Matches in SemOpenAlex for { <https://semopenalex.org/work/W3028971294> ?p ?o ?g. }
- W3028971294 endingPage "722" @default.
- W3028971294 startingPage "717" @default.
- W3028971294 abstract "The outbreak of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in China in December 2019. This disease now affects the whole world. Patients with rheumatic diseases are at higher risk of respiratory infections including influenza and pneumococcal pneumonia, which is attributed to the underlying disease, comorbidities and immunosuppressive therapy,1 but to date we lack good information about the virus SARS-CoV-2. Nonetheless, immunosuppressive treatments are essential to control disease activity and prevent functional deterioration in these patients. Rheumatologists need to be vigilant in preventing rheumatic disease patients from contracting the disease during this pandemic, especially patients with chronic lung problems (eg scleroderma with lung fibrosis) and chronic kidney disease (eg lupus nephritis) and those on high-dose glucocorticoids and immunosuppressants (Appendix 1). In the desperate search to find effective treatments for COVID-19, drugs largely used by rheumatologists have entered the spotlight, including the caution against use of non-steroidal anti-inflammatory drugs (NSAIDs), the potential of antimalarials and biologic disease-modifying anti-rheumatic drugs (bDMARDs), for example anti-interleukin-6 (IL-6) and targeted synthetic DMARDS (tsDMARDs) Janus-activated kinase (JAK) inhibitors to manage cytokine storm syndrome (CSS)/cytokine release syndrome associated with COVID-19. Here, we try to provide guidance regarding clinical decision-making both for patients with COVID-19 and those with rheumatic diseases, and strategies to mitigate further harm to these patients. An Asia-Pacific League Against Rheumatism (APLAR) COVID-19 task force comprising rheumatologists from 9 Asia-Pacific countries was convened on 31 March, 2020. A set of guidance statements was developed and refined based on best available evidence up to 26 April, 2020 and expert opinion. Given the overall limited nature of the data, a systematic review was not performed. The final guidance statements integrate both the task force members' assessment of the evidence quality and the ratio of risk and benefit from the treatment or action. We assert that the key guiding principle should be to “first do no harm,” especially given the unknown efficacy of proposed DMARDs and biologics and their established potential harms. This guidance document has been reviewed and endorsed by the APLAR executive committee and the APLAR scientific committee chairpersons. In the absence of a vaccine or a therapeutic agent, a “mitigation approach”, including “social distancing”, frequent hand washing and quarantining strategies are the primary interventions to hamper the spread of infection.2 Another approach, known as “suppression strategies” includes strict lockdown measures – social distancing in entire populations, the closure of schools and community spaces, aggressive case finding and contact tracing, have succeeded in maintaining low case counts of COVID-19. During this extraordinary time, the rheumatology community faces unprecedented challenges as care could be postponed/delayed or handled through virtual care to minimize contact exposure and to practice social distancing. Comorbid conditions are common in patients with COVID-19.3 Smoking can cause an increase in the release of IL-6 in bronchial epithelial cells,4 and upregulate angiotensin-converting enzyme-2 (ACE2) receptors, the known receptor for SARS-CoV.5 This is particularly relevant as some of the Asia-Pacific countries, for example China, has a high male smoking rate.6 Globally the quality of evaluation, monitoring and treatment of comorbidities in rheumatic disease patients is variable with considerable scope for improvement.7 Rheumatologists should be vigilant in assessing and managing comorbidities not only to improve morbidity and mortality, but hopefully to minimize risk of COVID-19 in rheumatic disease patients. In patients with acute respiratory tract infections, short-term use of NSAIDs are associated with increased risk of cardiovascular events and nephrotoxicity,8-10 higher rates of complications, and delays in the prescription of effective antibiotic treatment.11 Despite the lack of evidence relating specifically to people with COVID-19, regular NSAID use should not be recommended as the first line option for managing the symptoms of COVID-19.12 