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Anales de la Facultad de Ciencias Médicas (Asunción)

versão impressa ISSN 1816-8949


MATEOS, Edgard Alexis. Assembling the Physiopathology Puzzle of COVID-19. An. Fac. Cienc. Méd. (Asunción) [online]. 2020, vol.53, n.2, pp.105-126. ISSN 1816-8949.

A new coronavirus makes its appearance in China in late 2019, causing acute respiratory infection and respiratory failure. Due to its clinical and microbiological similarity to the agent of severe acute respiratory syndrome (SARS), SARS-CoV1, which affected China in 2003, was named SARS-CoV2, and the disease it produces as COVID-19 (COronaVIrus Disease 2019). Since its identification, the medical world has been flooded with statistical reports, tables and figures regarding the epidemiological behavior of SARS-CoV2, but few authors have focused their research on pathogenic mechanisms and if they have, their articles have been diluted by the maelstrom of statistical data.

The objective of the present work is to delve into the pathophysiological aspects of SARS-CoV2 infection, for which I carried out a literature review from the start of the current pandemic until June 2020, using Mendeley and PubMed for the search, focused above all on the ability of the virus to alter the delicate balance between angiotensin II and its antagonists, to analyze the possible reasons for the worse evolution in a subgroup of patients and to propose therapeutic measures focused on these findings.

SARS-CoV2 infects cells that express the primary receptor for the virus, the enzyme ACE2, present in the intestinal and respiratory epithelium, as well as the endothelium. Initially, it generates hypoxia due to alveolar injury and then generates endothelial dysfunction due to direct injury, antibody-mediated injury, cytokine storm and alteration of the balance between angiotensin II and its functional antagonists, with eventual thrombosis in pulmonary and systemic territory, as well as angiopathic hemolysis and due to macrophage hyperactivity. The positive feedback between hypoxia, inflammation and angiotensin II potentiates the development of a distress syndrome and multi-organ failure, with an increase in mortality.

The analysis of the probable pathophysiology in SARS-CoV2 infection allows us to draw some conclusions, the main ones being that the endothelium is one of the central actors in the pathogenesis of the disease and that the patients with the highest risk of complications are those with previous endothelial dysfunction, due to the presence of obesity, diabetes mellitus or hypertension, as well as that there are different phases or stages, each with a possible particular therapeutic intervention, that is, that COVID-19 is different between patients and in the same patient it is different in time, with each moment requiring a particular therapeutic intervention.

Palavras-chave : Coronavirus Infection; SARS-CoV2; Angiotensin..

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