S4726 An Acquired Double Pylorus Sign: A Rare Consequence of Recurrent Peptic Ulcer Disease

Introduction: Double pylorus is a rare gastrointestinal finding characterized by the presence of 2 distinct channels connecting the gastric antrum to the duodenal bulb. It may arise as either a congenital anomaly or as an acquired complication of peptic ulcer disease which has an estimated prevalence of 0.001–0.4%. We present a case of double pylorus identified during endoscopic evaluation, explore its potential etiologies, and review relevant management strategies and clinical implications. Case Description/Methods: A 67-year-old man with a history of decompensated alcoholic cirrhosis, prior perforated gastric ulcer requiring Graham patch repair, and chronic nonsteroidal anti-inflammatory drug use for pain management presented with melena. On arrival, he was hypotensive and tachycardic. Laboratory evaluation revealed a hemoglobin level of 10.7 g/dL (reference range: 13.5–17.5 g/dL), decreased from his baseline of 12.1 g/dL. He was emergently transfused with 2 units of packed red blood cells, started on an octreotide infusion, and received intravenous pantoprazole. Esophagogastroduodenoscopy (EGD) demonstrated non-bleeding type 2 gastroesophageal varices, portal hypertensive gastropathy, a cratered duodenal ulcer without active bleeding, and a double pylorus. We suspected that the double pylorus was acquired in setting of previous perforated gastric ulcer as was not seen on a prior EGD performed several years earlier. At discharge, the patient was advised to discontinue nonsteroidal anti-inflammatory drugs, transitioned to oral pantoprazole and scheduled for outpatient gastroenterology follow-up, including a repeat EGD in 6 weeks. Discussion: Penetrating gastroduodenal ulcers can form a fistulous tract between the stomach and duodenum, resulting in an acquired double pylorus. This condition is often discovered incidentally during endoscopy, as was the case with our patient. Management typically involves discontinuation of nonsteroidal anti-inflammatory drugs, initiation of proton pump inhibitor (PPI) therapy, and eradication of Helicobacter pylori, if present. While repeat endoscopy may be considered to assess healing and evaluate for fistula closure, the tract often persists as a stable anatomic variant. This case underscores the importance of recognizing double pylorus as a potential complication of peptic ulcer disease, particularly in the context of chronic nonsteroidal anti-inflammatory drug use. Early identification and targeted management of the underlying etiology are essential to minimizing further gastrointestinal morbidity.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001146364.23038.bf
Primary Topic
Gastrointestinal disorders and treatments
Type
article
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article

S4726 An Acquired Double Pylorus Sign: A Rare Consequence of Recurrent Peptic Ulcer Disease

Muhannad Kurtom, Shane Strange, Dustin Kilpatrick, Sadie De Silva
The American Journal of Gastroenterology
Gastrointestinal disorders and treatments
article

S4726 An Acquired Double Pylorus Sign: A Rare Consequence of Recurrent Peptic Ulcer Disease

Muhannad Kurtom, Shane Strange, Dustin Kilpatrick, Sadie De Silva
article en

Abstract

Introduction: Double pylorus is a rare gastrointestinal finding characterized by the presence of 2 distinct channels connecting the gastric antrum to the duodenal bulb. It may arise as either a congenital anomaly or as an acquired complication of peptic ulcer disease which has an estimated prevalence of 0.001–0.4%. We present a case of double pylorus identified during endoscopic evaluation, explore its potential etiologies, and review relevant management strategies and clinical implications. Case Description/Methods: A 67-year-old man with a history of decompensated alcoholic cirrhosis, prior perforated gastric ulcer requiring Graham patch repair, and chronic nonsteroidal anti-inflammatory drug use for pain management presented with melena. On arrival, he was hypotensive and tachycardic. Laboratory evaluation revealed a hemoglobin level of 10.7 g/dL (reference range: 13.5–17.5 g/dL), decreased from his baseline of 12.1 g/dL. He was emergently transfused with 2 units of packed red blood cells, started on an octreotide infusion, and received intravenous pantoprazole. Esophagogastroduodenoscopy (EGD) demonstrated non-bleeding type 2 gastroesophageal varices, portal hypertensive gastropathy, a cratered duodenal ulcer without active bleeding, and a double pylorus. We suspected that the double pylorus was acquired in setting of previous perforated gastric ulcer as was not seen on a prior EGD performed several years earlier. At discharge, the patient was advised to discontinue nonsteroidal anti-inflammatory drugs, transitioned to oral pantoprazole and scheduled for outpatient gastroenterology follow-up, including a repeat EGD in 6 weeks. Discussion: Penetrating gastroduodenal ulcers can form a fistulous tract between the stomach and duodenum, resulting in an acquired double pylorus. This condition is often discovered incidentally during endoscopy, as was the case with our patient. Management typically involves discontinuation of nonsteroidal anti-inflammatory drugs, initiation of proton pump inhibitor (PPI) therapy, and eradication of Helicobacter pylori, if present. While repeat endoscopy may be considered to assess healing and evaluate for fistula closure, the tract often persists as a stable anatomic variant. This case underscores the importance of recognizing double pylorus as a potential complication of peptic ulcer disease, particularly in the context of chronic nonsteroidal anti-inflammatory drug use. Early identification and targeted management of the underlying etiology are essential to minimizing further gastrointestinal morbidity.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 41%
Gastrointestinal disorders and treatments
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