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Social media has become an important venue for rheumatologists, patients, organizations, and other stakeholders to discuss recent research advances in diagnosis and management of rheumatic disorders. In this article, we describe the current state of how social media may enhance dissemination, discourse, and collaboration in rheumatology research. Social media may refer to social platforms like Twitter and Instagram or digital media like podcasts and other websites that are operated for providing as free, open-access medical education (FOAM). Twitter has been one of the most active social media venues and continues to host a vibrant rheumatology community. Examples of research discussions on Twitter include organic user tweets, educational threads (“tweetorials”), live-tweeting academic conferences, and journals posting recently-accepted articles. Some research collaborations have been initiated through social media interactions. Social media may also directly contribute to research by facilitating the recruitment of study participants and the collection of survey-based data. Thus, social media is an evolving and important tool to enhance research discourse, dissemination, and collaboration in rheumatology.

Highlights • This scoping review provides an up-to-date overview of published evidence regarding the frequency and severity of acute viral respiratory AEs related to antirheumatic disease therapies. • Glucocorticoid use was associated with a higher frequency of acute upper and lower respiratory viral events. • Mild viral respiratory infections occurred more frequently in several studies in which patients were treated with JAKi, most notably at higher doses. • TNFi and IL-17 inhibitors seemed to be associated with higher frequency of mild viral respiratory infections such as URTI and nasopharyngitis. • Our review identifies a knowledge gap for most antirheumatic medications and their acute respiratory viral complications; in the context of the COVID-19 pandemic, increased widespread respiratory viral PCR testing offers immediate research opportunities to clarify the safety of antirheumatic therapies in terms of viral respiratory complications., Introduction COVID-19 is an acute respiratory viral infection that threatens people worldwide, including people with rheumatic disease, although it remains unclear to what extent various antirheumatic disease therapies increase susceptibility to complications of viral respiratory infections. Objective The present study undertakes a scoping review of available evidence regarding the frequency and severity of acute respiratory viral adverse events related to antirheumatic disease therapies. Methods Online databases were used to identify, since database inception, studies reporting primary data on acute respiratory viral infections in patients utilizing antirheumatic disease therapies. Independent reviewer pairs charted data from eligible studies using a standardized data abstraction tool. Results A total of 180 studies were eligible for qualitative analysis. While acknowledging that the extant literature has a lack of specificity in reporting of acute viral infections or complications thereof, the data suggest that use of glucocorticoids, JAK inhibitors (especially high-dose), TNF inhibitors, and anti-IL-17 agents may be associated with an increased frequency of respiratory viral events. Available data suggest no increased frequency or risk of respiratory viral events with NSAIDs, hydroxychloroquine, sulfasalazine, methotrexate, azathioprine, mycophenolate mofetil, cyclophosphamide, or apremilast. One large cohort study demonstrated an association with leflunomide use and increased risk of acute viral respiratory events compared to non-use. Conclusion This scoping review identified that some medication classes may confer increased risk of acute respiratory viral infections. However, definitive data are lacking and future studies should address this knowledge gap.

The relative risk of SARS-CoV-2 infection and COVID-19 disease severity among people with rheumatic and musculoskeletal diseases (RMDs) compared to those without RMDs is unclear. This study was undertaken to quantify the risk of SARS-CoV-2 infection in those with RMDs and describe clinical outcomes of COVID-19 in these patients.We conducted a systematic literature review using 14 databases from January 1, 2019 to February 13, 2021. We included observational studies and experimental trials in RMD patients that described comparative rates of SARS-CoV-2 infection, hospitalization, oxygen supplementation/intensive care unit (ICU) admission/mechanical ventilation, or death attributed to COVID-19. Methodologic quality was evaluated using the Joanna Briggs Institute critical appraisal tools or the Newcastle-Ottawa scale. Risk ratios (RRs) and odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated, as applicable for each outcome, using the Mantel-Haenszel formula with random effects models.Of the 5,799 abstracts screened, 100 studies met the criteria for inclusion in the systematic review, and 54 of 100 had a low risk of bias. Among the studies included in the meta-analyses, we identified an increased prevalence of SARS-CoV-2 infection in patients with an RMD (RR 1.53 [95% CI 1.16-2.01]) compared to the general population. The odds of hospitalization, ICU admission, and mechanical ventilation were similar in patients with and those without an RMD, whereas the mortality rate was increased in patients with RMDs (OR 1.74 [95% CI 1.08-2.80]). In a smaller number of studies, the adjusted risk of outcomes related to COVID-19 was assessed, and the results varied; some studies demonstrated an increased risk while other studies showed no difference in risk in patients with an RMD compared to those without an RMD.Patients with RMDs have higher rates of SARS-CoV-2 infection and an increased mortality rate.

