering followed by withdrawal of DMARDs, STOP). The primary endpoint was the proportion of patients in sustained DAS28-ESR remission after 1 year. Results: 316 RA patients in sustained remission were included, 303 were randomized (CONT: N=100; TAP: N=102; STOP: N=101) and 282 (93%) had complete data sets after 1 year (CONT:N=93; TAP: N=93; STOP: N=96; Table 1). After 1 year, 81.2%, 58.6%, 43.3% of patients, maintained their remission state over 1 year in the CONT, TAP and STOP arms, respectively (p=0.0004 with log rank test for trend; Figure 1). Hazard ratios for flare were 3.02 (95%CI 1.69 to 5.40) and 4.34 (95%CI 2.48 to 7.60) for the TAP and STOP arms. RA patients who flared were more likely to be female, have longer disease duration, RF/ACPA positivity and higher baseline DAS-28 scores with standardized mean differences 〉 0.2. Serious adverse events were reported in 10.8%, 7.5%, and 13.5% in the CONT, TAP and STOP arms, respectively. Table 1. Baseline Characteristics Group Control Reduce Reduce/Stop Overall N 93 93 96 282 Age, mean(SD ) 55.9 (12.7) 56.9 (13.0) 56.5 (13.3) 56.5 (13.0) Female, n (% ) 53 (57.0) 57 (62.0) 57 (59.4) 167 (59.4) RF, n (% ) 52 (55.9) 58 (62.4) 52 (54.2) 162 (57.4) ACPA, n (% ) 53 (57.0) 50 (54.9) 55 (57.3) 158 (56.4) Disease duration, years, mean(SD ) 7.6 (6.9) 7.8 (6.9) 6.8 (8.1) 7.4 (7.3) Remission duration, months, mean(SD ) 20.6 (18.0) 16.5 (15.9) 22.7 (30.4) 20.0 (22.6) Biologics, n (% ) 39 (41.9) 44 (47.3) 39 (40.6) 122 (43.3) Methotrexate, n (% ) 71 (76.3) 67 (72.0) 75 (78.1) 213 (75.5) Other DMARDs, n (% ) 24 (25.8) 20 (21.5) 16 (16.7) 60 (21.3) Glucocorticoids, n (% ) 27 (29.0) 23 (24.7) 17 (17.7) 67 (23.8) CRP, mg/L, mean(SD ) 0.3 (0.3) 0.5 (0.5) 0.5 (0.6) 0.4 (0.5) ESR, mm/h, mean(SD ) 11.3 (8.4) 12.2 (8.8) 13.0 (10.0) 12.2 (9.1) Tender joint count, mean(SD ) 0.2 (0.6) 0.0 (0.2) 0.1 (0.3) 0.1 (0.4) Swollen joint count, mean(SD ) 0.1 (0.3) 0.1 (0.3) 0.1 (0.4) 0.1 (0.3) Physician VAS,mm, mean(SD ) 1.8 (4.2) 2.6 (4.4) 2.0 (3.9) 2.1 (4.2) Patient VAS,mm, mean(SD ) 6.4 (9.0) 5.5 (8.3) 4.5 (8.4) 5.5 (8.6) HAQ, standard, mean(SD ) 0.2 (0.4) 0.2 (0.3) 0.2 (0.4) 0.2 (0.4) HAQ, alternative, mean(SD ) 0.2 (0.4) 0.1 (0.3) 0.2 (0.3) 0.2 (0.3) DAS-28, mean(SD ) 1.7 (0.7) 1.7 (0.6) 1.7 (0.6) 1.7 (0.6) SDAI, mean(SD ) 1.4 (1.5) 1.4 (1.5) 1.3 (1.3) 1.3 (1.4) DAS-28 remission, n (% ) 91 (97.8) 93 (100.0) 95 (99.0) 279 (98.9) SDAI remission, n (% ) 79 (87.8) 79 (84.9) 88 (92.6) 246 (88.5) Boolean remission, n (% ) 69 (75.8) 71 (76.3) 76 (79.2) 216 (77.1) Conclusion: This randomized controlled study shows that half of RA patients in sustained remission relapse when tapering/stopping their DMARDs. Presence of autoantibodies, higher baseline DAS28-ESR and female sex are predictors for flares. References: [1]Schett G et al. Tapering biologic and conventional DMARD therapy in rheumatoid arthritis: current evidence and future directions. Ann Rheum Dis. 2016 Aug;75(8):1428-37. Disclosure of Interests: Melanie Hagen Speakers bureau: advisory boards, Koray Tascilar Speakers bureau: advisory board, Michaela Reiser: None declared, Larissa Valor: None declared, Judith Haschka Speakers bureau: advisory board, Arnd Kleyer Speakers bureau: advisory board, Axel Hueber Speakers bureau: advisory boards, Bernhard Manger Speakers bureau: advisory boards, Jayme Cobra Speakers bureau: advisory boards, Camille Figuereido Speakers bureau: advisory boards, Stephanie Finzel Speakers bureau: advisory boards, Hans-Peter Tony Speakers bureau: advisory boards, Joerg Wendler Speakers bureau: advisory boards, Stefan Kleinert Speakers bureau: advisory boards, Florian Schuch Speakers bureau: advisory boards, Monika Ronneberger: None declared, Martin Feuchtenberger Speakers bureau: advisory boards, Martin Fleck Speakers bureau: advisory boards, Karin Manger: None declared, Wolfgang Ochs: None declared, Matthias Schmitt-Haendle: None declared, Hanns-Martin Lorenz Speakers bureau: advisory boards, Rieke Alten Speakers bureau: advisory boards, Jörg Henes Speakers bureau: advisory boards, Klaus Krueger Speakers bureau: advisory boards, Jürgen Rech Speakers bureau: advisory boards, Georg Schett Speakers bureau: advisory boards.

