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Overview

MeSH Disease

Human Phenotype

Transmission

Seroprevalence
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    Hyaluronan is abundant in COVID-19 respiratory secretions

    Authors: Gernot Kaber; Michael J. Kratochvil; Elizabeth B Burgener; Egan L Peltan; Graham Barlow; Samuel Yang; Mark R Nicolls; Vinicio de Jesus Perez; Joelle I. Rosser; Andrew J. Wardle; Anissa Kalinowski; Michael G. Ozawa; Donald P. Regula; Nadine Nagy; Sarah C. Heilshorn; Carlos E. Milla; Angela J. Rogers; Paul L. Bollyky; Marcus VG Lacerda; Pedro M Moraes-Vieira; Helder I Nakaya; Qiao Wang; Hongbin Ji; Youhua Xie; Yihua Sun; Lu Lu; Yunjiao Zhou

    doi:10.1101/2020.09.11.20191692 Date: 2020-09-11 Source: medRxiv

    COVID-19 respiratory infections MESHD are associated with copious, adherent respiratory secretions that prolong chronic ventilation and contribute to the morbidity and mortality caused by the disease. We hypothesized that hyaluronan, an extracellular matrix glycosaminoglycan produced at sites of active inflammation MESHD that promotes edema HP edema MESHD in other settings, might be a component of these secretions. To interrogate this, we examined the respiratory secretions collected from eight intubated patients with COVID-19, six control patients with cystic fibrosis MESHD ( CF MESHD), a different respiratory disease MESHD also associated with thick adherent secretions, and eight healthy controls. In this sample set we found that hyaluronan content is increased approximately 20-fold in both CF MESHD and COVID-19 patients compared to healthy controls. The hyaluronan in COVID-19 samples was comprised of low-molecular weight fragments, the hyaluronan form most strongly linked with pro-inflammatory functions. Hyaluronan is similarly abundant in histologic sections from cadaveric lung tissue from COVID-19 patients. These findings implicate hyaluronan in the thick respiratory secretions characteristic of COVID-19 infection MESHD. Therapeutic strategies targeting hyaluronan should be investigated further for potential use in patients with COVID-19.

    Kawasaki Disease MESHD Outbreak in Children TRANS During COVID-19 Pandemic.

    Authors: Ewelina Gowin; Jacek Wysocki; Magdalena Frydrychowicz; Danuta Januszkiewicz-Lewandowska

    doi:10.21203/rs.3.rs-70123/v1 Date: 2020-09-01 Source: ResearchSquare

    BackgroundIn response to the recent information about the outbreak of Kawasaki disease MESHD ( KD MESHD) in children TRANS connected to SARS-Cov-2 pandemic, we would like to present a group of six patients hospitalized from March to May 2020 with an inflammatory disease similar to KD MESHD. Findings There were four girls and two boys, aged TRANS from 15 months to 16 years. They all presented with fever HP fever MESHD lasting at least five days, irritability HP irritability MESHD, bilateral nonexudative conjunctivitis HP conjunctivitis MESHD, lymphadenopathy, mucus membrane changes, rash MESHD, edema HP edema MESHD.Neither the patients nor the other members of the patients' households had a positive history of COVID-19 infection MESHD. None of the six children TRANS had a positive PCR result for SARS-CoV-2 or a positive results for antibodies to SARS-CoV-2 SERO. All patients received empiric antibiotic therapy. Four patients were diagnosed with KD MESHD. Three children TRANS received standard treatment. One boy did not respond and received an additional 14-days course of methylprednisolone.In two girls, the diagnosis of KD MESHD was not made. All patients survived ConclusionFinding a correlation with the Covid-19 pandemic is difficult regarding the situation in our country. According to ECDC, in May 2020 Poland wass still before the peak of the epidemy. The intention of this article is to report that increased hospitalization of children TRANS with the inflammatory syndrome MESHD is also observed in countries with low levels of transmission TRANS of the SARS-Cov-2 virus. Our observation may broaden the knowledge of new inflammatory syndrome MESHD, which is not necessarily caused by SARS-Cov-2 but may be worsened by co-infection MESHD.

