Brunner's gland hamartomas: Not always benign.

Brunner's gland hamartoma (BGH) is a rare, benign tumor of the duodenum. It is mostly asymptomatic and usually found incidentally on routine esophagogastroduodenoscopy (EGD). However, some BGHs present with major complications including anemia, bleeding, obstruction, or dysplasia, requiring management and resection of these lesions. Herein, we present two cases of large BGHs of the duodenum, one presenting as severe gastrointestinal bleeding and the other, noted on EGD for iron deficiency anemia, found to have high grade dysplasia. This literature review discusses the rare serious complications of BGH, including iron deficiency anemia, overt gastrointestinal bleeding, and malignant potential.

Endoloop pre-ligation assisted resection of a giant Brunner's gland adenoma of the duodenal bulb.

Brunner's gland adenoma (BGA), also known as Brunneroma or polypoid hamartoma, is a rare benign duodenal tumor that proliferates from Brunner's glands of the duodenum. They are usually asymptomatic and discovered by chance during endoscopy. Some giant lesions can sometimes present with chronic abdominal pain, nausea, vomiting, and anemia, including gastrointestinal bleeding and obstructive symptoms, and need to be resected by surgery or endoscopy. Here we report a giant BGA that was easily and safely removed by Endoloop pre-ligation assisted resection.

Brunner's gland adenoma: a robotic approach.

This report describes an unusual case of a symptomatic Brunner's gland adenoma arising in a man in his 40s that underwent robotic transduodenal resection. Initial investigations revealed a polypoidal, submucosal lesion that was found in the first part of the duodenum. Microscopically, there was neither dysplasia nor evidence of adenocarcinoma, suggesting differentials of gastrointestinal stroma tumour and duodenal adenoma. Given the size of the lesion, he underwent a surgical resection. Symptomatic Brunner's gland adenoma is uncommon and should be considered as a differential diagnosis in patients presenting with obstructive symptoms.

The Characteristics and Treatment Outcomes of 71 Duodenal Brunner's Gland Adenomas with Endoscopic Submucosal Dissection.

INTRODUCTION: The aim of this study was to investigate outcomes of patients with duodenal Brunner's gland adenomas (BGAs) that were treated endoscopically. METHODS: We identified 71 consecutive patients treated at our center with endoscopic submucosal dissection (ESD) for their duodenal tumors diagnosed pathologically as BGAs over the period between January 1, 2011 and December 31, 2021. We retrospectively analyzed our experience and short- and long-term outcomes of ESD therapy on patients with BGAs. RESULTS: Among 71 BGA patients with an average age of 57 ± 11.7 years (range: 30-82), 48 (67.6%) were male and 23 (32.4%) were female. The accuracy of preoperative diagnosis with endoscopic ultrasonography was 44.0% (22/50). The H. pylori infection was found in 29 patients (29/71, 40.8%). The median size of BGAs was 1.5 cm (interquartile range [IQR] 0.8-2.7 cm). The most common location was the duodenum bulb (50/71, 64.8%). For the ESD procedure, the median operation time was 15.0 min (IQR 9.5-25.5 min). The en bloc and the complete resection rates were 97.2% and 92.3%, respectively. ESD-related mild acute obstructive pancreatitis was present in 2 patients (2/4, 50%) with BGAs located in the ampulla region. During the follow-up period, 1 patient with a positive peripheral margin experienced tumor recurrence 2 years after the initial ESD. There was no disease-related death for the cohort. CONCLUSION: ESD was an effective and safe therapeutic option for BGA patients with excellent outcomes. Long-term follow-up is needed.

Brunner gland inflammation in Crohn's disease and Celiac disease: Overlapping inflammatory patterns suggest a possible link.

