Systemic lupus erythematosus after coronavirus disease-2019 (COVID-19) infection: Case-based review
TL;DR: A 38 year old Iranian woman presented with progressive icterus, pleuritic chest pain, palpitation, dyspnea, photosensitivity and arthralgia 18-days after COVID-19 symptoms proved by a positive polymerized chain reaction (PCR) as discussed by the authors.
About: This article is published in The Egyptian Rheumatologist.The article was published on 2022-04-01 and is currently open access. It has received 10 citations till now. The article focuses on the topics: Medicine & Hydroxychloroquine.
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TL;DR: In this article , the development of mast cell activation disorder (MCAS) was correlated with COVID-19 severity and the post-COVID syndrome (PCS), which is characterized by hyperactivation of mast cells with inappropriate and excessive release of chemical mediators.
Abstract: Abstract Most COVID-19 patients recovered with low mortality; however, some patients experienced long-term symptoms described as “long-COVID” or “Post-COVID syndrome” (PCS). Patients may have persisting symptoms for weeks after acute SARS-CoV-2 infection, including dyspnea, fatigue, myalgia, insomnia, cognitive and olfactory disorders. These symptoms may last for months in some patients. PCS may progress in association with the development of mast cell activation syndrome (MCAS), which is a distinct kind of mast cell activation disorder, characterized by hyper-activation of mast cells with inappropriate and excessive release of chemical mediators. COVID-19 survivors, mainly women, and patients with persistent severe fatigue for 10 weeks after recovery with a history of neuropsychiatric disorders are more prone to develop PCS. High D-dimer levels and blood urea nitrogen were observed to be risk factors associated with pulmonary dysfunction in COVID-19 survivors 3 months post-hospital discharge with the development of PCS. PCS has systemic manifestations that resolve with time with no further complications. However, the final outcomes of PCS are chiefly unknown. Persistence of inflammatory reactions, autoimmune mimicry, and reactivation of pathogens together with host microbiome alterations may contribute to the development of PCS. The deregulated release of inflammatory mediators in MCAS produces extraordinary symptoms in patients with PCS. The development of MCAS during the course of SARS-CoV-2 infection is correlated to COVID-19 severity and the development of PCS. Therefore, MCAS is treated by antihistamines, inhibition of synthesis of mediators, inhibition of mediator release, and inhibition of degranulation of mast cells.
17 citations
TL;DR: This report provides a model of COVID-19 heterogeneity with protean immune-related manifestations and a unique presentation that necessities its description, in order to provide a nidus for future studies in this new entity.
Abstract: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection may present with some systemic lupus erythematosus (SLE) manifestations intermingled with Kawasaki disease features. These emerging presentations were dubbed under the umbrella term ‘multisystem inflammatory syndrome in children (MIS-C)’. A one and half-year-old girl, admitted to Mansoura University Children’s Hospital (MUCH) with fever, bad general condition, vomiting, widespread maculopapular, vasculitic rash, hands and feet oedema, oral ulceration, arthralgia and lymphadenopathy. Moreover, bicytopenia, positive antinuclear, anti–double-stranded DNA antibodies and low C3 qualified her as a case of juvenile SLE. Despite the child received the initial therapy of immunosuppressive medication, her general condition deteriorated with fever persistence and rash exacerbation. At that time, the skin of her hands and feet started to peel. Thus, an expanded study for other alternatives was obligatory; SARS-CoV-2 infection testing revealed positive IgG serology, and retesting for lupus autoantibodies turned negative. HRCT chest showed bilateral basal consolidation with ground-glass appearance. Furthermore, Echo exhibited coronary artery dilation with thrombus inside. This evolution raised the concern for COVID-related MIS-C syndrome. This report provides a model of COVID-19 heterogeneity with protean immune-related manifestations. This case has a unique presentation that necessities its description, in order to provide a nidus for future studies in this new entity.
5 citations
TL;DR: In this paper , the frequency, clinical characteristics and outcome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in rheumatic diseases patients were investigated.
4 citations
TL;DR: In this article , the clinical manifestations, imaging findings and outcomes of corona virus disease 2019 (COVID-19) in patients with rheumatic diseases were assessed based on chest computed tomography severity score (CT-ss), the level of care, the number of patients who died and flare of underlying Rheumatic disease.
3 citations
TL;DR: In this article , the authors reported the first and unique case of new onset acute psychosis as a manifestation of lupus cerebritis following concomitant COVID-19 infection and vaccination in a previously healthy 26-year-old Tunisian female.
