<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1816-8949</journal-id>
<journal-title><![CDATA[Anales de la Facultad de Ciencias Médicas (Asunción)]]></journal-title>
<abbrev-journal-title><![CDATA[An. Fac. Cienc. Méd. (Asunción)]]></abbrev-journal-title>
<issn>1816-8949</issn>
<publisher>
<publisher-name><![CDATA[EFACIM. Editorial de la Facultad de Ciencias Médicas - Universidad Nacional de Asunción]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1816-89492020000200105</article-id>
<article-id pub-id-type="doi">10.18004/anales/2020.053.02.105</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Armando el Rompecabezas Fisiopatológico del COVID-19]]></article-title>
<article-title xml:lang="en"><![CDATA[Assembling the Physiopathology Puzzle of COVID-19]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Mateos]]></surname>
<given-names><![CDATA[Edgard Alexis]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional de Asunción Facultad de Ciencias Médicas, Hospital de Clínicas Servicio de Urgencias de Adultos]]></institution>
<addr-line><![CDATA[San Lorenzo ]]></addr-line>
<country>Paraguay</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>08</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>08</month>
<year>2020</year>
</pub-date>
<volume>53</volume>
<numero>2</numero>
<fpage>105</fpage>
<lpage>126</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.iics.una.py/scielo.php?script=sci_arttext&amp;pid=S1816-89492020000200105&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.iics.una.py/scielo.php?script=sci_abstract&amp;pid=S1816-89492020000200105&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.iics.una.py/scielo.php?script=sci_pdf&amp;pid=S1816-89492020000200105&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN Un nuevo coronavirus hace su aparición en China a fines del año 2019, produciendo infección respiratoria aguda y falla respiratoria. Debido a su similitud clínica y microbiológica con el agente del síndrome respiratorio agudo grave (SARS por sus siglas en inglés), el SARS-CoV1, que afecto a China en el año 2003, fue bautizado como SARS-CoV2, y la enfermedad que produce como COVID-19 (COronaVIrus Disease 2019). Desde su identificación el mundo médico se vio inundado de reportes estadísticos, tablas y cifras que hacen al comportamiento epidemiológico del SARS-CoV2, pero pocos autores han focalizado su investigación en los mecanismos patogénicos y si lo han hecho sus artículos han sido diluidos por la vorágine de datos estadísticos. El objetivo del presente trabajo es profundizar en los aspectos fisiopatológicos de la infección por SARS-CoV2 para lo cual realicé una revisión de la literatura desde el inicio de la actual pandemia hasta el mes de junio de 2020, utilizando para la búsqueda Mendeley y PubMed, centrado sobre todo en la capacidad del virus de alterar el delicado balance entre la angiotensina II y sus antagonistas, analizar las posibles razones de la peor evolución en un subgrupo de pacientes y proponer medidas terapéuticas enfocadas en estos hallazgos. El SARS-CoV2 infecta células que expresan el receptor primario para el virus, la enzima ACE2, presente en epitelio intestinal y respiratorio, así como en endotelio. Genera inicialmente hipoxia por lesión alveolar para luego generar disfunción endotelial por lesión directa, lesión mediada por anticuerpos, tormenta de citoquinas y alteración del balance entre la angiotensina II y sus antagonistas funcionales, con eventual trombosis en territorio pulmonar y sistémico, así como hemólisis angiopática y por hiperactividad macrofágica. La retroalimentación positiva entre hipoxia, inflamación y angiotensina II potencian el desarrollo de un síndrome de distrés y fallo multiorgánico, con escalada de la mortalidad. El análisis de la fisiopatología probable en la infección por SARS-CoV2 permite sacar algunas conclusiones siendo las centrales que el endotelio es uno de los actores centrales en la patogenia de la enfermedad y que los pacientes con mayor riesgo de complicaciones son aquellos con disfunción endotelial previa debida a la presencia de obesidad, diabetes mellitus o hipertensión, así como que existen diferentes fases o estadios, cada uno con una posible intervención terapéutica particular, es decir, que la COVID-19 es diferente entre pacientes y en el mismo paciente es diferente en el tiempo, con cada momento requiriendo una intervención terapéutica particular.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT 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.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Infecciones por Coronavirus (Coronavirus Infections)]]></kwd>
<kwd lng="es"><![CDATA[SARS-CoV2]]></kwd>
<kwd lng="es"><![CDATA[Angiotensinas (Angiotensins).]]></kwd>
<kwd lng="en"><![CDATA[Coronavirus Infection]]></kwd>
<kwd lng="en"><![CDATA[SARS-CoV2]]></kwd>
<kwd lng="en"><![CDATA[Angiotensin.]]></kwd>
</kwd-group>
</article-meta>
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