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more than 1) occurred in 533 (16.0%) patients; 207 (6.2%) were venous (3.2% PE and 3.9% DVT) and 365 (11.1%) were arterial (1.6% ischemic stroke, 8.9% MI, and 1.0% systemic thromboembolism; Table 1). Following multivariable adjustment, age, sex, Hispanic ethnicity, coronary artery disease, prior MI, and higher D-dimer levels at hospital presentation were associated with a thrombotic event (Table 2). All-cause mortality was 24.5% and was higher in those with thrombotic events (43.2% vs 21.0%; P < .001) (Table 1). After multivariable adjustment, a thrombotic event was independently associated with mortality (adjusted hazard ratio, 1.82; 95% CI, 1.54-2.15; P < .001). Both venous (adjusted hazard ratio, 1.37; 95% CI, 1.02-1.86; P = .04) and arterial (adjusted hazard ratio, 1.99; 95% CI, 1.65-2.40; P < .001) thrombosis were associated with mortality (P = .25 for interaction). Among 829 ICU patients, 29.4% had a thrombotic event (13.6% venous and 18.6% arterial). Among 2505 non-ICU patients, 11.5% had a thrombotic event (3.6% venous and 8.4% arterial). Discussion | In patients with COVID-19 hospitalized in a large New York City health system, a thrombotic event occurred in 16.0%. D-dimer level at presentation was independently associated with thrombotic events, consistent with an early coagulopathy. Prior studies varied regarding the precise incidence of thrombosis; however, all suggested a heightened risk in patients with COVID-19. 3,4 This analysis found variation by clinical setting and type of thrombosis event. While thrombosis is observed in other acute infections 5 (eg, 5.9% prevalence during the 2009 influenza pandemic), 6 the thrombotic risk appears higher in COVID-19. Thrombosis in patients with COVID-19 may be due to a cytokine storm, hypoxic injury, endothelial dysfunction, hypercoagulability, and/or increased platelet activity. This study has several limitations. A diagnosis of thrombosis may be underestimated because imaging studies were limited due to concerns of transmitting infection or competing risk of death. Type of MI was not confirmed with cardiac catheterization. Clinical practice changed over the study period, with increased awareness of thrombotic events and use of anticoagulation, which may affect the incidence of thrombosis.

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BackgroundSystemic juvenile idiopathic arthritis (SJIA) is an autoinflammatory disease associated with chronic arthritis. Early diagnosis and effective therapy of SJIA is desirable, so that complications are avoided. The PRO-KIND initiative of the German Society for Pediatric Rheumatology (GKJR) aims to define consensus-based strategies to harmonize diagnostic and therapeutic approaches in Germany.MethodsWe analyzed data on patients diagnosed with SJIA from 3 national registries in Germany. Subsequently, via online surveys and teleconferences among pediatric rheumatologists with a special expertise in the treatment of SJIA, we identified current diagnostic and treatment approaches in Germany. Those were harmonized via the formulation of statements and, supported by findings from a literature search. Finally, an in-person consensus conference using nominal group technique was held to further modify and consent the statements.ResultsUp to 50% of patients diagnosed with SJIA in Germany do not fulfill the International League of Associations for Rheumatology (ILAR) classification criteria, mostly due to the absence of chronic arthritis. Our findings suggest that chronic arthritis is not obligatory for the diagnosis and treatment of SJIA, allowing a diagnosis of probable SJIA. Malignant, infectious and hereditary autoinflammatory diseases should be considered before rendering a diagnosis of probable SJIA. There is substantial variability in the initial treatment of SJIA. Based on registry data, most patients initially receive systemic glucocorticoids, however, increasingly substituted or accompanied by biological agents, i.e. interleukin (IL)-1 and IL-6 blockade (up to 27.2% of patients). We identified preferred initial therapies for probable and definitive SJIA, including step-up patterns and treatment targets for the short-term (resolution of fever, decrease in C-reactive protein by 50% within 7 days), the mid-term (improvement in physician global and active joint count by at least 50% or a JADAS-10 score of maximally 5.4 within 4 weeks) and the long-term (glucocorticoid-free clinically inactive disease within 6 to 12 months), and an explicit treat-to-target strategy.ConclusionsWe developed consensus-based strategies regarding the diagnosis and treatment of probable or definitive SJIA in Germany.Electronic supplementary materialThe online version of this article (10.1186/s12969-018-0224-2) contains supplementary material, which is available to authorized users.

Our findings demonstrate an adverse treatment outcome for young patients with T1D and comorbid depressive symptoms underlining an urgent need for collaborative mental and somatic health care for patients with T1D and depression.