Abstract
Brunner's gland adenoma is a rare benign tumor of small bowel, often incidentally discovered during endoscopy or radiological imaging. Mostly they are asymptomatic or often present with nonspecific symptoms such as nausea, vomiting, gastrointestinal hemorrhage, iron deficiency anemia. We reported a 76 years old male case presented with chief complaints of vomiting and black tarry stool. General physical examination was normal except mild tenderness over epigastrium. Esophagogastroduodenoscopy revealed a pedunculated polypoid tubular structure with blind end distally of length approximately 10-12* 3.5*1.5 cm in the second section of the duodenum with multiple skipped ulcers on the exposed surface of it. Additionally, there were few erosions in the duodenum proximally and multiple superficial ulcerations in the antrum, associated with helicobacter pylori confirmed by rapid urease test kit. Surgical or endoscopic excision is the treatment of choice. We consider our case is the eldest case among Brunner's gland adenoma case in literature. Keywords: Brunner's gland adenoma; Brunner's gland hamartoma; Brunner's gland hyperplasia; case report.
Highlights
Brunner’s glands adenoma (BGA) is an extremely rare benign variant of small bowel neoplasm arising from the Brunner’s gland of the duodenum
Brunner’s glands account 10% of benign neoplasm of the duodenum,the first described by Brunner in 16881 whereas Curveilhier described first case in 1835.2,3 The pathophysiology of this is unknown; it is believed chronic insult of Brunner’s gland secondary to H. pylori infection would contribute to its hyperplasia
The exact pathophysiology of the Brunner’s gland adenoma remains obscure, there are many postulations regarding the etiology of BGH
Summary
Brunner’s glands adenoma (BGA) is an extremely rare benign variant of small bowel neoplasm arising from the Brunner’s gland of the duodenum. Brunner’s glands account 10% of benign neoplasm of the duodenum,the first described by Brunner in 16881 whereas Curveilhier described first case in 1835.2,3 The pathophysiology of this is unknown; it is believed chronic insult of Brunner’s gland secondary to H. pylori infection would contribute to its hyperplasia.
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