Nonetheless, arthritis patients taking NSAIDs for symptomatic relief should continue their treatment as needed. Epidemiologic studies have identified advanced age, male gender and presence of comorbidities (hypertension, obesity, diabetes, coronary heart disease, chronic obstructive lung disease and chronic kidney disease) as poor prognostic factors for COVID-19.13 Despite the lack of data on the true prevalence and risk of COVID-19 in rheumatic disease patients, immunosuppressed status (the use of chemotherapy or conditions requiring immunosuppressive treatment) was not reported to be a risk factor and risk for adverse outcome. One patient with systemic sclerosis-associated interstitial lung disease (SSC-ILD) on tocilizumab and 7 patients on bDMARDs or tsDMARDs who developed COVID-19 recovered uneventfully.14-16 Nonetheless, at least 2 patients on rituximab17 developed respiratory failure and 1 of them died despite treatment with tocilizumab.18 In order to gather real-world data to inform treatment strategies and better characterize individuals at increased risk of infection, the COVID-19 Global Rheumatology Alliance has successfully developed online portals and case report forms to enable healthcare providers around the world to enter information on individuals with rheumatic disease who have been diagnosed with COVID-19, with clinical data of the first 110 patients published.19 For now, patients with stable rheumatic diseases should continue their treatment. In case of infection (including COVID-19), treatment of infection gains precedence and immunosuppressive treatment may be de-escalated or temporarily withheld in consultation with the treating rheumatologist (Appendix 1). Acute lung injury and acute respiratory distress syndrome (ARDS) are partly caused by host immune responses. Severe COVID-19-associated pneumonia patients may exhibit features of systemic hyper-inflammation or CSS. COVID-19 infection with CSS typically occurs in subjects with ARDS and historically, non-survival in ARDS was linked to sustained IL-6 and IL-1 elevation.20 Corticosteroids suppress lung inflammation but also inhibit immune responses and pathogen clearance. The effectiveness of adjunctive glucocorticoid therapy in the management of COVID-19 infected patients remains controversial.21, 22 Until results from ongoing randomized-controlled trials are available, the World Health Organization (WHO) has advised against routine use of systemic corticosteroids for treatment of viral pneumonia outside of clinical trials unless they were indicated for other reasons (eg septic shock) (Appendix 2). In rheumatic disease patients on long-term steroids, it is very important to remind them not to stop their prednisone even if they develop symptoms suggestive of COVID-19 (Appendix 1). For patients with active rheumatic disease, after excluding concurrent active infection, the prednisone dose could be increased carefully according to the severity of the organ manifestation, in spite of the risk of COVID-19. Preclinical and limited clinical data suggested that hydroxychloroquine (HCQ) and chloroquine (CLQ) have antiviral activities against SARS-CoV-2.23-25 In contrast, a small but randomized study from China in patients with mild to moderate COVID-19 treated with HCQ or placebo found no difference in recovery rates,26 and French investigators failed to confirm antiviral activity or clinical benefit of the HCQ and azithromycin combination in 11 hospitalized patients with severe COVID-19.27 In a French series of 17 systemic lupus erythematosus (SLE) patients with COVID-19 on long-term HCQ, 11 (65%) and 5 (29%) developed respiratory failure and ARDS respectively despite having blood HCQ concentrations within the therapeutic range for the management of SLE.28 Whether blood HCQ concentrations may be effective for the antiviral activity against SARS-CoV-2 remained uncertain. Nonetheless, data from this study suggest that HCQ may not be able to prevent severe COVID-19 in these patients. The US Food and Drug Administration (FDA) cautioned against use of HCQ or CLQ for COVID-19 outside of the hospital setting or a clinical trial due to risk of heart rhythm problems (Appendix 2). The APLAR task force agreed there are insufficient clinical data to recommend either for or against HCQ or CLQ for COVID-19, and clinicians should monitor patients for adverse effects, especially prolonged QTc interval. Health authorities should ensure adequate supply of these drugs since the HCQ shortage not only will limit availability to patients