Abstract: We have previously reported that the presence of musculoskeletal pain in psoriasis patients is associated with a higher risk of developing psoriatic arthritis (PsA) (1). Furthermore, a subset of psoriasis patients shows evidence for structural entheseal lesions (SEL) in their hand joints (2), sometimes also referred as “Deep Koebner Phenomenon”, which are highly specific for psoriatic disease and virtually absent in healthy controls, rheumatoid arthritis and hand osteoarthritis patients (2-4). However, it remains unclear whether SEL alone or in combination with musculoskeletal pain are associated with the development of PsA. Objectives: To test whether the presence of SEL in psoriasis patients increases the risk for progression to PsA and how this is related to the presence of musculoskeletal pain. Methods: Psoriasis patients without evidence of PsA were enrolled in a prospective cohort study between 2011 and 2018. All patients underwent baseline assessment of SEL in their 2 nd and 3 rd MCP joints by high-resolution peripheral quantitative computed tomography (HR-pQCT). The risk of PsA development associated with SEL and arthralgia was explored using survival analyses and multivariable Cox regression models. Results: 114 psoriasis patients (72 men/42 women) with a mean (SD) follow-up duration of 28.2 (17.7) months were included, 24 of whom developed PsA (9.7 /100 patient-years, 95%CI 6.2 to 14.5) during the observation period. Patients with SEL (N=41) were at higher risk of developing PsA compared to patients without such lesions (21.4/100 patient-years, 95%CI 12.5 to 34.3, HR 5.10, 95%CI 1.53 to 16.99, p=0.008) (Kaplan Meier plot A). Furthermore, while patients without arthralgia and without SEL had a very low progression rate to PsA (1/29; 3.4%), patients with arthralgia but no SEL showed higher progression (5/33; 15.2%), which was in line with previous observations (1) (Kaplan Meier plot B). Presence of SEL further enhanced the risk for progression to PsA both in the absence (6/16; 37.5%) and presence (6/14; 42.8%) of arthralgia with the highest progression rate in those subjects with both arthralgia and SEL (p 〈 0.001 by log rank test for trend) (Kaplan Meier plot B). Conclusion: Presence of SEL is associated with an increased risk of developing PsA in patients with psoriasis. If used together with pain, SEL allow defining subsets of psoriasis patients with very low and very high risk to develop PsA. References: [1]Faustini F et al. Ann Rheum Dis. 2016;75:2068-2074 [2]Simon D et al. Ann Rheum Dis. 2016;75:660-6 [3]Finzel S et al. Ann Rheum Dis. 2011;70:122-7 [4]Finzel S et al. Arthritis Rheum. 2011;63:1231-6 Disclosure of Interests: David Simon Grant/research support from: Else Kröner-Memorial Scholarship, Novartis, Consultant of: Novartis, Lilly, Koray Tascilar: None declared, Arnd Kleyer Consultant of: Lilly, Gilead, Novartis,Abbvie, Speakers bureau: Novartis, Lilly, Sara Bayat Speakers bureau: Novartis, Eleni Kampylafka Speakers bureau: Novartis, BMS, Janssen, Axel Hueber Grant/research support from: Novartis, Lilly, Pfizer, Consultant of: Abbvie, BMS, Celgene, Gilead, GSK, Lilly, Novartis, Speakers bureau: GSK, Lilly, Novartis, Jürgen Rech Consultant of: BMS, Celgene, Novartis, Roche, Chugai, Speakers bureau: AbbVie, Biogen, BMS, Celgene, MSD, Novartis, Roche, Chugai, Pfizer, Lilly, Louis Schuster: None declared, Klaus Engel: None declared, Michael Sticherling Grant/research support from: Novartis, Consultant of: Advisory boards Abbvie, Celgene, Janssen Cilag, Lilly, Pfizer, MSD, Novartis, Amgen, Leo, Sanofi, UCB, Speakers bureau: Abbvie, Celgene, Janssen Cilag, Leo, MSD, Novartis, Pfizer, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Eli Lilly, Novartis, Roche and UCB

