Carrie Wong, MD; Ayaz Matin, MD; Muhammad A. Syed, MD; Gabriel S. Levi, MD; David L. Carr-Locke, MD


December 17, 2012

In This Article


Johann Conrad Brunner (1653-1727) was a Swiss anatomist from Diessenhofen who studied medicine in Schaffhausen, Strasbourg, and Paris and was a professor of anatomy and physiology at the University of Heidelberg. Although he was most revered for his contributions to pancreatic physiology, he discovered the duodenal submucosal structures known today as Brunner glands.

The highest concentration of Brunner glands is located in the proximal duodenum but can extend into the proximal jejunum. These structures secrete a viscous alkaline fluid that contains a glycoprotein that binds to the intestinal mucosa. The alkalinity protects the mucosa from potential injury from acidic gastric secretions. In addition, Brunner glands secrete enterogastrone, a hormone that inhibits gastric acid secretion.[1,2]

Benign duodenal lesions are rare and found in only 0.008% of patients. Brunner gland adenoma, also known as brunneroma, accounts for approximately 5%-10% of these benign lesions and presents most commonly in the fifth or sixth decade of life.[3,4,5,6] Although the etiology of brunneroma is unclear, it is believed to be caused by hyperplasia of the ductal and stromal elements of exocrine glands in the proximal duodenal mucosa. Helicobacter pylori infection may be involved in the pathogenesis. In a study by Kovacevic and colleagues,[7] 5 out of 7 patients who were diagnosed with Brunner gland adenoma had concurrent H pylori infections. Similar to simple tubular adenomas, brunneromas have a low malignant potential.

Few scattered reports of duodenal adenocarcinoma arising from Brunner glands are found in the literature. Dysplasia has been shown to occur in a background of gastric metaplasia. It is postulated that Brunner gland hyperplasia and gastric metaplasia may occur secondary to duodenal mucosal injury. A recent study from Japan looked at the occurrence of dysplasia and invasive carcinoma in Brunner gland hyperplasia.[8] The investigators noted dysplastic changes in 2.1% of cases of Brunner gland hyperplasia, with only 0.3% of those being invasive carcinoma.

In this case series, we examined 2 Brunner gland tumors. The first case was benign and the second was malignant. Both cases manifested as recurrent episodes of melena and iron-deficiency anemia.