Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

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Shew-Meei Sheu1, Jiunn-Jong Wu2,and Bor-Shyang Sheu3

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Follow-up Testing After Treatment of Helicobacter Pylori Infections: Cautions, Caveats, and Recommendations Taraq A. Attumi, MD, David Y. Graham, MD

Gastrointestinal pathogens: Helicobacter pylori

Figure 2 Inflammatory pathways affecting hepatic insulin resistance

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 2 Enteroids can model transport physiology

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Figure 1 Differential immune responses in the gut (oral tolerance)

Figure 5 Dendritic cells in liver inflammation

Figure 1 Contribution of the gut microbiota

Figure 4 Activation of clopidogrel via cytochrome P450

Figure 5 Therapeutic paradigms for interfering with the brain–gut axis

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Figure 1 Gut microorganisms at the intersection of several diseases

Figure 5 Lipid droplet consumption

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Figure 2 The microbiome–gut–brain axis

Figure 7 Clinical options for HCC therapy

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Figure 1 Biosimilar development process

Figure 3 The 'leaky gut' hypothesis

Figure 2 Effect of PPIs on gastric physiology

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Figure 4 Giant lipid droplet formation

Figure 1 Schematic outlining the results of Buffington et al.

Figure 6 Combination therapy for HCC

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Figure 2 Switching of biologic agents and biosimilars

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Follow-up Testing After Treatment of Helicobacter Pylori Infections: Cautions, Caveats, and Recommendations Taraq A. Attumi, MD, David Y. Graham, MD

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

to the liver and promote patient-derived xenograft tumour growth

Figure 7 Example colonic high-resolution manometry

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 1 Environmental factors contributing to IBD pathogenesis

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Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

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Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

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Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

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Relationships between H. pylori, inflammation, and acid secretion.

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Presentation transcript:

Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.117 Figure 3 Effect of acid inhibition with PPIs on Helicobacter pylori gastritis Figure 3 | Effect of acid inhibition with PPIs on Helicobacter pylori gastritis. A shift from antrum-predominant inflammation to fundus–corpus-predominant inflammation occurs with acid inhibition via proton-pump inhibitors (PPIs). The occurrence of Helicobacter pylori gastritis varies according to H. pylori virulence and host susceptibility genes and is related to diverse clinical outcomes. Corpus-predominant gastritis is associated with a markedly higher risk of developing malignancy than antrum-predominant gastritis. PPIs alter the gastric milieu by contributing to increased IL-1β, a potent pro-inflammatory factor, and ammonia (NH4). The catalytic activity of H. pylori urease on urea leads to the formation of NH4, and PPIs could further promote the production of ammonia through the biological nitrogen cycle involving other gut bacteria. IL-1β and NH4 contribute to as well as result from the fact that H. pylori shifts from the antrum to the corpus. Consequently, H. pylori might even totally disappear from the antrum, but it increases the inflammation in the fundus–corpus. Malfertheiner, P. et al. (2017) Proton-pump inhibitors: understanding the complications and risks Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.117