<?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>0872-8178</journal-id>
<journal-title><![CDATA[Jornal Português de Gastrenterologia ]]></journal-title>
<abbrev-journal-title><![CDATA[J Port Gastrenterol.]]></abbrev-journal-title>
<issn>0872-8178</issn>
<publisher>
<publisher-name><![CDATA[Sociedade Portuguesa de Gastrenterologia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0872-81782011000200004</article-id>
<title-group>
<article-title xml:lang="pt"><![CDATA[Permeabilidade Intestinal em Doentes com Cirrose Hepática: Correlação com Endotoxemia e Níveis Circulantes de TNF&#945;, IL - 1 e IL - 6]]></article-title>
<article-title xml:lang="en"><![CDATA[Intestinal Permealibity in Patients with Liver Cirrhosis: Correlation with Endotoxemia and Circulating Levels of TNF&#945;, IL - 1 and IL - 6]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ferro]]></surname>
<given-names><![CDATA[Susana Mão de]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Salazar]]></surname>
<given-names><![CDATA[Maria]]></given-names>
</name>
<xref ref-type="aff" rid="A03"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Machado]]></surname>
<given-names><![CDATA[Mariana]]></given-names>
</name>
<xref ref-type="aff" rid="A02"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ramalho]]></surname>
<given-names><![CDATA[Fernando]]></given-names>
</name>
<xref ref-type="aff" rid="A02"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pinto]]></surname>
<given-names><![CDATA[Helena Cortez]]></given-names>
</name>
<xref ref-type="aff" rid="A02"/>
</contrib>
</contrib-group>
<aff id="A01">
<institution><![CDATA[,Instituto Português de Oncologia de Lisboa, Francisco Gentil. EPE Serviços de Gastrenterologia ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<aff id="A02">
<institution><![CDATA[,Hospital de Santa Maria Serviços de Gastrenterologia ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<aff id="A03">
<institution><![CDATA[,Hospital da Força Aérea Serviços de Gastrenterologia ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2011</year>
</pub-date>
<volume>18</volume>
<numero>2</numero>
<fpage>66</fpage>
<lpage>72</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_arttext&amp;pid=S0872-81782011000200004&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_abstract&amp;pid=S0872-81782011000200004&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_pdf&amp;pid=S0872-81782011000200004&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="pt"><p><![CDATA[INTRODUÇÃO: A permeabilidade intestinal (PI) aumentada pode contribuir para a patogénese da cirrose hepática (CH) por aumento da translocação bacteriana e endotoxemia, com consequente elevação dos mediadores inflamatórios. OBJECTIVOS: Avaliar em doentes com CH se existe aumento da PI, e como este se correlaciona com a endotoxemia, resposta imunológica e a sua influência no risco de desenvolvimento de complicações. MÉTODOS: 19 doentes com CH, sem consumo alcoólico activo, e 19 controlos sem evidência de CH. PI avaliada pelo teste da lactulose-manitol (>Lac-Man). Níveis séricos de IL - 1, IL - 6 e TNF&#945; e endotoxemia. RESULTADOS: Permeabilidade intestinal: LAC/MAN: 0,16 ± 0,11 vs 0,40 ± 0,38, p=0,02 e endotoxemia: 0,38 ± 0,29 vs 0,28 ± 0,15 EU/mL, ns, nos doentes e controles respectivamente, sugerindo permeabilidade intestinal aumentada em ambos os grupos. A PI não se correlacionou com os níveis de endotoxemia e indivíduos com varizes esofágicas não apresentaram maior aumento da PI. IL- 1: 2,3 ± 0,3 vs. 1,8 ± 0,4 pg/mL,p = 0,03, IL - 6: 4,1 ± 3,4 vs.1,9 ± 2,2 pg/mL, p = 0,01; e TNF&#1048576;: 6,2±2,1 vs. 3,7±3,7 pg /mL, p = 0,001, nos doentes em relação aos controlos. CONCLUSÕES: Na cirrose hepática compensada, verificou-se PI e endotoxinemia aumentada, sem correlação com a presença de varizes esofágicas. Observou-se aumento significativo das citocinas circulantes, sem contudo se correlacionarem com o grau de PI ou endotoxemia.