As of the end of March 2020, the covid-19 pandemic has resulted in over 850 000 confirmed cases and an estimated 42 000 deaths worldwide.1 All agree that safe and effective therapies for treatment and prevention are urgently needed. In the midst of this rapidly progressing crisis, evidence has emerged suggesting that antimalarial medications, such as hydroxychloroquine (HCQ), may be efficacious for covid-19 treatment. After amplification from politicians, news outlets and social media, a rush to acquire supplies of HCQ resulted in worldwide shortages. Recent government policies may have exacerbated these issues, where wider use in both covid-19 treatment and prevention were authorised or recommended by India, the US Food and Drug Administration and other countries.2–4 In response to dwindling supplies, several US states have issued restrictions on HCQ use including limiting dispensation quantities and verifying indications.5–8 Rheumatologists, researchers and patient partners must advocate for the appropriate distribution and use of HCQ, as millions of people with rheumatic diseases worldwide depend on HCQ to control disease activity and maintain quality of life. In doing so, we must also remind ourselves to ‘make haste slowly’ ( festina lente ). Emanuel et al 9 published a well-timed commentary suggesting the following principles for fairly allocating scarce resources during the covid-19 crisis: equal treatment, attempts to maximise benefits and prioritising the most vulnerable. These recommendations echo prior guidance published in 2016 by the WHO on how to address future infectious disease outbreaks.10 The report cautioned that ‘special attention should be given to ensuring that persons who face heightened susceptibility to harm or injustice during infectious disease outbreaks are able to contribute to decisions about infectious disease outbreak planning and response’. This ethical framework offers health systems a structure for approaching the use and distribution of HCQ during the covid-19 pandemic to minimise …

Trauma remains a major cause of death throughout the world, especially for patients younger than 45 years. Due to rapid advances in clinical management, both in the acute and prehospital settings, trauma patients survive devastating injuries at unprecedented rates. However, these patients can often face life threatening complications that stem from the robust innate immune response induced by severe hemorrhage, leading to further tissue injury rather than repair. The complement and coagulation cascades are key mediators in this disordered reaction, which includes the development of trauma‐induced coagulopathy. There is increasing evidence that cross‐talk between these two pathways allows rapid amplification of their otherwise targeted responses and contributes to overwhelming and prolonged systemic inflammation. In this article, we summarize the initial steps of innate immune response to trauma and review the complex complement and coagulation cascades, as well as how they interact with each other. Despite progress in understanding these cascades, effective therapeutic targets have yet to be found and further research is needed both to improve survival rates as well as decrease associated morbidity.

