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Brunner’s Gland Hyperplasia Causing Complete Small Bowel Obstruction in a Patient With Helicobacter pylori

Brunner's gland hyperplasia is an uncommon pathology from the duodenum and is believed to be associated with infection with Helicobacter pylori. Patients commonly present with gastrointestinal bleeding, nausea, or abdominal pain. However, obstruction is an unusual clinical finding. A 47-year-ol...

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Detalles Bibliográficos
Autores principales: Lewis, Toni-Ann J, Kostanyan, Sofya, Kasmin, Franklin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10318853/
https://www.ncbi.nlm.nih.gov/pubmed/37408935
http://dx.doi.org/10.7759/cureus.41351
Descripción
Sumario:Brunner's gland hyperplasia is an uncommon pathology from the duodenum and is believed to be associated with infection with Helicobacter pylori. Patients commonly present with gastrointestinal bleeding, nausea, or abdominal pain. However, obstruction is an unusual clinical finding. A 47-year-old male presented to the emergency department with complaints of recurrent emesis, epigastric pain, and cramping for three days. Medical history was significant for duodenitis and diverticulitis, but there had been no prior abdominal surgeries. Epigastric tenderness to palpation without rebound tenderness was present on physical examination, H. pylori stool antigen was positive on admission, and treatment with triple therapy was initiated. Progressively the patient developed increasing emesis, with an associated cessation in flatus and bowel movements. On endoscopy, it was reported that the endoscope could not advance past the second portion of the duodenum. A nasogastric tube was placed for gastric decompression. Small bowel follow-through showed obstruction at the distal second duodenal segment. Bismuth quadruple therapy was initiated on day three. Push enteroscopy showed luminal narrowing and a transition point at the second duodenal segment with no identifiable mass or significant ulceration. Biopsy reports indicated Brunner's gland hyperplasia. By day seven, the patient reported increased bowel movements and flatus, with a resolution of his nausea and emesis, and the nasogastric tube was removed. The patient was discharged on day eight with outpatient prescriptions for quadruple therapy for six days. He was also instructed to follow up with the general surgery and gastroenterology teams for outpatient colonoscopy six weeks post-discharge and with his primary care physician (PCP) four weeks after completing quadruple therapy to ensure H. pylori eradication. Studies have shown that H. pylori were detected in most patients with Brunner's gland hyperplasia and may induce proliferation in Brunner's glands. Brunner's gland hyperplasia has a low incidence, with minimal cases reported. There is malignant potential but a low risk of progression into adenocarcinoma. Our case reinforces the idea that Brunner's gland hyperplasia should be included in the work-up, alongside testing for infection with H. pylori in assessing patients with gastric obstruction.