From the Guidelines
The answer is B. Duodenal ulcers. Depletion of somatostatin-producing antral cells in the gastric antrum leads to duodenal ulcers due to disruption of normal gastric acid regulation. The S-shaped, gram-negative bacteria described are Helicobacter pylori, which colonize the gastric mucosa and cause chronic inflammation. Somatostatin normally inhibits gastrin release, which in turn regulates gastric acid secretion. When somatostatin-producing cells are reduced, gastrin levels increase unchecked, resulting in hypersecretion of gastric acid. This excess acid flows into the duodenum, overwhelming the protective mechanisms of the duodenal mucosa and leading to ulcer formation. The duodenum is particularly susceptible to this acid-induced injury compared to the stomach, which has more robust protective mechanisms. This pathophysiological sequence explains why H. pylori infection is strongly associated with duodenal ulcer disease, rather than the other conditions listed in the question options, as supported by recent studies 1.
Some key points to consider:
- H. pylori infection is a major risk factor for peptic ulcer disease and gastric cancer, as highlighted in a 2022 review 1.
- The bacteria cause chronic inflammation in the gastric mucosa, leading to changes in acid secretion and somatostatin production.
- Eradication of H. pylori infection can prevent peptic ulcer disease and reduce the risk of gastric cancer, as discussed in a 2021 expert review 1.
- The relationship between H. pylori infection and duodenal ulcers is well-established, with the bacteria causing an increase in gastrin levels and subsequent hypersecretion of gastric acid, as noted in a 2019 study 1.
- The management of H. pylori infection involves eradication therapy, which can be effective in preventing duodenal ulcers and other complications, as outlined in a 2012 consensus report 1.
From the Research
Depletion of Somatostatin-Producing Antral Cells
- The depletion of somatostatin-producing antral cells from the gastric antrum is most likely to cause an increase in gastrin secretion, as somatostatin normally inhibits the release of gastrin 2.
- Elevated gastrin levels can lead to an increase in gastric acid secretion, which can cause duodenal ulcers.
- The studies provided show that proton pump inhibitors, such as omeprazole and lansoprazole, can effectively reduce gastric acid secretion and heal duodenal ulcers 3, 4, 5, 6.
- Therefore, the depletion of somatostatin-producing antral cells is most likely to cause duodenal ulcers.
Relationship Between Helicobacter pylori and Duodenal Ulcers
- The studies also show that Helicobacter pylori infection is associated with duodenal ulcer disease, and that eradication of the infection can prevent ulcer recurrence 3, 4, 5.
- The S-shaped, gram-negative bacteria mentioned in the question are likely Helicobacter pylori, which can colonize the gastric antrum and contribute to the development of duodenal ulcers.
- The depletion of somatostatin-producing antral cells, combined with the presence of Helicobacter pylori, can increase the risk of developing duodenal ulcers.