Abstract: Rare cases of COVID-19 infection- and vaccine-triggered autoimmune diseases have been separately reported in the literature. In this paper, we report the first and unique case of new onset acute psychosis as a manifestation of lupus cerebritis following concomitant COVID-19 infection and vaccination in a previously healthy 26-year-old Tunisian female.A 26-years old female with a family history of a mother diagnosed with schizophrenia, and no personal medical or psychiatric history, was diagnosed with mild COVID-19 infection four days after receiving the second dose of Pfizer-BioNTech COVID-19 vaccine. One month after receiving the vaccine, she presented to the psychiatric emergency department with acute psychomotor agitation, incoherent speech and total insomnia evolving for five days. She was firstly diagnosed with a brief psychotic disorder according to the DSM-5, and was prescribed risperidone (2 mg/day). On the seventh day of admission, she reported the onset of severe asthenia with dysphagia. Physical examination found fever, tachycardia, and multiple mouth ulcers. Neurological evaluation revealed a dysarthria with left hemiparesis. On laboratory tests, she had severe acute kidney failure, proteinuria, high CRP values, and pancytopenia. Immune tests identified the presence of antinuclear antibodies. Brain magnetic resonance imaging (MRI) revealed hyperintense signals in the left fronto-parietal lobes and the cerebellum. The patient was diagnosed with systemic lupus erythematosus (SLE) and put on anti-SLE drugs and antipsychotics, with a favorable evolution.The chronological relationship between COVID-19 infection, vaccination and the first lupus cerebritis manifestations is highly suggestive, albeit with no certainty, of the potential causal link. We suggest that precautionary measures should be taken to decrease the risk of SLE onset or exacerbation after COVID-19 vaccination, including a systematic COVID-19 testing before vaccination in individuals with specific predisposition.
3 citations
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Martin Aringer1, Karen H. Costenbader2, David I. Daikh3, Ralph Brinks4, Marta Mosca5, Rosalind Ramsey-Goldman6, Josef S Smolen7, David Wofsy3, Dimitrios T. Boumpas8, Diane L. Kamen9, David Jayne10, Ricard Cervera11, Nathalie Costedoat-Chalumeau, Betty Diamond12, Dafna D. Gladman13, Bevra H. Hahn14, Falk Hiepe15, Søren Jacobsen16, Dinesh Khanna17, Kirsten Lerstrøm, Elena Massarotti2, Joseph M. McCune17, Guillermo Ruiz-Irastorza18, Jorge Sanchez-Guerrero19, Matthias Schneider4, Murray B. Urowitz13, George Bertsias20, Bimba F. Hoyer15, Nicolai Leuchten1, Chiara Tani5, Sara K. Tedeschi2, Zahi Touma13, Gabriela Schmajuk3, Branimir Anić21, Florence Assan22, Tak Mao Chan23, Ann E. Clarke24, Mary K. Crow25, László Czirják26, Andrea Doria27, Winfried Graninger28, Bernadett Halda-Kiss26, Sarfaraz Hasni29, Peter M. Izmirly30, Michelle Jung24, Gábor Kumánovics26, Xavier Mariette31, Ivan Padjen21, José M. Pego-Reigosa32, Juanita Romero-Diaz, Íñigo Rúa-Figueroa Fernández, Raphaèle Seror22, Georg Stummvoll7, Yoshiya Tanaka33, Maria G Tektonidou8, Carlos Vasconcelos34, Edward M Vital35, Daniel J. Wallace36, Sule Yavuz37, Pier Luigi Meroni, Marvin J. Fritzler24, Ray Naden38, Thomas Dörner15, Sindhu R. Johnson19 •
Dresden University of Technology1, Brigham and Women's Hospital2, University of California, San Francisco3, University of Düsseldorf4, University of Pisa5, Northwestern University6, Medical University of Vienna7, National and Kapodistrian University of Athens8, Medical University of South Carolina9, University of Cambridge10, University of Barcelona11, The Feinstein Institute for Medical Research12, Toronto Western Hospital13, University of California, Los Angeles14, Humboldt University of Berlin15, Copenhagen University Hospital16, University of Michigan17, University of the Basque Country18, University Health Network19, University of Crete20, University of Zagreb21, University of Paris-Sud22, University of Hong Kong23, University of Calgary24, Hospital for Special Surgery25, University of Pécs26, University of Padua27, Medical University of Graz28, National Institutes of Health29, New York University30, Université Paris-Saclay31, University Hospital Complex Of Vigo32, University of Occupational and Environmental Health Japan33, University of Porto34, Leeds Teaching Hospitals NHS Trust35, Cedars-Sinai Medical Center36, Istanbul Bilim University37, McMaster University38
TL;DR: To develop new classification criteria for systemic lupus erythematosus (SLE) jointly supported by the European League Against Rheumatism and the American College of Rheumatology (ACR).
