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GER and Helicobacter pylori

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Gastroesophageal Reflux in Children

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Abstract

Helicobacter pylori (H. pylori) infection has been shown to affect the severity and course of gastroesophageal reflux disease (GERD). In this chapter, we have updated these complex relationships based on recent developments in children’s studies, taking into account findings from studies in adults.

The effect of H. pylori on GERD differs according to the anatomical location of H. pylori infection (antrum, corpus, or pangastritis). The type of gastritis is also very important in the course of reflux esophagitis (acute, chronic, atrophic). H. pylori-associated gastritis in the corpus causes hypoacidity while antral gastritis causes hyperacidity. During childhood, H. pylori is associated with antral predominant gastritis and duodenal ulcers.

Gastrin is affected by the gastric localization of H. pylori infection, atrophic changes, and acute/chronic nature. In antral gastritis, hypergastrinemia occurs during the destruction of somatostatin-secreting cells during infection and it triggers acid production, and hyperacidity leads to the development or progression of GER and erosive esophagitis. In cases of antral gastritis that causes hyperacidity, reflux esophagitis may improve after H. pylori is eradicated. Chronic gastritis can lead to atrophic gastritis. Atrophic gastritis causes hypoacidity due to cell damage. In this case, GERD manifestations are provoked by the eradication of H. pylori. Histological studies have shown that atrophic gastritis is rare in children.

The determining factors that trigger H. pylori-related GERD are the location of gastritis in both children and adults, CagA/VacA positivity, and substances released from the stomach which lead to transient lower esophageal sphincter relaxations. Pangastritis causing gastric atrophy is associated with CagA strains and its protective effect against GERD has been demonstrated in corpus gastritis. H. pylori infection with CagA strains is associated with less severe reflux esophagitis in children. But, antral nodularity was found more frequently in CagA-positive patients. VacA, s1b positivity was associated with a lower frequency of esophagitis rate in children. Further studies are required to explain this complex relationship in childhood.

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Abbreviations

BapA:

Blood group antigen-binding adhesin A

BE:

Barrett’s esophagus

BMI:

Body mass index

CagA:

Cytotoxin-associated gene A

DupA:

Duodenal ulcer promoting gene A protein

EAC:

Esophageal adenocarcinoma

GERD:

Gastroesophageal Reflux Disease

H. pylori :

Helicobacter pylori

HpSA:

H. pylori stool antigen

IL:

Interleukin

NO:

Nitric oxide

OipA:

Outer inflammatory protein

OMPs:

Outer membrane proteins

PGs:

Pepsinogens

PPIs:

Proton pump inhibitors

RE:

Reflux Esophagitis

SabA:

Sialic acid-binding adhesin

TLESR:

Transient lower esophageal sphincter relaxations

VacA:

Vacuolating cytotoxin A

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  1. Istanbul Kent University, Istanbul, Turkey

    Oya Yücel

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  1. Vrije Universitiet Brussel (VUB), UZ Brussel KidZ Health Castle, Brussels, Belgium

    Yvan Vandenplas

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Yücel, O. (2022). GER and Helicobacter pylori. In: Vandenplas, Y. (eds) Gastroesophageal Reflux in Children. Springer, Cham. https://doi.org/10.1007/978-3-030-99067-1_14

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  • DOI: https://doi.org/10.1007/978-3-030-99067-1_14

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