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Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children

Gastric outlet obstruction (GOO) in children is most commonly caused by idiopathic hypertrophic pyloric stenosis. Prior to proton pump inhibitors and H2 blockers, peptic ulcer disease (PUD) secondary to H. pylori was a cause of GOO. Both patients presented with a history of weight loss, vomiting, an...

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Detalles Bibliográficos
Autores principales: Patel, Raza A., Baker, Susan S., Sayej, Wael N., Baker, Robert D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3350168/
https://www.ncbi.nlm.nih.gov/pubmed/22606426
http://dx.doi.org/10.1155/2011/749850
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author Patel, Raza A.
Baker, Susan S.
Sayej, Wael N.
Baker, Robert D.
author_facet Patel, Raza A.
Baker, Susan S.
Sayej, Wael N.
Baker, Robert D.
author_sort Patel, Raza A.
collection PubMed
description Gastric outlet obstruction (GOO) in children is most commonly caused by idiopathic hypertrophic pyloric stenosis. Prior to proton pump inhibitors and H2 blockers, peptic ulcer disease (PUD) secondary to H. pylori was a cause of GOO. Both patients presented with a history of weight loss, vomiting, and abdominal pain. Their diagnosis of PUD and GOO was made by EGD and UGI. H. pylori testing was negative for both on multiple occasions but still received H. pylori eradication therapy. Patient 1 after failing pharmaceutical management underwent surgery for definitive treatment. Patient 2 underwent six therapeutic pyloric dilations before undergoing surgery as definitive treatment. These cases suggest that GOO secondary to PUD occurs in the absence of H. pylori infection and surgical management can provide definitive therapy.
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spelling pubmed-33501682012-05-17 Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children Patel, Raza A. Baker, Susan S. Sayej, Wael N. Baker, Robert D. Case Rep Gastrointest Med Case Report Gastric outlet obstruction (GOO) in children is most commonly caused by idiopathic hypertrophic pyloric stenosis. Prior to proton pump inhibitors and H2 blockers, peptic ulcer disease (PUD) secondary to H. pylori was a cause of GOO. Both patients presented with a history of weight loss, vomiting, and abdominal pain. Their diagnosis of PUD and GOO was made by EGD and UGI. H. pylori testing was negative for both on multiple occasions but still received H. pylori eradication therapy. Patient 1 after failing pharmaceutical management underwent surgery for definitive treatment. Patient 2 underwent six therapeutic pyloric dilations before undergoing surgery as definitive treatment. These cases suggest that GOO secondary to PUD occurs in the absence of H. pylori infection and surgical management can provide definitive therapy. Hindawi Publishing Corporation 2011 2011-08-25 /pmc/articles/PMC3350168/ /pubmed/22606426 http://dx.doi.org/10.1155/2011/749850 Text en Copyright © 2011 Raza A. Patel et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Case Report
Patel, Raza A.
Baker, Susan S.
Sayej, Wael N.
Baker, Robert D.
Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
title Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
title_full Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
title_fullStr Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
title_full_unstemmed Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
title_short Two Cases of Helicobacter pylori-Negative Gastric Outlet Obstruction in Children
title_sort two cases of helicobacter pylori-negative gastric outlet obstruction in children
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3350168/
https://www.ncbi.nlm.nih.gov/pubmed/22606426
http://dx.doi.org/10.1155/2011/749850
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