ObjectiveWe investigated prolonged COVID-19 symptom duration, defined as lasting 28 days or longer, among people with systemic autoimmune rheumatic diseases (SARDs).MethodsWe analysed data from the COVID-19 Global Rheumatology Alliance Vaccine Survey (2 April 2021–15 October 2021) to identify people with SARDs reporting test-confirmed COVID-19. Participants reported COVID-19 severity and symptom duration, sociodemographics and clinical characteristics. We reported the proportion experiencing prolonged symptom duration and investigated associations with baseline characteristics using logistic regression.ResultsWe identified 441 respondents with SARDs and COVID-19 (mean age 48.2 years, 83.7% female, 39.5% rheumatoid arthritis). The median COVID-19 symptom duration was 15 days (IQR 7, 25). Overall, 107 (24.2%) respondents had prolonged symptom duration (≥28 days); 42/429 (9.8%) reported symptoms lasting ≥90 days. Factors associated with higher odds of prolonged symptom duration included: hospitalisation for COVID-19 vs not hospitalised and mild acute symptoms (age-adjusted OR (aOR) 6.49, 95% CI 3.03 to 14.1), comorbidity count (aOR 1.11 per comorbidity, 95% CI 1.02 to 1.21) and osteoarthritis (aOR 2.11, 95% CI 1.01 to 4.27). COVID-19 onset in 2021 vs June 2020 or earlier was associated with lower odds of prolonged symptom duration (aOR 0.42, 95% CI 0.21 to 0.81).ConclusionMost people with SARDs had complete symptom resolution by day 15 after COVID-19 onset. However, about 1 in 4 experienced COVID-19 symptom duration 28 days or longer; 1 in 10 experienced symptoms 90 days or longer. Future studies are needed to investigate the possible relationships between immunomodulating medications, SARD type/flare, vaccine doses and novel viral variants with prolonged COVID-19 symptoms and other postacute sequelae of COVID-19 among people with SARDs.

Background: The impact and consequences of the COVID-19 pandemic on people with rheumatic disease are unclear. We developed the COVID-19 Global Rheumatology Alliance Patient Experience Survey to assess the effects of the COVID-19 pandemic on people with rheumatic disease worldwide. Methods: Survey questions were developed by key stakeholder groups and disseminated worldwide through social media, websites, and patient support organisations. Questions included demographics, rheumatic disease diagnosis, COVID-19 diagnosis, adoption of protective behaviours to mitigate COVID-19 exposure, medication access and changes, health-care access and communication with rheumatologists, and changes in employment or schooling. Adults age 18 years and older with inflammatory or autoimmune rheumatic diseases were eligible for inclusion. We included participants with and without a COVID-19 diagnosis. We excluded participants reporting only non-inflammatory rheumatic diseases such as fibromyalgia or osteoarthritis. Findings: 12 117 responses to the survey were received between April 3 and May 8, 2020, and of these, 10 407 respondents had included appropriate age data. We included complete responses from 9300 adults with rheumatic disease (mean age 46·1 years; 8375 [90·1%] women, 893 [9·6%] men, and 32 [0·3%] participants who identified as non-binary). 6273 (67·5%) of respondents identified as White, 1565 (16·8%) as Latin American, 198 (2·1%) as Black, 190 (2·0%) as Asian, and 42 (0·5%) as Native American or Aboriginal or First Nation. The most common rheumatic disease diagnoses included rheumatoid arthritis (3636 [39·1%] of 9300), systemic lupus erythematosus (2882 [31·0%]), and Sjogren's syndrome (1290 [13·9%]). Most respondents (6921 [82·0%] of 8441) continued their antirheumatic medications as prescribed. Almost all (9266 [99·7%] of 9297) respondents adopted protective behaviours to limit SARS-CoV-2 exposure. A change in employment status occurred in 2524 (27·1%) of 9300) of respondents, with a 13·6% decrease in the number in full-time employment (from 4066 to 3514). Interpretation: People with rheumatic disease maintained therapy and followed public health advice to mitigate the risks of COVID-19. Substantial employment status changes occurred, with potential implications for health-care access, medication affordability, mental health, and rheumatic disease activity. Funding: American College of Rheumatology.

