Corpus overview


Overview

MeSH Disease

Human Phenotype

Hypoxemia (2)

Edema (2)

Angioedema (1)


Transmission

There are no transmission terms in the subcorpus


Seroprevalence
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    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.

    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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