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Background Anti-rheumatic drugs can increase the predisposition to infection, and patients may be unaware of continuing their treatment during the COVID-19 pandemic. Objective This study aimed to assess whether patients maintain their treatment for rheumatic conditions during the pandemic period and determine the factors responsible for discontinuation. Methods Patients were randomly selected from the prospectively collected database of our tertiary referral center. The patients were interviewed by telephone through a standardized closed-ended questionnaire, which is targeting the continuity of the treatment plan and the considerations related to the individual choice. The patients were asked whether they hesitated to visit the hospital for follow-up or intravenous drug administration. Results A total of 278 patients completed the questionnaire. While 62 of the patients (22.3%) had reduced or interrupted the treatment, only 11 patients (3.9%) stopped the treatment completely. A significant difference was observed between the duration of illness and the discontinuation of treatment. (p = 0.023) There was a significant difference in disease activity between the group that stopped treatment and continued treatment. (p = 0.001) There was no statistically significant difference in other demographic characteristics. One hundred thirty-five patients (48.6%) made the treatment decision by themselves, and 80% continued the treatment. Reasons for stopping the treatment were anxiety (48.4%), not being able to go to the hospital for intravenous treatment (45.1%), and not being able to find the drug (6.5%). Conclusion Since patients with long-term illnesses were found to be significantly more likely to stop their treatment, this group of patients should be monitored.

Contemporary rheumatology is a field dealing with the phenomena of autoimmune states and inflammation. Rheumatic diseases cover a wide spectrum of diseases of the musculoskeletal system, connective tissue and vessels. The occurrence of an immune, autoimmune and autoinflammatory response is often linked to different kinds of infections. Which aspects of the coronavirus infection relate to rheumatological therapy and practice? In order to answer this question one needs to look at the pathogenesis of the SARS-CoV-2 infection. Antimalarial drugs may block antigen presentation of the viral peptides from antigen presenting cells, as they may alter the lysosomal proteases that mediate the viral entry in the cells and have demonstrated efficacy in improving the infection. Anti-IL-6 may interfere with cytokine storm in severe cases and use of tocilizumab has had good results in a small cohort. Baricitinib not only plays a role in inhibiting the synthesis of cytokines but it also has a function in suppressing receptor-mediated endocytosis. The constantly new and tested concepts in the treatment of COVID testify to the growing knowledge about the virus, but also to the need for more targeted therapy. Treatment regimens have been developed for both patients with COVID-19 and those with symptomatic SARS-CoV infection and rheumatic disease. This article is an attempt to discuss the management of COVID-19 and coexisting rheumatic disease.

As of June 10th 2020 about 7.2 million individuals have tested positive for, and more than 410,000 have died due to COVID-19. In this review we outline the pathophysiology that underpins the potential use of anti-rheumatic therapies for severe COVID-19 infection and summarize the current evidence regarding the risk and outcome of COVID-19 in patients with systemic autoimmune diseases. Thus far there is no convincing evidence that any disease-modifying anti-rheumatic drug (conventional synthetic, biologic or targeted synthetic) including hydroxychloroquine, may protect against severe COVID-19 infection; answers about their possible usefulness in the management of the cytokine storm associated with severe COVID-9 infection will only arise from ongoing randomized controlled trials. Evidence on COVID-19 risk and outcome in patients with systemic autoimmune diseases is extremely limited; thus, any conclusions would be unsafe and should be seen with great caution. At present, the risk and severity (hospitalization, intensive care unit admission and death) of COVID-19 infection in people with autoimmune diseases do not appear particularly dissimilar to the general population, with the possible exception of hospitalization in patients exposed to high glucocorticoid doses. At this stage it is impossible to draw any conclusions for differences in COVID-19 risk and outcome between different autoimmune diseases and between the various immunomodulatory therapies used for them. More research in the field is obviously required, including as a minimum careful and systematic epidemiology and appropriately controlled clinical trials.

Objective: In patients with rheumatoid arthritis (RA) in sustained remission, tapering of biological disease-modifying anti-rheumatic drugs can be considered. Tapering has already been investigated, but its feasibility remains to be determined. Therefore, we explored the feasibility of tapering etanercept in RA in a setting close to practice. Method: Patients with RA in 28-joint Disease Activity Score (DAS28) remission (>= 6 months) and treated with etanercept 50 mg weekly (>= 1 year) were included in the pragmatic 1 year open-label multicentre randomized controlled TapERA (Tapering Etanercept in Rheumatoid Arthritis) trial. Patients were assigned to continue etanercept weekly or to taper to every other week (EOW). Patients who lost remission [DAS28-C-reactive protein (CRP) >= 2.6] were re-escalated to etanercept weekly. The primary outcome was the proportion of patients maintaining DAS28-CRP remission for 6 months. Results: Sixty-six patients were randomized to etanercept weekly (n = 34) or EOW (n = 32). After 6 months, 26/34 patients (76%) in the weekly and 19/32 (59%) in the EOW group maintained disease control (p = 0.136). In the EOW group, 20/32 patients (63%) remained on their tapered treatment during the trial. Two patients reintroduced weekly etanercept themselves. Ten patients were re-escalated to etanercept weekly by the rheumatologist, after a median (interquartile range) interval of 3.0 (2.0-6.0) months. Among these patients, 7/10 regained remission after re-escalation, four of them at the next study visit. Conclusions: Although non-inferiority could not be demonstrated, tapering of etanercept to EOW appeared feasible in patients in sustained remission.

