Peptic ulcer disease is common, but its treatment shifted towards a non-surgical approach following a Nobel Prize-winning discovery, the Helicobacter pylori (H. pylori) infection. It was in 1982, that Barry Marshal and Robin Warren, from Australia, first isolated this bacterium from gastric mucosa biopsies. An innovative discovery was born. However, the medical community was convinced that no bacteria could live in the acidic environment of the stomach and that the stomach was sterile. So, it was not possible it could have a role in peptic ulcer disease, they said. Those old dogmas were blinding the experts at the time.
Barry Marshal kept thinking “out of the box” and kept his mind open to innovation. He was submitted to an upper endoscopy, and no changes were found in the gastric mucosa or in the biopsies. Then he drank a culture solution with H. pylori and was submitted to another upper endoscopy a few days later. Gastritis was evident, changes in gastric mucosa biopsies were now present, and gastritis-causing bacteria were found in the biopsies. Additionally, he was able to cure himself by taking antibiotics for 10 days. He managed to prove that antibiotics could heal gastritis. During the following years, the medical community accepted H. pylori as the cause of gastric and duodenal ulcers and recommended antibiotics to treat peptic ulcer disease. In 2004 (22 years after the first discovery of H. pylori) Barry Marshal and Robin Warren won the Nobel Prize.
In previous years, the dogma was “no acid - no ulcer”, and surgery was the baseline treatment. Thanks to Barry Marshal and Robin Warren today’s dogma is “no acid and no H. pylori - no ulcer.” In fact, the recurrence of peptic ulcer reflects the recurrence of H. pylori infection. This new concept completely changed peptic ulcer treatment, moving towards a medical and non-surgical approach. In the present day, surgery is indicated only for complications of peptic ulcer. Even in an emergent surgery for perforation or hemorrhage, vagotomy is not used anymore. Gastric resection for peptic ulcer treatment is a rarity in the present day.
In that setting, some concepts may be falling into oblivion. One of those may be the retained gastric antrum syndrome, which can cause peptic ulcer recurrence after gastrectomy. I found a case report from 2003, but many reports and publications have more than 20-30 years. Retained gastric antrum syndrome causes hypergastrinemia, with the consequent peptic ulcer, or peptic ulcer recurrence. Gastrin is produced by G cells and stimulates the parietal cells to produce acid. When the gastric pH falls to 3.0, gastrin production stops. Following gastric resection, a retained gastric antrum produces gastrin without negative feedback from the acid. Why? Because the retained antrum does not contact the acid secreted in the proximal gastric remnant. So… Gastrin is produced non-stop.
In 2003, Dr. Daniel Fontes, from Brazil, reported a case of a male patient already submitted to partial gastrectomy with Billroth II reconstruction, with a recurrent marginal peptic ulcer in the gastrojejunal anastomosis. The patient was on 40 mg/day of esomeprazole. Serum gastrin was 366 pg/ml (normal < 150 pg/ml). Following a CT scan and a celiac trunk angiography, a gastrinoma was suspected. However, during surgery, they found no gastrinoma but a retained gastric antrum. The authors decided to proceed with gastric remnant resection and retained antrum resection. Would a resection limited to the retained gastric antrum be enough to treat this patient? Probably yes, followed by H. pylori testing and eradication.
The retained gastric antrum syndrome is a rare complication following gastrectomy. It can be the cause of a peptic ulcer following a badly performed partial gastrectomy. A small amount of antrum is left near the duodenum, which produces gastrin in an undesired way, causing hypergastrinemia and the consequent peptic ulcer. However, there are other causes of hypergastrinemia that surgeons must take into consideration as differential diagnoses. According to the authors, possible causes of hypergastrinemia are:
Zollinger-Ellison syndrome;
G cells hyperplasia;
chronic renal insufficiency;
gastric emptying delay.
Differentiating a Zollinger-Ellison syndrome from a retained gastric antrum syndrome is not easy. Dr. Daniel Fontes et al state that serum gastrin > 500 pg/ml is very common in a gastrinoma, but serum gastrin 150-500 pg/ml is not diagnostic. Stimulation tests are good to diagnose gastrinoma (e.g., secretin stimulation test, calcium stimulation test). Secretin stimulation test is negative in both H. pylori infection and retained gastric antrum syndrome. Imaging tests are also crucial to diagnose both entities:
Ultrasonography and CT scan for Zollinger-Ellison syndrome;
Tc scintigraphy is the gold standard diagnostic tool for retained gastric antrum syndrome.
Remember that medical history is very important since retained gastric antrum syndrome means a previous gastrectomy. Finally, surgical resection is the only treatment for retained gastric antrum syndrome.
Nowadays, this entity, like many others, is falling into oblivion. This is true because of innovations in the diagnosis and treatment of diseases implicated in the etiology of those entities. As fewer and fewer surgeries are performed to treat peptic ulcers, complications, and consequent syndromes can be forgotten because they become a rarity. Surgeons must be updated but must never forget the older concepts and syndromes.
This is also happening with the emergence and widespread of laparoscopic surgery. Laparoscopy is limiting some open surgical techniques to the hardest scenarios. Will a surgeon used to the laparoscopic perspective be nervous about the need for open surgery?
Do you enjoy adrenal surgery? Must have this new book!
Costa Almeida CE, editor. Posterior Retroperitoneoscopic Adrenalectomy. Indications, Technical Steps and Outcomes. Switzerland: Springer; 2023.
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Dr. Carlos Eduardo Costa Almeida
General Surgeon
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