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Nodular localized cutaneous amyloidosis in an adult patient with Sjögren’s syndrome
Rheumatology ( IF 5.5 ) Pub Date : 2020-05-25 , DOI: 10.1093/rheumatology/keaa227
Fenjuan Yu 1 , Min Zhang 2 , Yanyan He 2 , Wei Zhang 2 , Haoxiang Xu 2
Affiliation  

In December 2019, a novel coronavirus, currently defined as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), was identified as the aetiological agent of a cluster of pneumonia in Wuhan, China [1]. Since this outbreak, the novel coronavirus disease (COVID-19) has spread worldwide. By 30 March 2020, COVID-19 had reached pandemic proportions, involving >110 countries and >600 000 cases [2]. Most cases of COVID-19 are self-limiting, but up to 20% of infected patients show a severe or critical disease, including severe pneumonia and multi-organ failure [3]. Systemic immune abnormalities feature in severe COVID-19. Despite peripheral blood showing a reduced lymphocyte number, there is a hyperactivation state of T cells, with an increase of Th17 and a high cytotoxic activity of CD8 [4]. Moreover, patients with severe COVID-19 show increased serum IL-6 levels and reduced number of circulating NK cells. Globally, these clinical and serological abnormalities characterize a cytokine release syndrome (CRS) [5]. During CRS, the systemic activation of immune cells causes the release of a large quantity of cytokines with the aim of limiting viral diffusion and clearing the infection. However, uncontrolled immune system activation can cause terminal organ damage, evolving towards multi-organ failure [6].
更新日期:2020-05-25
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