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OBJECTIVE: To describe characteristics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in patients with rheumatic immune-mediated inflammatory diseases (IMIDs) from Argentina, Mexico and Brazil, and to assess factors associated with mortality in this population. METHODS: Data from 3 national registries, SAR-COVID (Argentina), CMR-COVID (Mexico), and ReumaCoV-Brasil (Brazil), were combined. Adult patients with IMIDs and SARS-CoV-2 infection were recruited. Sociodemographic data, comorbidities, IMID clinical characteristics and treatment, and SARS-CoV-2 infection presentation and outcomes were recorded. RESULTS: A total of 4827 individuals were included: 2542 (52.7%) from SAR-COVID, 1167 (24.2%) from CMR-COVID, and 1118 (23.1%) from ReumaCoV-Brasil. Overall, 82.1% were female with a mean age of 49.7 (SD, 14.3) years; 22.7% of the patients were hospitalized, and 5.3% died because of COVID-19 (coronavirus disease 2019). Argentina and Brazil had both 4% of mortality and Mexico 9.4%. In the multivariable analysis, older age (≥60 years; odds ratio [OR], 7.4; 95% confidence interval [CI], 4.6-12.4), male sex (OR, 1.5; 95% CI, 1.1-2.1), living in Mexico (OR, 3.0; 95% CI, 2.0-4.4), comorbidity count (1 comorbidity: OR, 1.5; 95% CI, 1.0-2.1), diagnosis of connective tissue disease or vasculitis (OR, 1.8; 95% CI, 1.3-2.4), and other diseases (OR, 2.6; 95% CI, 1.6-4.1) compared with inflammatory joint disease, high disease activity (OR, 4.2; 95% CI, 2.5-7.0), and treatment with glucocorticoids (OR, 1.9; 95% CI, 1.4-2.5) or rituximab (OR, 4.2; 95% CI, 2.7-6.6) were associated with mortality. CONCLUSIONS: Mortality in patients with IMIDs was particularly high in Mexicans. Ethnic, environmental, societal factors, and different COVID-19 mitigation measures adopted have probably influenced these results.

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BACKGROUND: This article presents evidence and recommendations regarding the efficacy and safety of the approved and available therapies in Mexico to treat severe or established osteoporosis with the aim of developing a position regarding therapeutics in this stage of the disease, according to the descriptive cards of the National Drug Formulary of the National General Health Council of Mexico. METHODS: We performed a systematic and narrative review of the evidence of teriparatide and denosumab, from their pharmacological profile, effectiveness, and safety derived from clinical trials, as well as an analysis of the general recommendations of the national and international clinical practice guidelines. RESULTS: The evidence establishes that teriparatide and denosumab belong to different therapeutic classes, with biologically opposed mechanisms of action and indications of use, which are clearly differentiated in their respective national codes, therefore these drugs cannot be substitutable or interchangeable in severe osteoporosis therapy. Both represent the best options currently available for this stage of the disease; being similar in their efficacy in preventing new vertebral fragility fractures, with an RR of .35 (CI 95%; .22-.55) for teriparatide, and .32 (CI 95%: .26-.41) for denosumab. The absolute risk reduction is higher with teriparatide 9.3% (21 months) compared with denosumab at 4.8% (36 months). CONCLUSIONS: Our results agree with the recommendations available in national and international clinical practice guidelines, with both therapies proposed as a sequential, but not a substitute, treatment.

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Varios estudios han sugerido una asociación entre la periodontitissevera, la prevalencia de la bacteria Porphyromonas gingivalis y el desarrollo de artritis reumatoide. Como fundamento de esta relación, se ha observado que esta bacteria secreta una enzima, peptidil-arginina deiminasa, que es capaz de citrulinar proteínas del hospedero y así favorecer una respuesta autoinmune. Sin embargo, debido a la heterogeneidad de diseños experimentales, selección de pacientes y valoración de los desenlaces, los resultados no han mostrado la reproducibilidad deseada. Asimismo, observaciones recientes apuntan a que la actividad enzimática podría ser generada por otras especies bacterianas, lo que hace más compleja su relación. Sin embargo, por otro lado, algunos estudios sugieren que el tratamiento periodontal puede limitar el desarrollo de la artritis reumatoide.

Various studies have suggested a link between severe periodontitis,the prevalence of Porphyromonas gingivalis, and the development ofrheumatoid arthritis. As evidence of this relationship, P. gingivalis hasbeen found to secrete an enzyme, peptidyl arginine deiminase, which isable to citrullinate host proteins and thus help activate an autoimmuneresponse. However, due to the heterogeneity of experimental designs,patient selection, and assessment of clinical outcomes, the results havenot shown the desired reproducibility. Furthermore, recent fi ndingsindicate that the enzymatic activity may be produced by other species ofbacteria, which suggests the relationship is more complex. However, anumber of studies have shown that periodontal treatment could inhibitthe development of rheumatoid arthritis.

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OBJECTIVE: To evaluate the association between the clinical activity of RA patients and serum adipocytokines (Leptin, Adiponectin and Resistin) and inflammatory cytokines. METHODS: All RA patients fulfilled ACR 1987 criteria and were treated with DMARDs. Adipocytokine and inflammatory cytokine levels were evaluated using ELISA. RESULTS: 121 patients were included in the study. Stratifying according to DAS28 (low, moderate and high activity), there were significant differences for Leptin, Resistin, IL-6 and IL-17, however, no differences were seen for Adiponectin, TNFα or IL-1ß. Clinical activity positively correlated with Leptin, Resistin, IL-17 and IL-6 levels, but not with Adiponectin, TNFα or IL-1ß. Adiponectin levels negatively correlated with TNFα and positively correlated with IL-1ß. IL-1ß positively correlated with IL-6 and negatively correlated with TNFα and IL-17. CONCLUSION: Circulating Leptin, Resistin, IL-6 and IL-17 levels positively correlate with RA clinical activity in a manner independent of the subject's BMI. Complex relationships between inflammatory cytokines were observed in RA patients suggesting that other metabolic or inflammatory factors could be involved.

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OBJECTIVES: To assess whether baseline levels of leptin and adiponectin predict disease activity or response to treatment in patients with RA at 6 months, 1 and 2 years of follow-up. METHODS: A consecutive cohort of patients, classified according to the 2010 ACR/EULAR RA criteria, was evaluated at baseline, 6 months, 1 and 2 years. All were treated with steroids and/or DMARDs. None received biologics. Blood was taken at a baseline to determine plasma anti-CCP, leptin and adiponectin. The relationship between leptin, adiponectin, DAS28 and changes in DAS28 was assessed by multivariable linear and logistic regression from baseline to follow-up. RESULTS: 127 patients completed 6 months, 91 one year and 52 two years of follow-up. All were female, mean age 45 years (18-70), time since onset of disease 7.5 years (0-36). A U-shaped relationship between DAS28 and leptin baseline levels was seen. Adjusting for different factors, leptin levels at baseline predicted higher DAS28 at 6 months and, in patients who were not overweight or obese, predicted disease activity at 6 months, 1 and 2 years. In patients who were not overweight or obese, baseline leptin was able to predict response to treatment at 6 and 12 months. CONCLUSIONS: In the short term, baseline leptin levels predict disease activity in all RA patients and response to treatment in RA patients with normal weight.

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