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MeSH Disease

Human Phenotype

Transmission

Seroprevalence

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    Be-careful! Behind the storm of severe COVID-19, could be hidden macrophage activation syndrome MESHD. A case report with excellent outcome.

    Authors: Rafaela Silva Guimarães Gonçalves; André da Costa Victor; Ana Carolina Oliveira Cavalcanti Tavare; Angela Luzia Branco Pinto Duarte

    doi:10.21203/rs.3.rs-47499/v1 Date: 2020-07-22 Source: ResearchSquare

    In severe cases of COVID-19, it is important to note that some laboratory signs may alert to the presence of underlying macrophage activation syndrome MESHD (MAS), and we ratify that the classic signs of primary MAS are often not present. Here we show a case report of COVID-19 complicated by MAS treated with high doses of methylprednisolone and intravenous Immunoglobulin, with excellent clinical outcome, avoiding orotracheal intubation indeed. The interpretation of laboratory signs leads to early diagnosis and the introduction of effective therapy.

    Cytokine release syndrome MESHD is not usually caused by secondary hemophagocytic lymphohistiocytosis MESHD in a cohort of 19 critically ill COVID-19 patients

    Authors: Georg Lorenz; Philipp Moog; Quirin Bachmann; Paul La Rosee; Heike Schneider; Michaela Schlegl; Christoph Spinner; Uwe Heemann; Roland M Schmid; Hana Algül; Tobias Lahmer; Wolfgang Huber; Christoph Schmaderer

    doi:10.21203/rs.3.rs-31847/v1 Date: 2020-05-27 Source: ResearchSquare

    Background: Severe COVID-19 associated respiratory failure HP, poses the one challenge of our days. Assessment and treatment of COVID-19 associated hyperinflammation may be key to improve outcomes. It was speculated that in subgroups of patients secondary hemophagocytic lymphohistiocytosis MESHD (sHLH) or cytokine release syndrome MESHD (CRS) with features of macrophage activation syndrome MESHD might drive severe disease MESHD trajectories. If confirmed, profound immunosuppressive therapy would be a rationale treatment approach.Methods: Over a median observation period of 11 (IQR: 8; 16) days, 19 consecutive confirmed severe COVID-19-patients admitted to our intensive-care-unit were tested for presence of sHLH by two independent experts. HScores and 2004-HLH diagnostic criteria were assessed. Patients were grouped according to short-term clinical courses: discharge from ICU versus ongoing ARDS or death MESHD at time of analysis.Results: The median HScore at admission was 157 (IQR: 98;180), without the key clinical triad of HLH, i.e. progressive cytopenia, persistent fever MESHD fever HP and organomegaly. Independent expert chart review revealed the absence of sHLH in all cases. No patient reached more than 3/6 of modified HLH 2004 criteria. Nevertheless, patients presented hyperinflammation with peripheral neutrophilic signatures (neutrophil/lymphocyte-ratio>3.5). The latter best paralleled their short-term clinical courses, with declining relative neutrophil numbers prior to extubation (4.4, [IQR: 2.5;6.3]; n=8) versus those with unfavourable courses (7.6, [IQR: 5.2;31], n=9).Conclusion: Our study rules out virus induced sHLH as the leading cause of most severe-COVID-19 trajectories. Instead, an associated innate neutrophilic hyperinflammatory response or virus-associated-CRS appears dominant in patients with an unfavourable clinical course. Therapeutic implications are discussed.

    Pathophysiology of SARS-CoV-2: targeting of endothelial cells renders a complex disease MESHD with thrombotic microangiopathy MESHD and aberrant immune response. The Mount Sinai COVID-19 autopsy experience

    Authors: Clare Bryce; Zachary Grimes; Elisabet Pujadas; Sadhna Ahuja; Mary Beth Beasley; Randy Albrecht; Tahyna Hernandez; Aryeh Stock; Zhen Zhao; Mohamed Al Rasheed; Joyce Chen; Li Li; Diane Wang; Adriana Corben; Kenneth Haines; William Westra; Melissa Umphlett; Ronald E Gordon; Jason Reidy; Bruce Petersen; Fadi Salem; MariaIsabel Fiel; Siraj M El Jamal; Nadejda M Tsankova; Jane Houldsworth; Zarmeen Mussa; Wen-Chun Liu; Brandon Veremis; Emilia Sordillo; Melissa Gitman; Michael Nowak; Rachel Brody; Noam Harpaz; Miriam Merad; Sacha Gnjatic; Ryan Donnelly; Patricia Seigler; Calvin Keys; Jennifer Cameron; Isaiah Moultrie; Kae-Lynn Washington; Jacquelyn Treatman; Robert Sebra; Jeffrey Jhang; Adolfo Firpo; John Lednicky; Alberto Paniz-Mondolfi; Carlos Cordon-Cardo; Mary Fowkes

