Journal of autoimmunity
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Journal of autoimmunity · May 2020
ReviewThe epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak.
Coronavirus disease (COVID-19) is caused by SARS-COV2 and represents the causative agent of a potentially fatal disease that is of great global public health concern. Based on the large number of infected people that were exposed to the wet animal market in Wuhan City, China, it is suggested that this is likely the zoonotic origin of COVID-19. ⋯ Special attention and efforts to protect or reduce transmission should be applied in susceptible populations including children, health care providers, and elderly people. In this review, we highlights the symptoms, epidemiology, transmission, pathogenesis, phylogenetic analysis and future directions to control the spread of this fatal disease.
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Journal of autoimmunity · May 2020
ReviewRecommendations for coronavirus infection in rheumatic diseases treated with biologic therapy.
The Coronavirus-associated disease, that was first identified in 2019 in China (CoViD-19), is a pandemic caused by a bat-derived beta-coronavirus, named SARS-CoV2. It shares homology with SARS and MERS-CoV, responsible for past outbreaks in China and in Middle East. SARS-CoV2 spread from China where the first infections were described in December 2019 and is responsible for the respiratory symptoms that can lead to acute respiratory distress syndrome. ⋯ Checkpoints inhibitors such as anti-CD200 and anti-PD1 could have a role in the treatment of CoViD-19. Rheumatic disease patients taking immunosuppressive drugs should be recommended to maintain the chronic therapy, prevent infection by avoiding social contacts and pausing immunosuppressants in case of infection. National and international registries are being created to collect data on rheumatic patients with CoViD-19.
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Cryoglobulins are antibodies that precipitate at low temperatures and dissolve after rewarming. Cryoglobulinemia refers to the presence of circulating cryoglobulins and generally leads to a systemic inflammatory syndrome characterized by fatigue, arthralgia, purpura, ulcers, neuropathy and/or glomerulonephritis. The disease mainly involves small to medium-sized blood vessels and causes vasculitis due to cryoglobulin-containing immune complexes. ⋯ For patients with chronic HCV infection, antiviral therapy is indicated. Immunosuppressive or immunomodulatory therapy, including steroids, plasmapheresis and cytotoxic agents, is reserved for organ-threatening manifestations. In this review, we discuss the main clinical presentations, diagnostic approach and treatment options.
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Journal of autoimmunity · Sep 2019
Review Multicenter StudyCAPS criteria fail to identify most severely-ill thrombotic antiphospholipid syndrome patients requiring intensive care unit admission.
Catastrophic antiphospholipid syndrome (CAPS), the most severe manifestation of antiphospholipid syndrome (APS), is characterised by simultaneous thromboses in multiple organs. Diagnosing CAPS can be challenging but its early recognition and management is crucial for a favourable outcome. This study was undertaken to evaluate the frequencies, distributions and ability to predict mortality of "definite/probable" or "no-CAPS" categories of thrombotic APS patients requiring admission to the intensive care unit (ICU). ⋯ In this study, CAPS criteria were not associated with mortality of thrombotic APS patients requiring ICU admission. Further studies are need evaluate the adequacy of CAPS criteria for critically-ill APS patients.
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Journal of autoimmunity · Aug 2018
ReviewConnecting the immune system, systemic chronic inflammation and the gut microbiome: The role of sex.
Unresolved low grade systemic inflammation represents the underlying pathological mechanism driving immune and metabolic pathways involved in autoimmune diseases (AID). Mechanistic studies in animal models of AID and observational studies in patients have found alterations in gut microbiota communities and their metabolites, suggesting a microbial contribution to the onset or progression of AID. The gut microbiota and its metabolites have been shown to influence immune functions and immune homeostasis both within the gut and systematically. ⋯ We review herein how gut microbiota and its metabolites regulate immune function, intestinal permeability and possibly AID pathological processes. Further, we describe the dysbiosis within the gut microbiota observed in different AID and speculate how restoring gut microbiota composition and its regulatory metabolites by dietary intervention including prebiotics and probiotics could help in preventing or ameliorating AID. Finally, we suggest that, given consistent observations of microbiota dysbiosis associated with AID and the ability of SCFA and BA to regulate intestinal permeability and inflammation, further mechanistic studies, examining how dietary microbiota modulation can protect against AID, hold considerable potential to tackle increased incidence of AID at the population level.