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[INTRODUCTION: Increased intestinal permeability (IP) may contribute to the pathogenesis of liver cirrhosis (LC), allowing for an increase in bacterial translocation and endotoxemia, with subsequent rise in inflammatory mediators. AIMS: To evaluate IP in patients with LC and its correlation with endotoxemia, cytokine response, and risk of complications. METHODS: 19 patients with LC, without active alcohol consumption, and 19 controls, without evidence of LC. IP was evaluated with the lactulose-manitol test (Lac-Man), and serum levels of endotoxaemia, IL - 1, IL - 6, and TNF&#945;. RESULTS: Intestinal permeability: LAC/MAN: 0.16 ± 0.11 vs 0.40 ± 0.38, p=0.02, and endotoxaemia: 0.38 ± 0.29 vs 0.28 ± 0.15 EU/mL, ns, in patients and controls respectively, suggesting increased permeability in both groups. PI did not correlate with endotoxinemia and individuals with oesophageal varices did not present increased intestinal permeability. IL - 1: 2.3 ± 0.3 vs. 1.8 ± 0.4 pg/mL, p = 0.03, IL - 6: 4.1 ± 3.4 vs. 1.9 ± 2.2 pg/mL, p = 0.01; TNF&#945;: 6.2 ± 2.1 vs. 3.7 ± 3.7 pg /mL, p = 0.001, in patients and controls respectively. CONCLUSIONS: In compensated liver cirrhosis, intestinal permeability and endotoxaemia are increased, with no correlation with the presence of portal hypertension, although with a significant increase in circulating cytokines which did not correlate with the degree of intestinal permeability or endotoxaemia.]]></p></abstract>
<kwd-group>
<kwd lng="pt"><![CDATA[Cirrose hepática]]></kwd>
<kwd lng="pt"><![CDATA[permeabilidade intestinal]]></kwd>
<kwd lng="pt"><![CDATA[endotoxemia]]></kwd>
<kwd lng="en"><![CDATA[Liver cirrhosis]]></kwd>
<kwd lng="en"><![CDATA[intestinal permeability]]></kwd>
<kwd lng="en"><![CDATA[endotoxaemia]]></kwd>
</kwd-group>
</article-meta>
</front><body><![CDATA[ <p><b>Permeabilidade Intestinal em Doentes com Cirrose Hepática: Correlação com    Endotoxemia e Níveis Circulantes de TNF&#945;, IL - 1 e IL – 6</b></p>     <p>&nbsp;</p>        <p><b>Susana Mão de Ferro<sup>1</sup>, Maria Salazar<sup>3</sup>, Mariana Machado<sup>2</sup>,    Fernando Ramalho<sup>2</sup>, Helena Cortez Pinto<sup>2</sup></b></p>        <p>Serviços de Gastrenterologia <sup>1</sup>IPOLFG, EPE, <sup>2</sup>Hospital    de Santa Maria, <sup>3</sup>Hospital da Força Aérea</p>     <p> <a name="top0"></a><a href="#0">Correspond&ecirc;ncia</a></p>     <p>&nbsp; </p>        <p><b>RESUMO</b></p>     <p><b> INTRODU&Ccedil;&Atilde;O: </b>A permeabilidade intestinal (PI) aumentada    pode contribuir para a patogénese da cirrose hepática (CH) por aumento da translocação    bacteriana e endotoxemia, com consequente elevação dos mediadores inflamatórios.    OBJECTIVOS: Avaliar em doentes com CH se existe aumento da PI, e como este se    correlaciona com a endotoxemia, resposta imunológica e a sua influência no risco    de desenvolvimento de complicações. MÉTODOS: 19 doentes com CH, sem consumo    alcoólico activo, e 19 controlos sem evidência de CH. PI avaliada pelo teste    da lactulose-manitol (><i>Lac-Man</i>). Níveis séricos de IL - 1, IL - 6 e TNF&#945;    e endotoxemia. <b>RESULTADOS:</b> Permeabilidade intestinal: <i>LAC/MAN</i>:    0,16 ± 0,11 vs 0,40 ± 0,38, p=0,02 e endotoxemia: 0,38 ± 0,29 vs 0,28 ± 0,15    EU/mL, ns, nos doentes e controles respectivamente, sugerindo permeabilidade    intestinal aumentada em ambos os grupos. A PI não se correlacionou com os níveis    de endotoxemia e indivíduos com varizes esofágicas não apresentaram maior aumento    da PI. IL- 1: 2,3 ± 0,3 vs. 1,8 ± 0,4 pg/mL,p = 0,03, IL - 6: 4,1 ± 3,4 vs.1,9    ± 2,2 pg/mL, p = 0,01; e TNF&#1048576;: 6,2±2,1 vs. 3,7±3,7 pg /mL, p = 0,001,    nos doentes em relação aos controlos. <b>CONCLUSÕES:</b> Na cirrose hepática    compensada, verificou-se PI e endotoxinemia aumentada, sem correlação com a    presença de varizes esofágicas. Observou-se aumento significativo das citocinas    circulantes, sem contudo se correlacionarem com o grau de PI ou endotoxemia.  </p>      <p><b>PALAVRAS-CHAVE:</b> Cirrose hepática, permeabilidade intestinal, endotoxemia.</p>     <p>&nbsp;</p>          ]]></body>