The pharmacotherapy of Takayasu arteritis (TAK) with disease-modifying anti-rheumatic drugs (DMARDs) is an evolving area. A systematic review of Scopus, Web of Science, Pubmed Central, clinical trial databases and recent international rheumatology conferences for interventional and observational studies reporting the effectiveness of DMARDs in TAK identified four randomized controlled trials (RCTs, with another longer-term follow-up of one RCT) and 63 observational studies. The identified trials had some concern or high risk of bias. Most observational studies were downgraded on the Newcastle-Ottawa scale due to lack of appropriate comparator groups. Studies used heterogenous outcomes of clinical responses, angiographic stabilization, normalization of inflammatory markers, reduction in vascular uptake on positron emission tomography, reduction in prednisolone doses and relapses. Tocilizumab showed benefit in a RCT compared to placebo in a secondary per-protocol analysis but not the primary intention-to-treat analysis. Abatacept failed to demonstrate benefit compared to placebo for preventing relapses in another RCT. Pooled data from uncontrolled observational studies demonstrated beneficial clinical responses and angiographic stabilization in nearly 80% patients treated with tumour necrosis factor alpha inhibitors, tocilizumab or leflunomide. Certainty of evidence for outcomes from RCTs ranged from moderate to very low and was low to very low for all observational studies. There is a paucity of high-quality evidence to guide the pharmacotherapy of TAK. Future observational studies should attempt to include appropriate comparator arms. Multicentric, adequately powered RCTs assessing both clinical and angiographic responses are necessary in TAK. Supplementary Information The online version contains supplementary material available at 10.1007/s10067-021-05743-2.

Background Alterations in the composition of the fecal microbiota in children with juvenile idiopathic arthritis (JIA) have been observed in several studies, but it has not been determined whether the standard treatment for JIA changes the composition or function of the microbiota. The first-line disease-modifying anti-rheumatic drug for treatment of JIA is usually methotrexate, followed or supplemented by anti-tumor necrosis factor alpha drugs, such as etanercept. The aim of this study was to investigate the effects of methotrexate and etanercept treatments on the fecal microbiota and the fecal short-chain fatty acids (SCFAs) in children with JIA. Methods In this multicenter study, the composition of fecal microbiota from 45 treatment-naïve children with JIA was compared with that from 29 children treated with methotrexate and 12 children treated with etanercept. We also made pairwise comparisons of 15 children sampled before and during methotrexate treatment and 7 children sampled before and during etanercept treatment. The microbiota was determined using sequencing amplicons from the V3 and V4 regions of the 16S rRNA gene. Alpha-diversity, community composition, and relative abundances of bacterial taxa were analyzed in all comparisons. Analyses of fecal SCFAs, using a high-performance liquid chromatograph, were performed for the pairwise comparisons. Results We did not find any significant differences in α-diversity or community composition of microbiota. However, principal coordinate analysis indicated a change in community composition in 7 of the 15 paired samples before and during methotrexate and 2 of the 7 paired samples before and during etanercept. Comparisons of the relative abundance of taxa revealed minor differences before and during treatment with methotrexate or etanercept, but they were not significant after correction for multiple analyses, and the unpaired and paired analyses did not show similar changes. There were no significant differences in levels of fecal SCFAs before and during treatment with methotrexate or etanercept. Conclusions Treatment with methotrexate or etanercept had minor, but no significant or consistent changes either on composition of microbiota or on levels of SCFAs, suggesting that these changes are not related to the therapeutic effects of methotrexate or etanercept.

As doenças reumáticas podem causar distúrbios sexuais e reprodutivos. As razões destes distúrbios são multifatoriais. Manifestações e sintomas das doenças podem reduzir a libido e interferir no sucesso da reprodução, como ocorre na artrite reumatóide (AR), lúpus eritematoso sistêmico (LES), espondilite anquilosante (EA) e esclerose sistêmica (ES). A atividade da doença pode levar a uma alteração do eixo hipotálamo-hipófise, acarretando períodos de disfunção gonadal. Os auto-anticorpos e os distúrbios de hormônios sexuais, que podem estar presentes em muitas doenças reumáticas, podem influenciar negativamente na fertilidade. Além disso, algumas drogas usadas no tratamento de doenças reumatológicas por vezes representam um risco para a reprodução masculina, devido aos efeitos adversos que podem causar, como defeitos cromos-sômicos e gonadotoxicidade, prejudicando a espermatogênese e a motilidade dos espermatozóides. Conseqüentemente, há falência gonadal transitória ou permanente. Este trabalho faz uma revisão de um assunto pouco abordado na literatura brasileira. Rheumatic diseases affect all aspects of life, including sexuality and reproduction. The reasons for disturbing sexual functioning and reproduction are multifactorial. Manifestations and symptoms of disease can reduce libido and interfere with successful reproduction, for example, in rheumatoid arthritis (AR), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS) and systemic sclerosis (SSc). Active disease disturbs the hypothalamic-pituitary-axis, giving rise to periods of gonadal dysfunction. Autoantibodies, which are present in most of the rheumatic diseases, and disturbances of sex hormone status can negatively influence the fertilization. Furthermore, some antirheumatic drugs carry a risk for male reproduction, because can present adverse effects, which includes chromosomal defects and gonadotoxicity, damaging the spermatogenesis and sperm motility. It results in transient or permanent gonadal failure. We are presenting a review of this aspect. UFPB Departamento de Medicina Interna Sociedade Brasileira de Reumatologia (SBR) Projeto Pronuclear UFPB Universidade Federal de São Paulo (UNIFESP) SBR Projeto Pronuclear UNIFESP, EPM SciELO