with COVID-19 if efficacy is truly established but also represents a real risk to patients with rheumatic diseases. On the other hand, rheumatologists should remind patients to continue HCQ and not to taper the dosage even if they develop symptoms suggestive of COVID-19 and reassurance should be given that this drug should not increase their risk of infection. Once hospitalized, for some patients with COVID-19, death can occur within a few days, many with ARDS, and some with multi-organ dysfunction syndrome.14 In those critically ill patients, there are both clinical signs and symptoms, as well as laboratory abnormalities, that suggest a CSS is occurring in response to the viral infection. According to data from the Chinese cohorts, patients with severe disease and requiring intensive care often show leucopenia, lymphopenia, significantly higher levels of C-reactive protein (CRP), IL-6, IL-10, and tumor necrosis factor-α (TNF-α).29 In this setting, biologic drugs selectively blocking inflammatory cytokines, such as TNF-α inhibitors, anti-IL-6, anti-IL-1 and JAK inhibitors are currently employed in the treatment of severe cases of COVID-19 in an experimental manner or undergoing clinical trials (Appendix 2). Tocilizumab, has been shown effective in treating CSS, a common complication of chimeric antigen receptor-T cell therapy used for treating refractory acute lymphoblastic leukemia30 and may be effective in Chinese COVID-19 patients with severe and critical disease.31 Anti-IL-6R antibody is currently included in the treatment recommendation for Chinese COVID-19 patients (Appendix 2). These concepts have led to interests in JAK inhibitors, for example baricitinib, as potential treatments for CSS complicated with severe COVID-19. ACE2 is a cell-surface protein widely existing on cells in the heart, kidney, blood vessels, especially alveolar epithelial cells. SARS-CoV-2 was believed to invade and enter lung cells through ACE2-mediated endocytosis. One of the known regulators of endocytosis is the AP2-associated protein kinase 1 (AAK1). AAK1 inhibitors can interrupt the passage of the virus into cells and can be helpful in preventing virus infections. Baricitinib, apart from being a JAK inhibitor, is also an AAK1 inhibitor. Baricitinib was thought to be a possible candidate for treatment of COVID-19, considering its relative safety and high affinity.32 On the other hand, JAK–STAT (signal transducer and activator of transcription) signal blocking by baricitinib produces an impairment of interferon-mediated antiviral response, with a potential facilitating effect on the evolution of SARS-CoV-2 infection, and therefore may not be a suitable treatment.33 While we are waiting for the results from the control trials to resolve this controversy, rheumatologists should be particularly cautious of serious infectious events on the use of this agent, in particular viral infection, for example herpes zoster. Rheumatologists worldwide are trying new strategies to optimize care for rheumatic disease patients during this unprecedented COVID-19 pandemic. Concerted efforts from healthcare providers in different healthcare systems are required to continue clinical assessments and ensure adequate supply of immunosuppressive therapy. Worsening of rheumatic disease may induce a systemic inflammatory state which may represent an adjunctive risk factor for major susceptibility to viral infection. On the other hand, rheumatologists are cautiously enthusiastic that a variety of immune-modulating drugs and targeted cytokine inhibitors available for rheumatic disease patients may also benefit patients as prophylaxis for COVID-19 or with COVID-19-induced CSS. Because of insufficient data, APLAR could not recommend any specific treatments for patients with COVID-19. Nevertheless, rheumatologists/immunologists are expert in the use of these agents and we should be to the forefront in advising around their application, noting risks and benefits are not yet clear and should not be taken for granted in COVID-19. We emphasize the ongoing importance of critical review of emerging literature to inform current and future treatment decisions. International registries have been created to collect data on rheumatic patients with COVID-19. Ultimately, time and these registries will tell what the right decision is regarding maintaining current therapy for patients with rheumatic diseases. The APLAR task force will respond quickly and efficiently to place the evidence base behind our recommendations and update them should