Abstract: The first vaccine against SARS-CoV-2 was approved in December 2020. Immunogenicity of SARS-CoV2 vaccines in patients with immune-mediated inflammatory disease (IMID) have so far been evaluated in the 2-6 weeks following complete vaccination and risk groups for poor early vaccine response have been identified leading to specific vaccination recommendations. However, data on the long-term course and persistence of vaccine response in IMID patients, as well as the outcomes of the specific recommendations are lacking. Objectives To evaluate the long-term course of humoral response to SARS-CoV-2 vaccination in a large prospective cohort of IMID patients and non-IMID controls with a follow-up duration of up-to to 10 months after the first vaccine dose. Methods We have initiated a prospective dynamic cohort of IMID patients and healthy controls in February 2020 to monitor immune response to SARS-CoV-2 and respiratory infections including COVID-19 (1). Participants who contributed data starting from the 4 weeks before their first vaccination onwards were included in this analysis. Antibodies against SARS-CoV-2 spike protein were quantified with an ELISA from Euroimmun (Lübeck, Germany) with an optical density cutoff of 0.8. We fitted linear mixed-effect models for log-transformed antibody levels using time splines with adjustment for age and sex. Marginal mean antibody levels with 95% confidence intervals (CI) were estimated at selected time points for IMID patients and controls with double vaccination. We descriptively analyzed the observed antibody levels over time in cohort participants receiving two vaccinations vs. three vaccinations. Results Among 5076 cohort participants, 3147 IMID patients and healthy controls (mean (SD) age 49 (16)) provided 4756 samples for this analysis between December 2020 and 2021, with a median (IQR) 28 (14-31) weeks of follow-up after the first vaccination (Table 1). 2965 (94%) participants had received at least 2 and 223 (7%) participants had received three vaccine doses by the date of their latest sampling. In IMID patients, age and sex-adjusted estimated marginal mean antibody levels waned after week 16 and were substantially reduced at all time points compared to the controls, finally dropping to the borderline range (1.01, 95%CI 0.86 to 1.19) at week 40 (Figure 1A, Table 1). A third dose was given to 128 (7%) of IMID patients with a poor response to 2 vaccine doses after a median 20 weeks of the second dose (IQR 10 to 26 weeks). After the third dose, antibody levels in IMID patients were comparable to those of healthy controls at 40 weeks who had three vaccine doses. These were also higher than that of IMID patients and controls who did not receive a third dose (Figure 1B). Table 1. Participant characteristics and antibody levels Healthy controls IMID  N 1199 1948  Age, mean (SD) 40.8 (13.5) 54.3 (14.8)  Follow-up, weeks, median (IQR) 31.1 (23.8-36.6) 19.6 (12.3-26.6)  Follow-up range, weeks, 1.6-46.1 1.7-46.3 Sex, n(%)  Female 554 (46.2) 1136 (58.3) Vaccine intervals, ´median (IQR)  1 st to 2 nd dose 4.6 (3.0-6.0) 6.0 (5.0-6.1)  2 nd to 3 rd dose 29.6 (26.9-36.4) 19.9 (10.0-26.1) Diagnosis, n (%)  Spondyloarthritis - 713 (36.6)  Rheumatoid arthritis - 489 (25.1)  Autoimmune disease, systemic+ - 420 (21.5)  Inflammatory bowel disease - 219 (11.2)  Psoriasis - 107 (5.5) Mean* antibody levels after 1 st dose  Week-8 4.16 (3.89 to 4.45) 2.97 (2.83 to 3.12)  Week-16 8.39 (7.81 to 9.02) 5.04 (4.81 to 5.28)  Week-32 5.02 (4.73 to 5.33) 2.52 (2.32 to 2.74)  Week-40 2.14 (1.95 to 2.35) 1.01 (0.86 to 1.19) + Systemic lupus, systemic sclerosis, Sjögren’s syndrome, vasculitis * Estimated marginal means adjusted for age and sex. Figure 1. Conclusion Humoral response to vaccination against SARS-CoV-2 was weaker in IMID patients compared to controls at all time points after the first vaccine dose and practically disappeared after 1 year. IMID patients can still achieve a good antibody response with a third dose even after a weak response with two doses. References [1]Simon D et al Nat Commun 2020 Disclosure of Interests None declared

Abstract: While MRI evaluation of joints has been primarily used to quantify inflammation at a cross-sectional and longitudinal level, less is known about the potential of MRI in distinguishing different patterns of inflammation in the various forms of arthritis. Objectives To evaluate (i) whether deep learning using neural networks can be trained to distinguish between seropositive rheumatoid arthritis (RA+), seronegative RA (RA-), and psoriatic arthritis (PsA) based on structural inflammatory patterns on hand magnetic resonance imaging and (ii) to assess if psoriasis patients with subclinical inflammation fit into such patterns. Methods ResNet 3D [1] neural networks were trained to distinguish (i) RA+ vs. PsA, (ii) RA- vs. PsA and (iii) RA+ vs. RA- with respect to hand MRI data. Diagnosis of patients was determined using the following guidelines: ACR/EULAR 2010 [2] for RA and CASPAR [3] for PsA. Results from T1 coronal, T2 coronal, T1 coronal and axial fat suppressed contrast-enhanced (CE) and T2 fat suppressed axial sequences were used. The performance of such trained networks was analyzed by the area-under-the-receiver-operating-characteristic curve (AUROC) with and without imputation of demographic and clinical parameters (Figure 1A). Additionally, the trained networks were applied to psoriasis patients without clinical signs of PsA. Figure 1. (A) Neural network combining MR sequences with optional additional clinical data. The prediction for a single case is formed by averaging the prediction of all sequences and the clinical data. (B) Plot of the AUROC for increasing percentages (0.6 – 60%) of training data for the differentiation between RA+ and PsA by the neural network. The light blue area around the dark blue mean indicates the uncertainty measured using a 5-fold cross-validation. Results MRI scans from 649 patients (135 RA-, 190 RA+, 177 PsA, 147 psoriasis) were included (Table 1). The AUROC for differentiation between disease entities was 75% (SD 3%) for RA+ vs. PsA, 74% (SD 8%) for RA- vs. PsA, and 67% (6%) for RA+ vs. RA-. All MRI sequences were relevant for classification, however, when deleting CE sequences, the loss of performance was only marginal. The addition of patient-specific data to the networks did not provide significant improvements. Increasing amounts of training data demonstrated improved performance of the networks (Figure 1B). Psoriasis patients were mostly assigned to PsA by the neural networks, suggesting that PsA-like MRI pattern may be present early in the course of psoriatic disease. Table 1. Overview of demographic and clinical information. RA+ RA - PsA Psoriasis Total Number (N) 649 Number (N) 190 135 177 147 Age (years), mean±SD 56.9±12.6 60.5±10.3 56.3±12.0 