Patients with inflammatory arthritis represent a possible high-risk group to COVID-19 due to their immunosuppressive regimen designed to maintain low disease activity. Thus, substantial effort has been put forth to understand the impact of COVID-19 on these patients. Patients with rheumatic diseases as a whole do not appear to be more susceptible to acquiring COVID-19. Furthermore, immunosuppression generally did not increase the likelihood of developing severe COVID-19, with the important exception of medium and high-dose glucocorticoid use. In addition, a small number of COVID-19 patients have developed new inflammatory arthritis; whether this represents an unmasking of previous subclinical disease or a bone fide virus-induced arthritis is unclear. Nevertheless, it appears that inflammatory arthritis patients currently on immunosuppression should continue their medication to prevent future flares and limit glucocorticoid usage. While this continues to be a rapidly evolving field, these data are reassuring to both patients with and providers treating inflammatory arthritides.

Introduction Several months into the COVID-19 pandemic, safe and effective treatments against this global health disaster have yet to be identified. Clinical research trials around the world are underway testing a wide array of possible medications. In particular, the off-label use of hydroxychloroquine for COVID-19 prophylaxis and treatment has created many unprecedented challenges for the scientific community and the public. Areas covered We critically assessed major events from February – May 2020 that contributed to widespread use of hydroxychloroquine for the treatment and prophylaxis of COVID-19. We aimed to explore how opinions toward hydroxychloroquine may shift from early enthusiasm (based on in vitro and preliminary clinical data) to the hope for a miracle cure (through communication and promotion of questionable results) and, finally, to a rise of skepticism as more in-depth analyses are emerging. Expert opinion Mindful and rigorous acquisition of data, as well as its interpretation, are essential to an effective pandemic response. The rapid and premature promotion of results has had major implications for global crisis management, even creating distrust among the public. It is crucial for the medical and scientific community to incorporate the lessons learned from this situation.

We appreciate the interest of Lo et al in our opinion piece and thank them for the data presented in their letter.1 2 Several reports of QT prolongation and torsades de pointes in patients with COVID-19 receiving antimalarials have been published.3–5 These and other reports have indirectly raised questions regarding the arrhythmogenic potential of hydroxychloroquine (HCQ) when used to treat rheumatic disease. Lo et al used the unique resource of the National Health Insurance Research Database of Taiwan. Through propensity scores, they matched patients who used HCQ and who did not use HCQ for the treatment of newly diagnosed rheumatoid arthritis (RA). Data about other disease-modifying antirheumatic drugs used by the patients was not reported. Therefore, it is unclear if the groups were similar in their RA disease severity, although they seemed similar related to comorbidities. The authors did not find differences in the cumulative risk of arrhythmia between the two groups after 1 year of follow-up. However, a prior meta-analysis on reported cardiotoxic events of antimalarials found that cardiac conduction abnormalities were the most common cardiac adverse events and were associated with higher cumulative doses (median cumulative HCQ dose of 1235 g, …

We thank Santos-Moreno et al for their response to our commentary.1 2 The authors provide data on cardiovascular adverse events associated with maintenance antimalarial use for patients with rheumatoid arthritis (RA). In addition to our previous correspondence response3 from Erre et al ,4 these additional data are reassuring to patients with rheumatic diseases on chronic doses of antimalarials regarding the continued safety of these medications. However, as we have also addressed in a previous response, the safety profile of antimalarials in patients with COVID-19 infection compared with patients with rheumatic disease may differ widely. Observational data regarding cardiovascular events in hospitalised patients with COVID-19 treated with hydroxychloroquine (HCQ) with or …

We read the comment on our article by Lopez-Gonzalez et al with great interest.1 2 The authors detail the presentation of four cases of acute arthritis in patients hospitalised with COVID-19 and underlying gout (three cases) or recurrent arthritis of unknown origin (one case). Although we await further reports, there have been anecdotes of newly diagnosed inflammatory arthritis in the context of COVID-19 infection, perhaps representing either a viral-associated arthritis or a reactive arthritis.3 4 However, as the authors note, common causes of acute inflammatory arthritis must continue to be considered in the differential diagnosis—these include crystal-associated arthritis, such as gout or pseudogout. Acute …