<body><![CDATA[<p><b>Intestinal Permealibity in Patients with Liver Cirrhosis: Correlation with    Endotoxemia and Circulating Levels of TNF&#945;, IL - 1 and IL - 6</b></p>          <p><b>ABSTRACT</b></p>     <p><b>INTRODUCTION</b>: Increased intestinal permeability (IP) may contribute    to the pathogenesis of liver cirrhosis (LC), allowing for an increase in bacterial    translocation and endotoxemia, with subsequent rise in inflammatory mediators.    AIMS: To evaluate IP in patients with LC and its correlation with endotoxemia,    cytokine response, and risk of complications. <b>METHODS:</b> 19 patients with    LC, without active alcohol consumption, and 19 controls, without evidence of    LC. IP was evaluated with the lactulose-manitol test (Lac-Man), and serum levels    of endotoxaemia, IL - 1, IL - 6, and TNF&#945;. <b>RESULTS:</b> Intestinal permeability:    LAC/MAN: 0.16 ± 0.11 vs 0.40 ± 0.38, p=0.02, and endotoxaemia: 0.38 ± 0.29 vs    0.28 ± 0.15 EU/mL, ns, in patients and controls respectively, suggesting increased    permeability in both groups. PI did not correlate with endotoxinemia and individuals    with oesophageal varices did not present increased intestinal permeability.    IL - 1: 2.3 ± 0.3 vs. 1.8 ± 0.4 pg/mL, p = 0.03, IL - 6: 4.1 ± 3.4 vs. 1.9 ±    2.2 pg/mL, p = 0.01; TNF&#945;: 6.2 ± 2.1 vs. 3.7 ± 3.7 pg /mL, p = 0.001, in    patients and controls respectively. <b>CONCLUSIONS:</b> In compensated liver    cirrhosis, intestinal permeability and endotoxaemia are increased, with no correlation    with the presence of portal hypertension, although with a significant increase    in circulating cytokines which did not correlate with the degree of intestinal    permeability or endotoxaemia. </p>      <p><b>KEYWORDS:</b> Liver cirrhosis, intestinal permeability, endotoxaemia<i>.</i></p>     <p>&nbsp;</p>     <p>Texto completo dispon&iacute;vel apenas em PDF.</p>     <p>Full text only available in PDF format.</p>     <p>&nbsp;</p>      <p><b>REFERÊNCIAS</b></p>      <p>1. Campillo B, Pernet P, Bories PN, <i>et al. </i>Intestinal permeability in liver cirrhosis: relationship with severe septic complications. Eur J Gastroenterol Hepatol 1999;11:755-759.</p>      ]]></body>
<body><![CDATA[<p>2. Gunnarsdottir SA, Sadik R, Shev S, <i>et al. </i>Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension. Am J Gastroenterol 2003;98:1362-1370.</p>      <p>3. Bauer TM, Steinbruckner B, Brinkmann FE, <i>et al. </i>Small intestinal bacterial overgrowth in patients with cirrhosis: prevalence and relation with spontaneous bacterial peritonitis. Am J Gastroenterol 2001;96:2962-2967.</p>      <p>4. Barakat M, Mostafa M, Mahran Z, <i>et al. </i>Portal hypertensive duodenopathy: clinical, endoscopic, and histopathologic profiles. Am J Gastroenterol 2007;102:2793-2802.</p>      <p>5. Figueiredo P, Almeida N, Lérias C, <i>et al. </i>Effect of portal hypertension in the small bowel: an endoscopic approach. Dig Dis Sci 2008;53:2144-2150.</p>      <p>6. Such J, Guardiola JV, de Juan J, <i>et al. </i>Ultrastructural characteristics of distal duodenum mucosa in patients with cirrhosis. Eur J Gastroenterol Hepatol 2002;14:371-376.</p>      <p>7. Cirera I, Bauer TM, Navasa M, <i>et al. </i>Bacterial translocation of enteric organisms in patients with cirrhosis. J Hepatol 2001;34:32-37.</p>      <p>8. Adachi Y, Moore LE, Bradford BU, <i>et al. </i>Antibiotics prevent liver injury in rats following long-term exposure to ethanol. Gastroenterology 1995;108:218-224.