RESUMO
Objective: Gout is a crystal-induced inflammatory arthritis caused by elevated uric acid. Physical activity has the potential to reduce serum uric acid (SUA), thus improving the disease burden of gout. In this study, we examined the association of objectively-measured physical activity and SUA. Methods: A cross-sectional study was conducted using survey, laboratory, and accelerometer data from the 2003-2004 National Health and Nutrition Examination Survey (NHANES). SUA concentrations (mg/dL) were obtained during an initial exam, and then physical activity (kCal/day) was measured with 7 days of ActiGraph accelerometry in participants (n = 3,475) representative of the ambulatory, non-institutionalized US civilian population. Regression, including restricted cubic splines, was used to assess the relation of physical activity and SUA in bivariate and adjusted models. Covariates included age, gender, race/ethnicity, alcohol use, body mass index, renal function, and urate-lowering therapy. Results: In the bivariate model, physical activity was correlated with SUA concentrations and included a non-linear component (p < 0.01). In the adjusted model, linear splines were employed with a node at the SUA nadir of 5.37mg/dL; this occurred at 703 kCal/day of physical activity. The association of physical activity and SUA was negative from 0 to 703 kCal/day (p = 0.07) and positive >703 kCal/day (p < 0.01 for the change in slope). Conclusion: Physical activity and SUA are associated in a non-linear fashion, with a minimum estimated SUA at 703 kCal/day of objectively-measured physical activity. These findings raise intriguing questions about the use of physical activity as a potential adjunctive therapy in patients with gout, and further interventional studies are needed to elucidate the effects of moderate intensity exercise on SUA concentrations.
RESUMO
Primary Sjögren's syndrome, a chronic inflammatory process, is among the most commonly occurring rheumatologic diseases. The clinical hallmark of this disease is exocrine gland dysfunction, resulting predominately in dry eyes and dry mouth. However, the disease often extends beyond the exocrine glands to seriously affect other organs systems, such as the lungs, kidneys, and nervous system. Moreover, patients with primary Sjögren's syndrome develop non-Hodgkin's B cell lymphoma at a substantially higher rate than the general population. New research has improved our understanding of disease mechanisms, with notable advances in our knowledge about the genetic susceptibility of disease, the molecular details of the chronic inflammatory response in the salivary glands, and the complex role of the type 1 interferon pathway. The pipeline of drugs under development for the treatment of primary Sjögren's syndrome is enriched with novel biologics and small molecular entities targeting the pathogenic process. Herein, we summarize the latest advances in elucidating the pathogenesis of primary Sjögren's syndrome and highlight new drugs in clinical development aiming to reverse the glandular dysfunction and favorably impact the systemic features of this disease.