new findings emerge from clinical trials. aConcerning glucocorticoids, immunosuppressants, csDAMRDs, bDMARDs and JAK inhibitors, the balance of safety and efficacy in viral infection as well as pulmonary inflammation remains unclear. Taylor & Francis: https://taylorandfrancis.com/coronavirus/ Elsevier: https://www.elsevier.com/connect/coronavirus-information-center Wiley: https://novel-coronavirus.onlinelibrary.wiley.com/ Springer Nature: https://www.springernature.com/jp/researchers/campaigns/coronavirus/coronavirus-further-articles Oxford University Press: https://academic.oup.com/journals/pages/coronavirus?cc=us&lang=en& BMJ: https://www.bmj.com/coronavirus New England Journal of Medicine: https://www.nejm.org/coronavirus The Lancet: https://www.thelancet.com/coronavirus European League Against Rheumatism (EULAR) guidance for patients on COVID 19: https://www.eular.org/eular_guidance_for_patients_covid19_outbreak.cfm American College of Rheumatology (ACR): https://www.rheumatology.org/announcements World Health Organization (WHO): Coronavirus disease (COVID-19) outbreak German Society for Rheumatology - Patient section. (German only): Deutsche Gesellschaft für Rheumatologie - Patienten Bereich British Society for Rheumatology guidance for rheumatologists: https://www.rheumatology.org.uk/news-policy/details/covid19-coronavirus-update-members Shielding policy in UK: https://www.gov.uk/government/publications/guidance-on-shielding-and-protecting-extremely-vulnerable-persons-from-covid-19/guidance-on-shielding-and-protecting-extremely-vulnerable-persons-from-covid-19) National Rheumatoid Arthritis Society: Coronavirus: What we know so far. https://www.nras.org.uk/coronavirus. Medical Council of India: Telemedicine Practice Guidelines - Ministry of Health and Family WHO clinical management of severe acute respiratory infection (SARI) when COVID-19 disease is suspected: https://www.who.int/publications-detail/clinical-management-of-severe-acute-respiratory-infection-when-novel-coronavirus-(ncov)-infection-is-suspected National Institute of Health treatment guideline https://covid19treatmentguidelines.nih.gov/introduction/ US Food and Drug Administration (FDA) cautions against the use of antimalarial agents outside hospital setting or clinical trial: https://www.fda.gov/drugs/drug-safety-and-availability/fda-cautions-against-use-hydroxychloroquine-or-chloroquine-covid-19-outside-hospital-setting-or Treatment recommendation for Chinese COVID-19 patients: http://kjfy.meetingchina.org/msite/news/show/cn/3337.html The Australasian Society of Clinical Immunology and Allergy (ASCIA) positional statement: https://www.allergy.org.au/hp/papers Clinicaltrial.gov: https://clinicaltrials.gov/ct2/results?cond=COVID-19 Hydroxychloroquine as post-exposure prophylaxis: https://clinicaltrials.gov/ct2/show/NCT04308668 Hydroxychloroquine for the Treatment of Patients with Mild to Moderate COVID-19 to Prevent Progression to Severe Infection or Death: https://clinicaltrials.gov/ct2/show/NCT04323631?cond=COVID-19&draw=4&rank=21 Tocilizumab: https://clinicaltrials.gov/ct2/show/NCT04317092?cond=COVID-19&draw=2&rank=10 Sarilumab: https://clinicaltrials.gov/ct2/show/NCT04315298?cond=COVID-19&draw=3&rank=12 Baricitinib: https://www.clinicaltrials.gov/ct2/show/NCT04320277 https://clinicaltrials.gov/ct2/show/NCT04321993?cond=COVID-19&draw=2&rank=18 The COVID-19 Global Rheumatology Alliance: https://rheum-covid.org/ EULAR: https://www.eular.org/eular_covid19_database.cfm" @default.
- W3028971294 created "2020-06-05" @default.
- W3028971294 creator A5001540288 @default.
- W3028971294 creator A5005417867 @default.
- W3028971294 creator A5013144482 @default.
- W3028971294 creator A5015953107 @default.
- W3028971294 creator A5022591267 @default.
- W3028971294 creator A5036051895 @default.
- W3028971294 creator A5059300419 @default.
- W3028971294 creator A5062983264 @default.
- W3028971294 creator A5065412132 @default.
- W3028971294 creator A5072385805 @default.
- W3028971294 creator A5075284186 @default.
- W3028971294 creator A5086410909 @default.
- W3028971294 date "2020-05-27" @default.
- W3028971294 modified "2023-10-18" @default.
- W3028971294 title "Care for patients with rheumatic diseases during COVID‐19 pandemic: A position statement from APLAR" @default.
- W3028971294 cites W2102746921 @default.
- W3028971294 cites W2583291982 @default.
- W3028971294 cites W2727983289 @default.
- W3028971294 cites W2741315312 @default.
- W3028971294 cites W2792497289 @default.
- W3028971294 cites W2799298609 @default.
