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      Characteristics of COVID-19 and Impact of Disease Activity in Patients with Adult-Onset Still’s Disease

      case-report

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          Abstract

          Introduction

          This study aimed to characterize the morbidity, hospitalization, and mortality rates among patients with adult-onset Still’s disease (AOSD) affected by coronavirus disease 2019 (COVID-19) and explore the impact of COVID-19 on the disease activity of AOSD.

          Methods

          Data on the clinical and demographic characteristics, COVID-19-related symptoms, and outcomes were retrospectively collected. Patients were stratified according to COVID-19 severity and associations between risk factors and outcomes were analyzed using multivariate logistic regression. The disease activity of patients with AOSD flares after COVID-19 was described.

          Results

          A total of 188 patients with AOSD were followed up, of whom 75.5% ( n = 142) had a confirmed or highly suspected COVID-19. Patients on medium or high-dose oral glucocorticoids or Janus kinase (JAK) inhibitors were at increased risk of developing moderate to severe COVID-19. Six patients suffered flares of AOSD following COVID-19 in a short period; however, the relapse rate was not statistically increased compared with patients without COVID-19.

          Conclusion

          Patients with AOSD receiving medium or high-dose glucocorticoid therapy or JAK inhibitors had worse COVID-19 outcomes. Further work is needed to explore risk factors affecting COVID-19 outcomes and the impact of COVID-19 on disease activity in AOSD.

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          The Role of Cytokines including Interleukin-6 in COVID-19 induced Pneumonia and Macrophage Activation Syndrome-Like Disease

          Dennis McGonagle, Kassem Sharif, Anthony O'Regan … (2020)
          Severe COVID-19 associated pneumonia patients may exhibit features of systemic hyper-inflammation designated under the umbrella term of macrophage activation syndrome (MAS) or cytokine storm, also known as secondary haemophagocytic lymphohistocytosis (sHLH). This is distinct from HLH associated with immunodeficiency states termed primary HLH -with radically different therapy strategies in both situations. COVID-19 infection with MAS typically occurs in subjects with adult respiratory distress syndrome (ARDS) and historically, non-survival in ARDS was linked to sustained IL-6 and IL-1 elevation. We provide a model for the classification of MAS to stratify the MAS-like presentation in COVID-19 pneumonia and explore the complexities of discerning ARDS from MAS. We discuss the potential impact of timing of anti-cytokine therapy on viral clearance and the impact of such therapy on intra-pulmonary macrophage activation and emergent pulmonary vascular disease.
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            Characteristics associated with hospitalisation for COVID-19 in people with rheumatic disease: data from the COVID-19 Global Rheumatology Alliance physician-reported registry

            Milena Gianfrancesco, Kimme L Hyrich, Sarah Al-Adely … (2020)
            Objectives COVID-19 outcomes in people with rheumatic diseases remain poorly understood. The aim was to examine demographic and clinical factors associated with COVID-19 hospitalisation status in people with rheumatic disease. Methods Case series of individuals with rheumatic disease and COVID-19 from the COVID-19 Global Rheumatology Alliance registry: 24 March 2020 to 20 April 2020. Multivariable logistic regression was used to estimate ORs and 95% CIs of hospitalisation. Age, sex, smoking status, rheumatic disease diagnosis, comorbidities and rheumatic disease medications taken immediately prior to infection were analysed. Results A total of 600 cases from 40 countries were included. Nearly half of the cases were hospitalised (277, 46%) and 55 (9%) died. In multivariable-adjusted models, prednisone dose ≥10 mg/day was associated with higher odds of hospitalisation (OR 2.05, 95% CI 1.06 to 3.96). Use of conventional disease-modifying antirheumatic drug (DMARD) alone or in combination with biologics/Janus Kinase inhibitors was not associated with hospitalisation (OR 1.23, 95% CI 0.70 to 2.17 and OR 0.74, 95% CI 0.37 to 1.46, respectively). Non-steroidal anti-inflammatory drug (NSAID) use was not associated with hospitalisation status (OR 0.64, 95% CI 0.39 to 1.06). Tumour necrosis factor inhibitor (anti-TNF) use was associated with a reduced odds of hospitalisation (OR 0.40, 95% CI 0.19 to 0.81), while no association with antimalarial use (OR 0.94, 95% CI 0.57 to 1.57) was observed. Conclusions We found that glucocorticoid exposure of ≥10 mg/day is associated with a higher odds of hospitalisation and anti-TNF with a decreased odds of hospitalisation in patients with rheumatic disease. Neither exposure to DMARDs nor NSAIDs were associated with increased odds of hospitalisation.
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              Inflammasome activation in infected macrophages drives COVID-19 pathology

