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According to the title of our article, we believe that the cause of pain, pangastritis, and refractory gastric ulcer in our patient is hypoperfusion resulting from compression of the celiac artery by the median arcuate ligament. Which is not inconsistent with the fact that <span class="elsevierStyleItalic">Helicobacter pylori (H. pylori)</span> infection damages the gastric mucosa even after the bacterium has been eradicated and that this factor would have favoured such an aggressive clinical manifestation.</p><p id="par0010" class="elsevierStylePara elsevierViewall">By adhering to the gastric epithelium, disrupting the mucous layer, and releasing enzymes and toxins, <span class="elsevierStyleItalic">H. pylori</span> infection makes the gastric mucosa more vulnerable to damage by peptic acid. Moreover, the host's immune response to <span class="elsevierStyleItalic">H. pylori</span> causes an inflammatory reaction that further perpetuates tissue damage.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Electron microscopy has confirmed the presence of close adherence of <span class="elsevierStyleItalic">H. pylori</span> to the gastric cell surface. At the site of this, bacterial membrane proteins open channels in the epithelial cell membrane that allow direct contact of bacterial factors with the cytoplasm, improving the antigen presentation to the lamina propria and facilitating local and systemic immune stimulation.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">3</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">H. pylori</span> infection induces a significant increase in white blood cells flow and in the development of platelet aggregates, suggesting that platelet activation and aggregation contribute to associated microvascular dysfunction and to the recruitment of inflammatory cells. Platelet aggregation mediated by an interaction of <span class="elsevierStyleItalic">H. pylori</span> with the von Willebrand factor is believed to contribute to ulcer disease associated with infection, but also possibly to non-GI manifestations of infection such as cardiovascular disease and idiopathic thrombocytopenia.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">4</span></a></p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:2 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Cepeda González C, Culebras Requena J. Réplica. Med Clin (Barc). 2020;155:90.</p>" ] 1 => array:2 [ "etiqueta" => "☆☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0009"><span class="elsevierStyleInterRef" id="intr0009" href="https://doi.org/10.1016/j.medcli.2019.05.029">10.1016/j.medcli.2019.05.029</span><span class="elsevierStyleInterRef" id="intr0006" href="https://doi.org/10.1016/j.medcle.2019.07.013">10.1016/j.medcle.2019.07.013</span></p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:4 [ 0 => array:3 [ "identificador" => "bib0025" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Medial arcuate ligament syndrome as an infrequent cause of refractory gastric ulcer" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "C. Cepeda" 1 => "J. Culebras" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Med Clin (Barc)" "fecha" => "2019" "volumen" => "152" "paginaInicial" => "288" "paginaFinal" => "289" ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0030" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Pathogenesis of <span class="elsevierStyleItalic">Helicobacter pylori</span> infection" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "J.G. Kusters" 1 => "H.A. van Vliet" 2 => "E.J. Kuipers" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1128/CMR.00054-05" "Revista" => array:6 [ "tituloSerie" => "Clin Microbiol Rev" "fecha" => "2006" "volumen" => "19" "paginaInicial" => "449" "paginaFinal" => "490" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16847081" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0035" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Immunology of <span class="elsevierStyleItalic">Helicobacter pylori</span>: insights into the failure of the immune response and perspectives on vaccine studies" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "K.T. Wilson" 1 => "J.E. Crabtree" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1053/j.gastro.2007.05.008" "Revista" => array:6 [ "tituloSerie" => "Gastroenterology" "fecha" => "2007" "volumen" => "133" "paginaInicial" => "288" "paginaFinal" => "308" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/17631150" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0040" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "<span class="elsevierStyleItalic">Helicobacter pylori</span> binds von Willebrand factor and interacts with GPIb to induce platelet aggregation" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "M.F. Byrne" 1 => "S.W. Kerrigan" 2 => "P.A. Corcoran" 3 => "J.C. Atherton" 4 => "F.E. Murray" 5 => "D.J. Fitzgerald" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/s0016-5085(03)00397-4" "Revista" => array:5 [ "tituloSerie" => "Gastroenterology" "fecha" => "2003" "volumen" => "124" "paginaInicial" => "1846" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/12806618" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000015500000002/v1_202007190713/S2387020620302552/v1_202007190713/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000015500000002/v1_202007190713/S2387020620302552/v1_202007190713/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020620302552?idApp=UINPBA00004N" ]
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Vol. 155. Issue 2.
Pages 90 (July 2020)
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Vol. 155. Issue 2.
Pages 90 (July 2020)
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Med Clin. 2020;155:89-9010.1016/j.medcle.2019.05.027
Javier A. Cienfuegos, Fernando Rotellar, Luis Hurtado-Pardo
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