- W3028971294 cites W2948453538 @default.
- W3028971294 cites W2974826704 @default.
- W3028971294 cites W2978519000 @default.
- W3028971294 cites W3004919484 @default.
- W3028971294 cites W3005212621 @default.
- W3028971294 cites W3005403371 @default.
- W3028971294 cites W3009567932 @default.
- W3028971294 cites W3010673910 @default.
- W3028971294 cites W3010930696 @default.
- W3028971294 cites W3010992334 @default.
- W3028971294 cites W3011260630 @default.
- W3028971294 cites W3012809680 @default.
- W3028971294 cites W3013025026 @default.
- W3028971294 cites W3013702546 @default.
- W3028971294 cites W3013899502 @default.
- W3028971294 cites W3014003872 @default.
- W3028971294 cites W3014270994 @default.
- W3028971294 cites W3014663601 @default.
- W3028971294 cites W3014972620 @default.
- W3028971294 cites W3015018920 @default.
- W3028971294 cites W3016350662 @default.
- W3028971294 cites W3016647362 @default.
- W3028971294 cites W3019517138 @default.
- W3028971294 cites W3020403921 @default.
- W3028971294 cites W3020578654 @default.
- W3028971294 cites W3022970339 @default.
- W3028971294 cites W3028971294 @default.
- W3028971294 cites W3165656738 @default.
- W3028971294 doi "https://doi.org/10.1111/1756-185x.13863" @default.
- W3028971294 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7283887" @default.
- W3028971294 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32462761" @default.
- W3028971294 hasPublicationYear "2020" @default.
- W3028971294 type Work @default.
- W3028971294 sameAs 3028971294 @default.
- W3028971294 citedByCount "21" @default.
- W3028971294 countsByYear W30289712942020 @default.
- W3028971294 countsByYear W30289712942021 @default.
- W3028971294 countsByYear W30289712942022 @default.
- W3028971294 countsByYear W30289712942023 @default.
- W3028971294 crossrefType "journal-article" @default.
- W3028971294 hasAuthorship W3028971294A5001540288 @default.
- W3028971294 hasAuthorship W3028971294A5005417867 @default.
- W3028971294 hasAuthorship W3028971294A5013144482 @default.
- W3028971294 hasAuthorship W3028971294A5015953107 @default.
- W3028971294 hasAuthorship W3028971294A5022591267 @default.
- W3028971294 hasAuthorship W3028971294A5036051895 @default.
- W3028971294 hasAuthorship W3028971294A5059300419 @default.
- W3028971294 hasAuthorship W3028971294A5062983264 @default.
- W3028971294 hasAuthorship W3028971294A5065412132 @default.
- W3028971294 hasAuthorship W3028971294A5072385805 @default.
- W3028971294 hasAuthorship W3028971294A5075284186 @default.
- W3028971294 hasAuthorship W3028971294A5086410909 @default.
- W3028971294 hasBestOaLocation W30289712941 @default.
- W3028971294 hasConcept C116675565 @default.
- W3028971294 hasConcept C126322002 @default.
- W3028971294 hasConcept C159047783 @default.
- W3028971294 hasConcept C17744445 @default.
- W3028971294 hasConcept C177713679 @default.
- W3028971294 hasConcept C199539241 @default.
- W3028971294 hasConcept C2777026412 @default.
- W3028971294 hasConcept C2778137277 @default.
- W3028971294 hasConcept C2779134260 @default.
- W3028971294 hasConcept C2779473830 @default.
- W3028971294 hasConcept C2909376813 @default.
- W3028971294 hasConcept C2994133304 @default.
- W3028971294 hasConcept C3006700255 @default.
- W3028971294 hasConcept C3007834351 @default.
- W3028971294 hasConcept C3008058167 @default.
- W3028971294 hasConcept C512399662 @default.
- W3028971294 hasConcept C524204448 @default.
- W3028971294 hasConcept C71924100 @default.
- W3028971294 hasConcept C89623803 @default.
- W3028971294 hasConceptScore W3028971294C116675565 @default.
- W3028971294 hasConceptScore W3028971294C126322002 @default.
- W3028971294 hasConceptScore W3028971294C159047783 @default.