Abstract: Objective To develop new classification criteria for systemic lupus erythematosus (SLE) jointly supported by the European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR). Methods This international initiative had four phases. 1) Evaluation of antinuclear antibody (ANA) as an entry criterion through systematic review and meta-regression of the literature and criteria generation through an international Delphi exercise, an early patient cohort, and a patient survey. 2) Criteria reduction by Delphi and nominal group technique exercises. 3) Criteria definition and weighting based on criterion performance and on results of a multi-criteria decision analysis. 4) Refinement of weights and threshold scores in a new derivation cohort of 1,001 subjects and validation compared with previous criteria in a new validation cohort of 1,270 subjects. Results The 2019 EULAR/ACR classification criteria for SLE include positive ANA at least once as obligatory entry criterion; followed by additive weighted criteria grouped in 7 clinical (constitutional, hematologic, neuropsychiatric, mucocutaneous, serosal, musculoskeletal, renal) and 3 immunologic (antiphospholipid antibodies, complement proteins, SLE-specific antibodies) domains, and weighted from 2 to 10. Patients accumulating ≥10 points are classified. In the validation cohort, the new criteria had a sensitivity of 96.1% and specificity of 93.4%, compared with 82.8% sensitivity and 93.4% specificity of the ACR 1997 and 96.7% sensitivity and 83.7% specificity of the Systemic Lupus International Collaborating Clinics 2012 criteria. Conclusion These new classification criteria were developed using rigorous methodology with multidisciplinary and international input, and have excellent sensitivity and specificity. Use of ANA entry criterion, hierarchically clustered, and weighted criteria reflects current thinking about SLE and provides an improved foundation for SLE research.
1,018 citations
TL;DR: Surprisingly, not only the TNFR1, but also theTNFR2, was able to mediate the antiviral effects of TNF‐α in viv, whilst the antiv viral activity observed following CD40‐CD40L interaction is a newly defined function which may involve apoptosis of infected cells.
Abstract: In this review, we discuss two broad approaches we have taken to study the role of cytokines and chemokines in antiviral immunity. Firstly, recombinant vaccinia viruses were engineered to express genes encoding cytokines and chemokines of interest. Potent antiviral activity was mediated by many of these encoded factors, including IL-2, IL-12, IFN-gamma, TNF-alpha, CD40L, Mig and Crg-2. In some cases, host defense mechanisms were induced (IL-2, IL-12, Mig and Crg-2), whilst for others, a direct antiviral effect was demonstrated (IFN-gamma, TNF-alpha and CD40L). In sharp contrast, vector-directed expression of IL-4, a type 2 factor, greatly increased virus virulence, due to a downregulation of host type 1 immune responses. Our second experimental approach involved the use of strains of mice deficient for the production of particular cytokines or their receptors, often in combination with our engineered viruses. Mice deficient in either IFN-gamma, IFN-gamma R, IFN-alpha/beta R, TNFRs, CD40 or IL-6 were, in general, highly susceptible to poxvirus infection. Surprisingly, not only the TNFR1, but also the TNFR2, was able to mediate the antiviral effects of TNF-alpha in vivo, whilst the antiviral activity observed following CD40-CD40L interaction is a newly defined function which may involve apoptosis of infected cells. Through the use of perforin-deficient mice, we were able to demonstrate a requirement for this molecule in the clearance of some viruses, such as ectromelia virus, whilst for others, such as vaccinia virus, perforin was less important but IFN-gamma was essential.
266 citations
236 citations
TL;DR: There is insufficient evidence for SARS-CoV-2 infected hepatocytes or virus-related liver injury in COVID-19 at present, but the clinical, pathological and laboratory characteristics as well as underlying pathophysiology and etiology of liver injury remain largely unclear.
Abstract: An outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (2019 coronavirus disease, COVID-19) since December 2019, from Wuhan, China, has been posing a significant threat to global human health. The clinical features and outcomes of Chinese patients with COVID-19 have been widely reported. Increasing evidence has witnessed the frequent incident liver injury in COVID-19 patients, and it is often manifested as transient elevation of serum aminotransferases; however, the patients seldom have liver failure and obvious intrahepatic cholestasis, unless pre-existing advanced liver disease was present. The underlying mechanisms of liver injury in cases of COVID-19 might include psychological stress, systemic inflammation response, drug toxicity, and progression of pre-existing liver diseases. However, there is insufficient evidence for SARS-CoV-2 infected hepatocytes or virus-related liver injury in COVID-19 at present. The clinical, pathological and laboratory characteristics as well as underlying pathophysiology and etiology of liver injury in COVID-19 remain largely unclear. In this review, we highlight these important issues based on the recent developments in the field, for optimizing the management and treatment of liver injury in Chinese patients with COVID-19.
233 citations
TL;DR: A 67-year-old female presented with upper respiratory symptoms and was diagnosed with COVID-19 and found to have a large hemorrhagic pericardial effusion with echocardiographic signs of tamponade and mild left ventricular impairment.
Abstract: A 67-year-old woman presented with upper respiratory symptoms and was diagnosed with coronavirus disease-2019 (COVID-19). She was found to have a large hemorrhagic pericardial effusion wit...
149 citations