              Esen Sefik, Rihao Qu, Caroline Junqueira … (2022)
              Severe COVID-19 is characterized by persistent lung inflammation, inflammatory cytokine production, viral RNA, and sustained interferon (IFN) response all of which are recapitulated and required for pathology in the SARS-CoV-2 infected MISTRG6-hACE2 humanized mouse model of COVID-19 with a human immune system 1 – 20 . Blocking either viral replication with Remdesivir 21 – 23 or the downstream IFN stimulated cascade with anti-IFNAR2 in vivo in the chronic stages of disease attenuated the overactive immune-inflammatory response, especially inflammatory macrophages. Here, we show SARS-CoV-2 infection and replication in lung-resident human macrophages is a critical driver of disease. In response to infection mediated by CD16 and ACE2 receptors, human macrophages activate inflammasomes, release IL-1 and IL-18 and undergo pyroptosis thereby contributing to the hyperinflammatory state of the lungs. Inflammasome activation and its accompanying inflammatory response is necessary for lung inflammation, as inhibition of the NLRP3 inflammasome pathway reverses chronic lung pathology. Remarkably, this same blockade of inflammasome activation leads to the release of infectious virus by the infected macrophages. Thus, inflammasomes oppose host infection by SARS-CoV-2 by production of inflammatory cytokines and suicide by pyroptosis to prevent a productive viral cycle.
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                Author and article information

                Contributors
                Huihui Chi:
                ORCID: http://orcid.org/0000-0001-9587-1180
                chh_210@126.com
                Journal
                Journal ID (nlm-ta): Rheumatol Ther
                Journal ID (iso-abbrev): Rheumatol Ther
                Title: Rheumatology and Therapy
                Publisher: Springer Healthcare (Cheshire )
                ISSN (Print): 2198-6576
                ISSN (Electronic): 2198-6584
                Publication date (Electronic): 6 January 2024
                Publication date PMC-release: 6 January 2024
                Publication date Collection: February 2024
                Volume: 11
                Issue: 1
                Pages: 201-212
                Affiliations
                [1 ]GRID grid.412277.5, ISNI 0000 0004 1760 6738, Department of Rheumatology and Immunology, , Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, ; No. 197 Ruijin Second Road, Shanghai, 200025 China
                [2 ]GRID grid.412277.5, ISNI 0000 0004 1760 6738, Department of General Medicine, , Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, ; Shanghai, China
                Author information
                http://orcid.org/0000-0001-9587-1180
                Article
                Publisher ID: 632
                DOI: 10.1007/s40744-023-00632-3
                PMC ID: 10796879
                PubMed ID: 38183598
                SO-VID: c8aded87-0785-4894-86f9-40ea5d08806d
                Copyright © © The Author(s) 2024
                License:

                Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

                History
                Date received : 16 October 2023
                Date accepted : 11 December 2023
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 82101883
                Award Recipient :
                Funded by: Natural Science Foundation of Shanghai
                Award ID: 23ZR1440100
                Award Recipient :
                Funded by: Shanghai Sailing Program
                Award ID: 21YF1426300
                Award Recipient :
                Categories
                Subject: Brief Report
                Custom metadata
                issue-copyright-statement © Springer Healthcare Ltd., part of Springer Nature 2024

                Keywords: adult-onset still’s disease,covid-19,glucocorticoids,jak inhibitors
                Data availability:
                Keywords: adult-onset still’s disease, covid-19, glucocorticoids, jak inhibitors

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