</p>      <p>9. Wigg AJ, Roberts-Thomson IC, Dymock RB, <i>et al. </i>The role of small intestinal bacterial overgrowth, intestinal permeability, endotoxaemia, and tumour necrosis factor alpha in the pathogenesis of non-alcoholic steatohepatitis. Gut 2001;48:206-211.</p>      <p>10. Thurman RG, Bradford BU, Iimuro Y, <i>et al. </i>Role of Kupffer cells, endotoxin and free radicals in hepatotoxicity due to prolonged alcohol consumption: studies in female and male rats. J Nutr 1997;127:903S-906S.</p>      <p>11. Miki K, Butler R, Moore D, <i>et al. </i>Rapid and simultaneous quantification of rhamnose, mannitol, and lactulose in urine by HPLC for estimating intestinal permeability in pediatric practice. Clin Chem 1996;42:71-75.</p>      ]]></body>
<body><![CDATA[<p>12. Cariello R, Federico A, Sapone A, <i>et al. </i>Intestinal permeability in patients with chronic liver diseases: It's relationship with the aetiology and the entity of liver damage. Dig Liver Dis 2010;42:200-204.</p>      <p>13. Keshavarzian A, Holmes EW, Patel M, <i>et al. </i>Leaky gut in alcoholic cirrhosis: a possible mechanism for alcohol-induced liver damage. Am J Gastroenterol 1999;94:200-207.</p>      <!-- ref --><p>14. Juby LD, Rothwell J, Axon AT. Lactulose/mannitol test: an ideal screen for celiac disease. Gastroenterology 1989;96:79-85.&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;[&#160;<a href="javascript:void(0);" onclick="javascript: window.open('/scielo.php?script=sci_nlinks&ref=000035&pid=S0872-8178201100020000400001&lng=','','width=640,height=500,resizable=yes,scrollbars=1,menubar=yes,');">Links</a>&#160;]<!-- end-ref --><p>15. Vilela EG, Torres HO, Ferrari ML, <i>et al. </i>Gut permeability to lactulose and mannitol differs in treated Crohn's disease and celiac disease patients and healthy subjects. Braz J Med Biol Res 2008;41:1105-1109.</p>      <p>16. Secondulfo M, Iafusco D, Carratu R, <i>et al.</i>Ultrastructural mucosal alterations and increased intestinal permeability in non-celiac, type I diabetic patients. Dig Liver Dis 2004;36:35-45.</p>      <p>17. Webster CJ. Principles of a quantitative assay for bacterial endotoxins in blood that >uses Limulus lysate and a chromogenic substrate.J Clin Microbiol 1980;12:644-650.</p>      <p>18. Bajaj JS, Zadvornova Y, Heuman DM, <i>et al. </i>Association of proton    pump inhibitor therapy with spontaneous bacterial peritonitis in cirrhotic patients    with ascites. Am J Gastroenterol 2009;104:1130-1134.</p>     <p>&nbsp;</p>     <p><a name="0"></a><a href="#top0">Correspond&ecirc;ncia</a>: Susana M&atilde;o    de Ferro, Servi&ccedil;o de Gastrenterologia, IPOLFG, EPE, R. Prof. Lima Basto    1099-023 Lisboa &#8211; Portugal; E-mail: <a href="mailto:smaodeferro@gmail.com">smaodeferro@gmail.com</a></p>     <p>&nbsp;</p>     ]]></body>
<body><![CDATA[<p><b>PATROCÍNIOS</b></p>     <p>Trabalho patrocinado por Bolsa de Investigação da Sociedade Portuguesa de Gastrenterologia.    Comunicado sob a forma de Poster na <i>44th Annual Meetingof the European Association    for the Study of the Liver </i>(EASL), 2009, Copenhaga – Dinamarca, e no XXVIII    Congresso Nacional de Gastrenterologia, 2008.</p>     <p>&nbsp;</p>     <p>Recebido para Publica&ccedil;&atilde;o: 31/03/2010 e Aceite para Publica&ccedil;&atilde;o:    19/12/2010.</p>         ]]></body><back>
<ref-list>
<ref id="B1">
<label>14</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Juby]]></surname>
<given-names><![CDATA[LD]]></given-names>
</name>
<name>
<surname><![CDATA[Rothwell]]></surname>
<given-names><![CDATA[J]]></given-names>
</name>
<name>
<surname><![CDATA[Axon]]></surname>
<given-names><![CDATA[AT]]></given-names>
</name>
</person-group>
<article-title xml:lang="en"><![CDATA[Lactulose/mannitol test: an ideal screen for celiac disease]]></article-title>
<source><![CDATA[Gastroenterology]]></source>
<year>1989</year>
<volume>96</volume>
<page-range>79-85</page-range></nlm-citation>
</ref>
</ref-list>
</back>
</article>
