<?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>0026-1742</journal-id>
<journal-title><![CDATA[Revista de la Facultad de Medicina (México)]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. Fac. Med. (Méx.)]]></abbrev-journal-title>
<issn>0026-1742</issn>
<publisher>
<publisher-name><![CDATA[Universidad Nacional Autónoma de México, Facultad de Medicina]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0026-17422020000500045</article-id>
<article-id pub-id-type="doi">10.22201/fm.24484865e.2020.63.5.08</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Fisiología de la hemostasia y su alteración por la coagulopatía en COVID-19]]></article-title>
<article-title xml:lang="en"><![CDATA[Physiology of Hemostasis and its Alteration by Coagulopathy in COVID-19]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[González-Villalva]]></surname>
<given-names><![CDATA[Adriana]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Peña-Díaz]]></surname>
<given-names><![CDATA[Aurora de la]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rojas-Lemus]]></surname>
<given-names><![CDATA[Marcela]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López-Valdez]]></surname>
<given-names><![CDATA[Nelly]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ustarroz-Cano]]></surname>
<given-names><![CDATA[Martha]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[García-Peláez]]></surname>
<given-names><![CDATA[Isabel]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bizarro-Nevares]]></surname>
<given-names><![CDATA[Patricia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Fortoul]]></surname>
<given-names><![CDATA[Teresa I.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México Facultad de Medicina Departamento de Biología Celular]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Nacional Autónoma de México Facultad de Medicina Departamento de Farmacología]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>10</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>10</month>
<year>2020</year>
</pub-date>
<volume>63</volume>
<numero>5</numero>
<fpage>45</fpage>
<lpage>57</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0026-17422020000500045&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0026-17422020000500045&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0026-17422020000500045&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La pandemia de la enfermedad COVID-19, ocasionada por el virus Sars-CoV-2, ha preocupado al personal de salud, entre otras cosas, por la alta incidencia de coagulopatía asociada a aumento en la mortalidad que se presenta en los pacientes. La coagulopatía es principalmente trombótica, inicialmente en pulmón y posteriormente sistémica, macro y microvascular, asociada al daño endotelial, inflamación, trampas extracelulares de neutrófilos (NETs), activación de macrófagos y tormenta de citocinas que perpetúan el círculo vicioso de trombosis e inflamación. Se ha reportado el aumento de factores protrombóticos en los pacientes: aumento del factor tisular, factor de Von Willebrand, fibrinógeno, factor VIII, entre otros y, además, la disminución de algunos anticoagulantes naturales como la proteína S y la antitrombina. Además, se menciona la insuficiencia de la fibrinólisis, asociada con el aumento del PAI-1 (inhibidor del activador tisular de plasminógeno). Durante la enfermedad, hay depósito de fibrina intraalveolar que también es degradada. Tanto la fibrinólisis del trombo, como la degradación de fibrina intraalveolar, hacen que aumenten los dímeros D y, por esta razón, este es uno de los mejores predictores de la severidad de la enfermedad COVID-19. En este artículo se revisa la fisiología de la hemostasia, la tromboinflamación secundaria a la infección por el virus Sars-Cov-2, la evidencia clínica y lo que se sabe de la fisiopatología de la coagulopatía en COVID-19, para tratar de entenderla desde la mirada de la ciencia básica.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract COVID-19 global pandemic caused by Sars-CoV-2 virus, has worried to health care providers due to the high mortality rate related to coagulopathy in many patients. COVID-19 coagulopathy is mainly thrombotic, first locally in lungs but later on it becomes micro and macrovascular systemic coagulopathy. It has been associated to endothelial damage, inflammation, neutrophil-extracellular traps, monocyte and macrophage activation, cytokines storm that induce a vicious cycle of thrombosis and inflammation. The increased levels of prothrombotic factors as tissue factor, Von Willebrand factor, fibrinogen, VIII factor and the decreased levels of antithrombotic factos, such as: antithrombin and Protein S have been reported in COVID-19 patients. Insufficiency of fibrinolysis because of the increased levels of PAI-1 (plasminogen activator inhibitor 1) have been reported also. During this disease there are intraalveolar fibrin deposits that needs to be degraded. Fibrinolysis of thrombus and fibrin intraalveolar degradation are responsible for the high increase of D-dimers levels that are an important predictor of severity of the disease. In this report, the physiology of hemostasis, thromboinflamation secondary to Sars-CoV-2 infection are reviewed, as well as the clinical evidence and the physiopathology of COVID-19 coagulopathy from the basic sciences point of view.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Hemostasia]]></kwd>
<kwd lng="es"><![CDATA[coagulación]]></kwd>
<kwd lng="es"><![CDATA[trombosis]]></kwd>
<kwd lng="es"><![CDATA[coagulopatía]]></kwd>
<kwd lng="es"><![CDATA[Sars-CoV-2]]></kwd>
<kwd lng="es"><![CDATA[COVID-19]]></kwd>
<kwd lng="en"><![CDATA[Hemostasis]]></kwd>
<kwd lng="en"><![CDATA[coagulation]]></kwd>
<kwd lng="en"><![CDATA[thrombosis]]></kwd>
<kwd lng="en"><![CDATA[coagulopathy]]></kwd>
<kwd lng="en"><![CDATA[Sars-CoV-2]]></kwd>
<kwd lng="en"><![CDATA[COVID-19]]></kwd>
</kwd-group>
</article-meta>
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<person-group person-group-type="author">
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<article-title xml:lang=""><![CDATA[The versatile heparin in COVID-19]]></article-title>
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