    Pharmacological inhibition of the kinin-kallikrein system in severe COVID-19 A proof-of-concept study

    Authors: Eli Mansour; Andre C Palma; Raisa G Ulaf; Luciana C Ribeiro; Ana Flavia Bernardes; Thyago A Nunes; Marcus V Agrela; Bruna Bombassaro; Milena Monfort-Pires; Rafael L Camargo; Eliana P Araujo; Natalia S Brunetti; Alessandro S Farias; Antonio L Falcao; Thiago M Santos; Plinio Trabasso; Rachel P Dertkigil; Sergio S Dertkigil; Maria Luiza Moretti; Licio A Velloso

    doi:10.1101/2020.08.11.20167353 Date: 2020-08-14 Source: medRxiv

    Coronavirus disease-19 (COVID-19) can develop into a severe respiratory syndrome MESHD that results in up to 40% mortality. Acute lung inflammatory edema HP edema MESHD is a major pathological finding in autopsies explaining O2 diffusion failure and hypoxemia HP hypoxemia MESHD. Only dexamethasone has been shown to reduce mortality in severe cases, further supporting a role for inflammation MESHD in disease severity. SARS-CoV-2 enters cells employing angiotensin converting enzyme 2 (ACE2) as a receptor, which is highly expressed in lung alveolar MESHD cells. ACE2 is one of the components of the cellular machinery that inactivates the potent inflammatory agent bradykinin, and SARS-CoV-2 infection MESHD could interfere with the catalytic activity of ACE2, leading to accumulation of bradykinin. In this open-label, randomized clinical trial, we tested two pharmacological inhibitors of the kinin-kallikrein system that are currently approved for the treatment of hereditary angioedema MESHD angioedema HP, icatibant and inhibitor of C1 esterase/kallikrein, in a group of 30 patients with severe COVID-19. Neither icatibant nor inhibitor of C1 esterase/kallikrein resulted in significant changes in disease mortality and time to clinical improvement. However, both compounds promoted significant improvement of lung computed tomography scores and increased blood SERO eosinophils, which has been reported as an indicator of disease recovery. In this small cohort, we found evidence for a beneficial role of pharmacological inhibition of the kinin-kallikrein system in two markers that indicate improved disease recovery.

    Clinical and intestinal histopathological findings in SARS-CoV-2/COVID-19 patients with hematochezia HP hematochezia MESHD

    Authors: Margaret Cho; Weiguo Liu; Sophie Balzora; Yvelisse Suarez; Deepthi Hoskoppal; Neil D Theise; Wenqing Cao; Suparna A Sarkar

    doi:10.1101/2020.07.29.20164558 Date: 2020-08-07 Source: medRxiv

    Gastrointestinal ( GI MESHD) symptoms of SARS-CoV2/COVID-19 in the form of anorexia HP anorexia MESHD, nausea, vomiting HP nausea, vomiting MESHD vomiting MESHD, abdominal pain HP abdominal pain MESHD and diarrhea HP diarrhea MESHD are usually preceeded by respiratory manifestations and are associated with a poor prognosis. Hematochezia HP Hematochezia MESHD is an uncommon clinical presentation of COVID-19 disease and we hypothesize that older patients with significant comorbidites ( obesity HP obesity MESHD and cardiovascular) and prolonged hospitalization are suspectible to ischemic injury MESHD to the bowel. We reviewed the clinical course, key laboratory data including acute phase reactants, drug/medication history in two elderly TRANS male TRANS patients admitted for COVID-19 respiratory failure HP respiratory failure MESHD. Both patients had a complicated clinical course and suffered from hematochezia HP hematochezia MESHD and acute blood SERO blood MESHD loss anemia HP requiring blood SERO transfusion around day 40 of their hospitalization. Colonoscopic impressions were correlated with the histopathological findings in the colonic biopies and changes compatible with ischemia MESHD to nonspecific acute inflammation MESHD, edema HP edema MESHD and increased eosinophils in the lamina propria were noted.Both patients were on anticoagulants, multiple antibiotics and antifungal agents due to respiratory infections MESHD at the time of lower GI bleeding MESHD. Hematochezia HP Hematochezia MESHD resolved spontaneously with supportive care. Both patients eventually recovered and were discharged. Elderly TRANS patients with significant comorbid conditions are uniquely at risk for ischemic injury MESHD to the bowel. Hypoxic conditions MESHD due to COVID-19 pneumonia HP pneumonia MESHD and respiratory failure HP respiratory failure MESHD, compounded by preexisting cardiovascular complications, and/or cytokine storm orchestrated by the viral infection leading to alteration in coagulation profile and/or drug/medication injury can be difficult to distinguish in these critically ill patients. Presentation of hematochezia HP hematochezia MESHD may further increase the mortality and morbidity of COVID-19 patients, and prompt consultation and management by gastroenterology is therefore warranted.

