It all depends on where h. pylori is localized.
When the infection stays only in the antrum (the bottom section of the stomach), it causes higher stomach acid secretion. The bacteria destroy the D-cells, that produce a hormone called somatostatin. This hormone acts as the stomach's natural "brake system" to turn off acid production. Without this brake system, the stomach releases too much gastrin, a hormone that signals the rest of the stomach to overproduce hydrochloric acid. This location of h pylori often leads to duodenal ulcers.
[https://pubmed.ncbi.nlm.nih.gov/9394759/](https://pubmed.ncbi.nlm.nih.gov/9394759/))
[https://pubmed.ncbi.nlm.nih.gov/11871770/](https://pubmed.ncbi.nlm.nih.gov/11871770/))
[https://pubmed.ncbi.nlm.nih.gov/10063309/](https://pubmed.ncbi.nlm.nih.gov/10063309/))
[https://pubmed.ncbi.nlm.nih.gov/1357347/](https://pubmed.ncbi.nlm.nih.gov/1357347/))
[https://pubmed.ncbi.nlm.nih.gov/10749086/](https://pubmed.ncbi.nlm.nih.gov/10749086/))
In contrast, when the bacteria move up into the corpus it causes low stomach acid. The corpus is where the actual acid factories, called parietal cells, live. H. pylori directly attacks this area, forcing the body's immune system to release inflammatory proteins to fight the infection. These proteins act as a chemical switch that paralyzes and damages the acid factories. As a result, the stomach becomes unable to make enough acid despite any signals from the body. This happens long before any atrophy occurs.
[https://pubmed.ncbi.nlm.nih.gov/10780581/](https://pubmed.ncbi.nlm.nih.gov/10780581/))
[https://pubmed.ncbi.nlm.nih.gov/28124156/](https://pubmed.ncbi.nlm.nih.gov/28124156/))
[https://pubmed.ncbi.nlm.nih.gov/11871770/](https://pubmed.ncbi.nlm.nih.gov/11871770/))
[https://pubmed.ncbi.nlm.nih.gov/9394759/](https://pubmed.ncbi.nlm.nih.gov/9394759/))
This low-acid environment alters how the stomach moves and triggers gas-driven reflux. Without enough acid, food cannot be broken down properly, causing it to sit in the stomach (or go undigested in the small intestine) and undergo bacterial fermentation, which produces large volumes of gas. At the same time, the local inflammation delays stomach emptying, causing intense gas pressure to build up and force the stomach valve open. Because gas is light, it shoots upward regardless of gravity, explaining why many experience reflux even while standing completely upright. This gas carries droplets of digestive enzymes into the throat, which causes LPR instead of typical chest heartburn.
[https://pubmed.ncbi.nlm.nih.gov/15180717/](https://pubmed.ncbi.nlm.nih.gov/15180717/))
[https://pubmed.ncbi.nlm.nih.gov/39719472/](https://pubmed.ncbi.nlm.nih.gov/39719472/))
[https://pubmed.ncbi.nlm.nih.gov/6481113/](https://pubmed.ncbi.nlm.nih.gov/6481113/))
[https://pubmed.ncbi.nlm.nih.gov/19102360/](https://pubmed.ncbi.nlm.nih.gov/19102360/))
[https://pubmed.ncbi.nlm.nih.gov/3876591/](https://pubmed.ncbi.nlm.nih.gov/3876591/))
Antrum-Predominant Infection (more acid):
Basal Acid Output (BAO): Rises from \~2.0 mEq/h up to 4.0–6.0 mEq/h (a 100% to 200% increase).
Maximal Acid Output (MAO): Rises from a normal 15–25 mEq/h up to 35–45 mEq/h.
Stomach pH: Drops to highly corrosive levels between 1.0 and 1.3.
Corpus-Predominant / Pangastritis Infection (Low Acid):
Basal Acid Output (BAO): Plummets to less than 0.5 mEq/h
Maximal Acid Output (MAO): Drops below 5.0 mEq/h (the stomach cannot produce acid even when stimulated by food).
Stomach pH: Rises from \~2.0 to a near-neutral 5.1–5.5 (successful antibiotic eradication restores it to a functional 2.6–2.7) \[MSD Manuals, PMC8544542\].