The use of hydroxychloroquine (HCQ) in the prophylaxis and treatment of coronavirus disease 2019 (COVID-19) has received significant attention by politicians and media figures. This has occurred despite limited data supporting its efficacy in COVID-19 as well as considerable concern about its safety when used at high doses (>400 mg daily) and in combination with other QT interval prolonging drugs.1–4 An inaccurate narrative has emerged in recent weeks that patients with systemic lupus erythematosus (SLE) who are taking HCQ as a baseline therapy are less affected by or do not develop COVID-19.5–7 This assumption has been challenged by Monti and Montecucco,8 referencing data from the COVID-19 Global Rheumatology Alliance registry on patients with rheumatic disease that previously identified 19/110 (17%) patients with SLE.9 A case series of 17 patients with lupus or antiphospholipid syndrome who developed COVID-19 on a median HCQ dose of 400 mg daily (median HCQ blood level of 648 ng/mL) has since become available.10 As of 17 April 2020, we have now identified 80 patients with SLE and COVID-19 in the global physician-reported registry. Patients were predominantly female (72/80, 90%) and less than 65 years of age (69/80, 86%). Importantly, 64% (51/80) of patients with SLE were taking an antimalarial (HCQ or chloroquine) prior to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (30% as monotherapy). Notably, 21.1% (121/573) of all reported patients with rheumatic disease in the registry were treated with an antimalarial prior to onset of COVID-19, yet 49.6% (60/121) required hospitalisation. In patients with SLE, frequency of hospitalisation with COVID-19 …

Hydroxychloroquine, an essential treatment for many patients with rheumatologic conditions, has garnered widespread attention as a potential treatment for COVID-19 infection. The authors appraise t...

We appreciated the letter from Monti et al , which was the first dedicated report of patients with rheumatic disease who have been diagnosed with COVID-19.1 We have also reviewed the response from Joob and Wiwanitkit,2 which unfortunately perpetuates the notion that individuals with systemic lupus erythematosus (SLE) or other rheumatic disease may be protected from COVID-19 infection via hydroxychloroquine use. Although the origins of this claim are not entirely clear, they may arise from the fact that rheumatic or autoimmune diseases were not initially reported among other comorbidities in the first large Chinese case …

We read the comment by Erre et al to our correspondence about hydroxychloroquine (HCQ) use during the COVID-19 with great interest.1 2 As also highlighted by others, antimalarial use such as HCQ during the COVID-19 pandemic has the potential for cardiotoxicity.3 4 Patients with COVID-19 and those with rheumatic disease represent distinct populations with different dosing strategies. We agree that the potential for cardiotoxicity from antimalarials may also be different related to these issues. The authors present interesting data on QTc intervals in patients with rheumatoid arthritis (RA) on maintenance HCQ, drawn from an established cohort of patients without known significant underlying cardiovascular disease. While these patients had statistically significant higher QT intervals on HCQ compared with those on other disease-modifying antirheumatic drugs (DMARDs), the mean remained within normal limits so this difference is unlikely to have a …

The mechanisms by which signals are transmitted across the plasma membrane to regulate signaling are largely unknown for receptors with single-pass transmembrane domains such as the epidermal growth factor receptor (EGFR). A crystal structure of the extracellular domain of EGFR dimerized by epidermal growth factor (EGF) reveals the extended, rod-like domain IV and a small, hydrophobic domain IV interface compatible with flexibility. The crystal structure and disulfide cross-linking suggest that the 7-residue linker between the extracellular and transmembrane domains is flexible. Disulfide cross-linking of the transmembrane domain shows that EGF stimulates only moderate association in the first two α-helical turns, in contrast to association throughout the membrane over five α-helical turns in glycophorin A and integrin. Furthermore, systematic mutagenesis to leucine and phenylalanine suggests that no specific transmembrane interfaces are required for EGFR kinase activation. These results suggest that linkage between ligand-induced dimerization and tyrosine kinase activation is much looser than was previously envisioned.