    Myocardial Injury MESHD in Post Mortem Biopsies of Patients with COVID-19

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytinsky Moura; Jose Rocha Faria Neto; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v1 Date: 2020-07-17 Source: ResearchSquare

    Background: Myocardial injury MESHD is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury MESHD in COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide.Aim: This histopathological and immunohistochemical study seeks to clarify the pathogenesis of myocardial injury MESHD in COVID-19.Methods: Postmortem minimally invasive autopsies were performed in two patients who died from COVID-19, and the myocardium samples were compared to a control patient. Immunohistochemistry (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen.Results: The histopathological analysis showed severe pericellular interstitial edema HP edema MESHD surrounding each of the cardiomyocytes. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. On the other hand, no difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. Conclusion: Our findings point to a pathogenesis related with pyroptosis leading to endothelial disfunction. The subsequent inflammation MESHD with associated interstitial edema HP edema MESHD could explain the myocardial disfunction and arrythmias MESHD in COVID-19 patients. The presence of Th2 response, MMP-9 and type-3 collagen suggests progression to myocardial fibrosis HP myocardial fibrosis MESHD in the long term.

    The Pathogenisis of COVID-19 Myocardial Injury MESHD: an Immunohistochemical Study of Postmortem Biopsies 

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Sarah Fagundes Grobe; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytynski Moura; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v2 Date: 2020-07-17 Source: ResearchSquare

    Rationale: M yocardial injury MESHDis significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of m yocardial injury MESHDin COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide. Objective: This histopathological and immunohistochemical study seeks to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 m yocardial injury. MESHD Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control patient. Histopathological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen. The samples were also subjected to a TUNEL assay to detect potential apoptosis. The histopathological analysis showed severe pericellular interstitial edema HP dema MESHDsurrounding each of the cardiomyocytes and higher mast cells count by high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. No difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. The TUNEL assay was positive in all the COVID-19 samples confirming the presence of endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 m yocardial injury MESHDseems to be related with pyroptosis leading to endothelial cell injury and disfunction. The subsequent i nflammation MESHDwith associated interstitial edema HP dema MESHDcould explain the myocardial disfunction and a rrythmias MESHDin these patients. Our findings also show that COVID-19 m yocardial injury MESHDmay cause myocardial fibrosis HP yocardial fibrosis MESHDin the long term. These patients should be monitored for m yocardial dysfunction MESHDand a rrythmias MESHDafter the acute phase of COVID-19.

