<?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>0120-9957</journal-id>
<journal-title><![CDATA[Revista colombiana de Gastroenterología]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. colomb. Gastroenterol.]]></abbrev-journal-title>
<issn>0120-9957</issn>
<publisher>
<publisher-name><![CDATA[Asociación Colombiana de Gastroenterología  ]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0120-99572022000400420</article-id>
<article-id pub-id-type="doi">10.22516/25007440.952</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Non-alcoholic fatty liver disease part 1: general aspects, epidemiology. pathophysiology and natural history]]></article-title>
<article-title xml:lang="es"><![CDATA[Hígado graso (parte 1): aspectos generales, epidemiología, fisiopatología e historia natural]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Prieto-Ortiz]]></surname>
<given-names><![CDATA[Jhon Edison]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sánchez-Luque]]></surname>
<given-names><![CDATA[Carlos Bernardo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ortega-Quiroz]]></surname>
<given-names><![CDATA[Rolando]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Centro de enfermedades hepáticas y digestivas (CEHYD)  ]]></institution>
<addr-line><![CDATA[Bogotá ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Centro de enfermedades hepáticas y digestivas (CEHYD)  ]]></institution>
<addr-line><![CDATA[Bogotá ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Clínica del Norte  ]]></institution>
<addr-line><![CDATA[Barranquilla ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2022</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2022</year>
</pub-date>
<volume>37</volume>
<numero>4</numero>
<fpage>420</fpage>
<lpage>432</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0120-99572022000400420&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0120-99572022000400420&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0120-99572022000400420&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Fatty liver or NAFLD is defined by the presence of fat or steatosis in hepatocytes and covers a spectrum that goes from simple steatosis, through steatohepatitis (NASH), with inflammation and fibrosis and ending in cirrhosis. It is considered a global world prevalence close to 25% in the general population and is diagnosed between 40 and 50 years, with variations regarding the predominant sex and with ethnic differences, affecting more the Hispanic population. Fatty liver is associated with metabolic syndrome (MS), and obesity is considered the main risk factor for its presence and progression. Fatty liver is a complex and very heterogeneous disorder in its pathophysiology, resulting from the interaction of multiple elements, genetic, epigenetic, environmental, cultural factors, etc. All this together leads to an accumulation of hepatic fat, insulin resistance, hormonal and intestinal microbiota alterations, generating hepatocellular damage through the formation of free oxygen radicals and activation of hepatic fibrogenesis. The natural history of fatty liver is dynamic, patients with simple steatosis have a low risk of progression to cirrhosis, in patients with NASH this risk is increased, however, the process may be reversible, and some people will have spontaneous improvement. Fibrosis seems to be the determinant of overall mortality and outcomes associated with liver disease, it is considered that in all patients fibrosis worsens one stage every 14 years, in NASH it worsens one stage every seven years. Previous studies conclude that approximately 20% of cases of simple steatosis progress to NASH and that approximately 20% of them progress to cirrhosis, with the presence of hepatocellular carcinoma (HCC) in 5 to 10% of them.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El hígado graso no alcohólico (NAFLD) se define por la presencia de grasa o esteatosis en los hepatocitos y abarca un espectro que va desde la esteatosis simple, pasa por la esteatohepatitis no alcohólica (NASH) con inflamación y fibrosis, y finaliza en la cirrosis. Se considera una prevalencia mundial global cercana al 25% en la población general y se diagnóstica entre los 40 y 50 años, con variaciones respecto al sexo predominante y con diferencias étnicas (la población hispana es la más afectada). El hígado graso está asociado al síndrome metabólico (SM), y la obesidad se considera el principal factor de riesgo con su presencia y con su progresión. El hígado graso es un trastorno complejo y muy heterogéneo en su fisiopatología, que resulta de la interacción de múltiples elementos: factores genéticos, epigenéticos, ambientales, culturales, entre otros. Todo ello en conjunto lleva a incremento paulatino de grasa hepática, resistencia a la insulina y alteraciones hormonales y de la microbiota intestinal, lo que genera un daño hepatocelular a través de la formación de radicales libres de oxígeno y activación de la fibrogénesis hepática. La historia natural del hígado graso es dinámica: los pacientes con esteatosis simple tienen bajo riesgo de progresión a cirrosis, mientras que en los pacientes con NASH este riesgo se aumenta; sin embargo, el proceso puede ser reversible y algunas personas tendrán una mejoría espontánea. La fibrosis parece ser el determinante de la mortalidad global y de los desenlaces asociados a la enfermedad hepática; se considera que en todos los pacientes la fibrosis empeora una etapa cada 14 años y en NASH empeora en una etapa cada 7 años. Estudios previos concluyen que aproximadamente 20% de los casos de esteatosis simple progresan a NASH y que, de ellos, aproximadamente el 20% progresan a cirrosis, con presencia de hepatocarcinoma (HCC) en el 5% a 10% de ellos.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Non-alcoholic Fatty liver disease]]></kwd>
<kwd lng="en"><![CDATA[pathophysiology]]></kwd>
<kwd lng="en"><![CDATA[natural history]]></kwd>
<kwd lng="es"><![CDATA[Hígado graso]]></kwd>
<kwd lng="es"><![CDATA[fisiopatología]]></kwd>
<kwd lng="es"><![CDATA[historia natural]]></kwd>
</kwd-group>
</article-meta>
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