    doi:10.1101/2020.05.18.20099960 Date: 2020-05-22 Source: medRxiv

    BACKGROUND Severe Acute Respiratory Syndrome MESHD Coronavirus-2 (SARS-CoV-2) and its associated clinical syndrome MESHD COVID-19 are causing overwhelming morbidity and mortality around the globe, disproportionately affecting New York City. A comprehensive, integrative autopsy series that advances the mechanistic discussion surrounding this disease MESHD process is still lacking. METHODS Autopsies were performed at the Mount Sinai Hospital on 67 COVID-19 positive patients and data from the clinical records were obtained from the Mount Sinai Data Warehouse. The experimental design included a comprehensive microscopic examination carried out by a team of expert pathologists, along with transmission TRANS electron microscopy, immunohistochemistry, RNA in situ hybridization, as well as immunology and serology assays. RESULTS Laboratory results of our COVID-19 cohort show elevated inflammatory markers, abnormal coagulation values, and elevated cytokines IL-6, IL-8 and TNF. Autopsies revealed large pulmonary emboli in four cases. We report microthrombi in multiple organ systems including the brain, as well as conspicuous hemophagocytosis HP and a secondary hemophagocytic lymphohistiocytosis MESHD-like syndrome MESHD in many of our patients. We provide electron microscopic, immunofluorescent and immunohistochemical evidence of the presence of the virus and the ACE2 receptor in our samples. CONCLUSIONS We report a comprehensive autopsy series of 67 COVID-19 positive patients revealing that this disease MESHD, so far conceptualized as a primarily respiratory viral illness, also causes endothelial dysfunction, a hypercoagulable state, and an imbalance of both the innate and adaptive immune responses. Novel findings reported here include an endothelial phenotype of ACE2 in selected organs, which correlates with clotting abnormalities and thrombotic microangiopathy MESHD, addressing the prominent coagulopathy and neuropsychiatric symptoms. Another original observation is that of macrophage activation syndrome MESHD, with hemophagocytosis HP and a hemophagocytic lymphohistiocytosis MESHD-like disorder, underlying the microangiopathy and excessive cytokine release. We discuss the involvement of critical regulatory pathways.

    Management of rheumatic diseases MESHD in the times of COVID-19 pandemic- perspectives of rheumatology practitioners from India

    Authors: Latika Gupta; Durga Misra; Vishwesh Agarwal; Suma Balan; Vikas Agarwal

    doi:10.1101/2020.04.03.20048389 Date: 2020-04-07 Source: medRxiv

    Background. The Coronavirus disease MESHD 19 (COVID-19) pandemic has led to widespread concerns about the risk of infection TRANS risk of infection TRANS infection MESHD in patients with rheumatic diseases MESHD (RD) receiving disease MESHD modifying ant-rheumatic drugs (DMARDs) and other immunosuppressants (IS). Methods. A SurveyMonkey based electronic survey was conducted amongst members of the Indian Rheumatology Association to understand the need for changes in prevailing practices. Results. Of the 861 invitees, 221 responded. In the wake of the pandemic, 47.5% would reduce biological DMARDs (bDMARDs) while only 12.2% would reduce the use of conventional synthetic DMARDs. 64.2% were likely to defer change in IS, the reluctance being most with rituximab (58.3%) followed by cyclophosphamide (53.3%), anti-tumor necrosis MESHD factor alpha agents (52.4%) and Janus kinase inhibitors (34.39%). Hydroxychloroquine was the preferred choice (81.9%) for the treatment of COVID-19 followed by protease inhibitors (22.1%) and intravenous immunoglobulin (8.1%). Chloroquine was less preferred (19%). More than two-thirds (70.5%) believed that COVID-19 might trigger macrophage activation syndrome MESHD. Social distancing (98.1%) and hand hygiene (74.6%) were recommended by majority. 62.8% would avoid touch for clinical examination whenever feasible. Conclusion. Most rheumatologists perceived the need to change treatment of RDs during the COVID-19 pandemic; reduce immunosuppression and defer the usage of rituximab and bDMARDs.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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