    Multisystem inflammatory syndrome MESHD with features of Atypical Kawasaki disease MESHD during COVID-19 pandemic: Report of a case from India

    Authors: Abdul Rauf; Ajay Vijayan; Shaji Thomas John; Raghuram A Krishnan; Abdul Latheef

    doi:10.21203/rs.3.rs-29369/v1 Date: 2020-05-15 Source: ResearchSquare

    There is a global concern of increasing number of children TRANS presenting with inflammatory syndrome MESHD with clinical features simulating Kawasaki disease, during ongoing COVID-19 pandemic. We report a very similar case of 5-year-old boy from a COVID-19 hotspot area in Kerala state of India who presented in late April 2020 with acute febrile illness MESHD with abdominal pain HP abdominal pain MESHD and loose stools followed by shock HP. On examination, child TRANS had bulbar conjunctivitis HP conjunctivitis MESHD and extremity edema HP edema MESHD. Initial investigations showed high inflammatory parameters, elevated serum creatinine HP serum SERO creatinine and liver enzymes. Echocardiography showed moderate LV dysfunction MESHD and normal coronaries. Cardiac enzymes were also elevated, suggesting myocarditis HP myocarditis MESHD. He was treated with inotropic support, respiratory support with High Flow Nasal Cannula, IV Immunoglobulins, aspirin, steroids and diuretics. RT PCR for SARS-CoV-2 was negative twice. His clinical condition improved rapidly, was afebrile from day 2, inflammatory parameters decreased, left ventricular function improved and was discharged after 6 days of hospital stay.

    Placental pathology in COVID-19

    Authors: Elisheva D Shanes; Leena B Mithal; Sebastian Otero; Hooman A Azad; Emily S Miller; Jeffery A Goldstein

    doi:10.1101/2020.05.08.20093229 Date: 2020-05-12 Source: medRxiv

    Objectives: To describe histopathologic findings in the placentas of women with COVID-19 during pregnancy. Methods: Pregnant women with COVID-19 delivering between March 18, 2020 and May 5, 2020 were identified. Placentas were examined and compared to historical controls and women with placental evaluation for a history of melanoma HP melanoma MESHD. Results: 16 placentas from patients with SARS-CoV-2 were examined (15 with live birth in the 3rd trimester 1 delivered in the 2nd trimester after intrauterine fetal demise). Compared to controls, third trimester placentas were significantly more likely to show at least one feature of maternal vascular malperfusion (MVM), including abnormal or injured maternal vessels, as well as delayed villous maturation, chorangiosis, and intervillous thrombi MESHD. Rates of acute and chronic inflammation MESHD were not increased. The placenta from the patient with intrauterine fetal demise showed villous edema MESHD edema HP and a retroplacental hematoma MESHD. Conclusions: Relative to controls, COVID-19 placentas show increased prevalence SERO of features of maternal vascular malperfusion (MVM), a pattern of placental injury reflecting abnormalities in oxygenation within the intervillous space associated with adverse perinatal outcomes. Only 1 COVID-19 patient was hypertensive MESHD despite the association of MVM with hypertensive disorders MESHD and preeclampsia HP. These changes may reflect a systemic inflammatory or hypercoagulable state influencing placental physiology.

    Interference of SARS-CoV-2 with the Homeostasis of Ventilation and Perfusion in the Lung

    Authors: Clemente F. Arias; Francisco J. Acosta; Federica Bertocchini; Cristina Fernández-Arias

    id:10.20944/preprints202005.0177.v1 Date: 2020-05-10 Source: Preprints.org

    A growing number of studies suggest that SARS-CoV-2 could interfere with homeostatic mechanisms in the lung but the implications of this possible interference have not been fully explored in the literature. In this work, we examine the consequences that can be drawn from this hypothesis according to currently available knowledge. We suggest that one such consequence is the potential disruption of normal ventilation and perfusion of lung regions that may be distant from the infection sites. Loss of ventilation might result in local alveolar hypoxia MESHD and contribute to hypoxemia HP hypoxemia MESHD, which in turn could trigger homeostatic responses that enhance blood SERO oxygenation by redistributing pulmonary blood SERO circulation. Sudden changes in perfusion might then lead to the development of hydrostatic edema MESHD edema HP and eventually to vascular remodeling and inflammation MESHD. Therefore, the immune response might not be the only source of the substantial inflammation MESHD observed in lung tissues of patients with severe COVID-19, as is often assumed in the literature. The balance between the homeostatic and the immune reaction in each patient could account for the observed heterogeneity of the clinical manifestations of COVID-19.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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