49.6±13.8 Sex (female/male) 126/64 93/42 92/85 71/76 BMI (kg/m 2 ), mean±SD 26.6±10.5 27.6 ±9.3 29.1±11.3 26.7±6.9 Disease duration (years), mean±SD 2.6±4.9 1.3±2.3 0.8±2.3 4.2±5.1 DAS28, mean±SD 3.3±1.3 3.4±1.2 3.2±1.3 - CRP (mg/L), mean±SD 0.9±2.5 0.7±1.2 0.5±0.8 0.5±1.3 HAQ, mean±SD 0.8±0.6 0.9±0.8 0.6±0.6 0.3±0.4 Medication bDMARD 88.46% 83.87% 81.32% 35.01% csDMARD 89.52% 88.89% 80.54% 12.28% Conclusion Deep learning can be successfully applied to differentiate MRI inflammatory patterns related to RA+, RA-, and PsA. Early changes in psoriasis patients can be recognized by neural networks and are characterized by a pattern that allowed the networks to classify them as PsA. References [1]Kensho Hara, Hirokatsu Kataoka, and Yutaka Satoh 2018. Can Spatiotemporal 3D CNNs Retrace the History of 2D CNNs and ImageNet? In Proceedings of the IEEE Conference on Computer Vision and Pattern Recognition (CVPR) (pp. 6546–6555). [2]Aletaha D, Neogi T et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010 Sep;62(9):2569-81. [3]Helliwell PS, Taylor WJ. Classification and diagnostic criteria for psoriatic arthritis. Annals of the Rheumatic Diseases 2005;64:ii3-ii8. Acknowledgements The study was supported by the Deutsche Forschungsgemeinschaft (DFG-FOR2886 PANDORA and the CRC1181 Checkpoints for Resolution of Inflammation). Additional funding was received by the Bundesministerium für Bildung und Forschung (BMBF; project MASCARA), the ERC Synergy grant 4D Nanoscope, the IMI funded projects HIPPOCRATES and RTCure, the Emerging Fields Initiative MIRACLE of the Friedrich-Alexander-Universität Erlangen-Nürnberg and the Else Kröner-Memorial Scholarship (DS, no. 2019_EKMS.27). Furthermore, infrastructural and hardware support was provided by the d.hip Digital Health Innovation Platform. Disclosure of Interests None declared

Abstract: We investigated associations between baseline use of immunosuppressive drugs and severity of Coronavirus Disease 2019 (COVID‐19) in autoimmune hepatitis (AIH). Patients and methods Data of AIH patients with laboratory confirmed COVID‐19 were retrospectively collected from 15 countries. The outcomes of AIH patients who were on immunosuppression at the time of COVID‐19 were compared to patients who were not on AIH medication. The clinical courses of COVID‐19 were classified as (i)‐no hospitalization, (ii)‐hospitalization without oxygen supplementation, (iii)‐hospitalization with oxygen supplementation by nasal cannula or mask, (iv)‐intensive care unit (ICU) admission with non‐invasive mechanical ventilation, (v)‐ICU admission with invasive mechanical ventilation or (vi)‐death and analysed using ordinal logistic regression. Results We included 254 AIH patients (79.5%, female) with a median age of 50 (range, 17‐85) years. At the onset of COVID‐19, 234 patients (92.1%) were on treatment with glucocorticoids (n = 156), thiopurines (n = 151), mycophenolate mofetil (n = 22) or tacrolimus (n = 16), alone or in combinations. Overall, 94 (37%) patients were hospitalized and 18 (7.1%) patients died. Use of systemic glucocorticoids (adjusted odds ratio [aOR] 4.73, 95% CI 1.12‐25.89) and thiopurines (aOR 4.78, 95% CI 1.33‐23.50) for AIH was associated with worse COVID‐19 severity, after adjusting for age‐sex, comorbidities and presence of cirrhosis. Baseline treatment with mycophenolate mofetil (aOR 3.56, 95% CI 0.76‐20.56) and tacrolimus (aOR 4.09, 95% CI 0.69‐27.00) were also associated with more severe COVID‐19 courses in a smaller subset of treated patients. Conclusion Baseline treatment with systemic glucocorticoids or thiopurines prior to the onset of COVID‐19 was significantly associated with COVID‐19 severity in patients with AIH.