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Aortitis is an over-arching term used to describe inflammation of the aortic wall. It can lead to serious complications such as aneurysm formation, dissection and aortic rupture. Due to its rarity and variability of presentation, diagnosis and management can be challenging. We present a case of a patient who presented with inflammatory aortitis of the paravisceral aorta with pseudoaneurysm formation and proximal superior mesenteric artery thrombosis resulting in acute on chronic mesenteric ischemia. Complex operative fixation using two chimney grafts and one periscope graft, combined with hepatorenal bypass successfully excluded the pseudoaneurysms. The inflammatory aortitis resolved with a short course of high dose steroids. This report highlights the role of hybrid open and endovascular techniques to treat challenging aortic pathology.

Background: Rheumatoid arthritis has been associated with severe COVID-19, but few studies have investigated how phenotypes of rheumatoid arthritis affect these associations. We aimed to investigate the associations between rheumatoid arthritis and phenotypes of interstitial lung disease, serostatus, and bone erosions with COVID-19 severity., Methods: We did a retrospective, comparative, multicentre cohort study at two large health-care systems (Mayo Clinic [19 hospitals and affiliated outpatient centres] and Mass General Brigham [14 hospitals and affiliated outpatient centres]) in the USA. Consecutive patients with rheumatoid arthritis meeting the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria and who had COVID-19 between March 1, 2020, and June 6, 2021, were matched 1:5 on age, sex, and calendar date with patients without rheumatoid arthritis (comparators). Data were received from electronic health records from Mayo Clinic and Mass General Brigham. We examined subgroups of patients with rheumatoid arthritis by phenotypic features: rheumatoid arthritis-associated interstitial lung disease, seropositivity (for anti-cyclic citrullinated peptide, rheumatoid factor, or both), and bone erosions. Severe COVID-19 was a composite of hospitalisation or death. We used Cox regression to estimate hazard ratios (HR) for severe COVID-19, comparing rheumatoid arthritis and subgroups to the comparator group., Findings: We identified 582 patients with rheumatoid arthritis and 2875 matched comparators, all of whom had COVID-19 within the study dates. The mean age of those with rheumatoid arthritis was 62 [SD 14] years, 421 (72%) of 582 were women and 161 (28%) were men, 457 (79%) were White, 65 (11%) were Hispanic or Latino, and 41 (7%) were Black. Among patients with rheumatoid arthritis, 50 (9%) of 582 had interstitial lung disease, 388 (68%) of 568 were seropositive, and 159 (27%) of 582 had bone erosions. Severe COVID-19 occurred in 126 (22%) of 582 patients with rheumatoid arthritis versus 363 (13%) 2875 in the comparator group. Patients with rheumatoid arthritis had an HR of 1·75 (95% CI 1·45-2·10) for severe COVID-19 versus the comparator group. Patients with rheumatoid arthritis-associated interstitial lung disease had an HR of 2·50 (1·66-3·77) versus the comparator group for severe COVID-19. The risk for severe COVID-19 was also higher in patients with rheumatoid arthritis who were seropositive (HR 1·97 [95% CI 1·58-2·46]) or had erosive disease (1·93 [1·41-2·63]) than for those in the comparator group., Interpretation: Patients with rheumatoid arthritis have an increased risk of severe COVID-19 across phenotypic subgroups, especially among patients with interstitial lung disease. These findings suggest that rheumatoid arthritis with interstitial lung disease, or its treatment, might be a substantial contributor to severe COVID-19 outcomes for patients with rheumatoid arthritis., Funding: None., Competing Interests: NJP reports consulting fees from FVC Health, unrelated to this work; and is supported by the US National Institutes of Health Ruth L Kirschstein Institutional National Research Service Award (T32-AR-007258). JAS has received research support from Bristol Myers Squibb; consulted for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Optum, and Pfizer, unrelated to this work; and is supported by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR077607, P30 AR070253, and P30 AR072577) and the R Bruce and Joan M Mickey Research Scholar Fund. ZSW reports research support from Bristol-Myers Squibb and Principia/Sanofi; consulting fees from Viela Bio, Horizon, Zenas Biopharma, Shionogi, Sanofi, and MedPace, unrelated to this work; and is supported by the US National Institute of Arthritis and Musculoskeletal and Skin Diseases (K23AR073334 and R03AR078938), the Rheumatology Research Foundation, and Massachusetts General Hospital Department of Medicine. AD-G has received unrelated grant funding from the US Centers for Disease Control and Prevention, the Rheumatology Research Foundation Career Development Award, and the Robert D and Patricia E Kern Center for the Science of Health Care Delivery. All other authors have no competing interests. The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard University, its affiliated academic health-care centres, or the US National Institutes of Health., (© 2022 Elsevier Ltd. All rights reserved.)