Similar to celiac disease, inflammatory bowel disease frequently manifests in the duodenum. Histopathologic studies focused on mucosal alterations with little attention to submucosal Brunner glands. Recently, several studies have demonstrated overlapping features between Crohn's disease and celiac disease suggesting a putative link. However, histopathologic studies evaluating this possible link are limited, and those that are focused on Brunner glands are lacking. The present study aims to explore whether Crohn's disease and celiac disease display shared or overlapping inflammatory changes in Brunner glands. We performed a retrospective review study over 17-years retrieving duodenal biopsy specimens containing Brunner gland lobules in patients with Crohn's disease, celiac disease, and ulcerative colitis. We found 10 out of 126 duodenal biopsies (8 %) in patients with Crohn's disease and 6 out of 134 (4.5 %) duodenal biopsies in patients with celiac disease sharing inflammatory patterns in duodenal Brunner gland lobules. Both diseases showed interstitial intralobular and interlobular mixed chronic inflammation with variable fibrosis. Focally enhanced active inflammation of Brunner gland lobules was more characteristic of Crohn's disease. Intralobular epithelioid granulomas and multinucleated giant cells were specific to Crohn's disease. Ulcerative colitis patients did not show similar features. The interstitial focally enhanced chronic inflammatory pattern was significantly (p < 0.05) associated with both diseases, while the other inflammatory patterns were not (p > 0.05). This overlapping inflammatory pattern in Brunner glands in patients with Crohn's disease and celiac disease is supportive of the previously reported link between the two diseases. Pathologists should pay more attention to Brunner glands when evaluating duodenal biopsies. Further studies are warranted to validate these observations and their relevance in the pathogenesis of autoinflammatory gastrointestinal diseases.

Intestinal obstruction secondary to Brunner's glands hyperplasia.

Brunner's gland hyperplasia constitutes 10.6% of benign tumors of the duodenum, with an incidence of 0.008%. It is usually an incidental finding during endoscopy or imaging tests as they are small and asymptomatic. In the case of symptomatic tumors, resection of the lesion is indicated. In lesions ≤2 cm, endoscopic resection can be chosen, reserving surgery for larger lesions or endoscopically inaccessible ones. We present the case of a patient with a history of vomiting and hyporexia of months of evolution who presented peptic ulcer perforation and underwent surgery. During follow-up, she presented intestinal obstruction due to pyloric stenosis. Given the impossibility of ruling out a neoplastic process with certainty in diagnostic tests, surgical resection (antrectomy) was decided with an anatomopathological finding of Brunner's gland hyperplasia.

Comprehensive proteogenomic characterization of early duodenal cancer reveals the carcinogenesis tracks of different subtypes.

The subtypes of duodenal cancer (DC) are complicated and the carcinogenesis process is not well characterized. We present comprehensive characterization of 438 samples from 156 DC patients, covering 2 major and 5 rare subtypes. Proteogenomics reveals LYN amplification at the chromosome 8q gain functioned in the transmit from intraepithelial neoplasia phase to infiltration tumor phase via MAPK signaling, and illustrates the DST mutation improves mTOR signaling in the duodenal adenocarcinoma stage. Proteome-based analysis elucidates stage-specific molecular characterizations and carcinogenesis tracks, and defines the cancer-driving waves of the adenocarcinoma and Brunner's gland subtypes. The drug-targetable alanyl-tRNA synthetase (AARS1) in the high tumor mutation burden/immune infiltration is significantly enhanced in DC progression, and catalyzes the lysine-alanylation of poly-ADP-ribose polymerases (PARP1), which decreases the apoptosis of cancer cells, eventually promoting cell proliferation and tumorigenesis. We assess the proteogenomic landscape of early DC, and provide insights into the molecular features corresponding therapeutic targets.

Duodenal gastric-type neoplasm with uncertain malignant potential in a lipoma.

The pathologic diagnosis of duodenal tumors is a developing field; however, its overview remains unclear. We describe a rare case of a duodenal gastric-type neoplasm in a 50-year-old woman. She visited her primary care doctor with complaints of upper abdominal pain, tarry stools, and shortness of breath on exertion. She was admitted owing to a stalked polyp with erosion and hemorrhage in the descending part of the duodenum. Endoscopic mucosal resection (EMR) was performed on the polyp. Histologically, the resected polyp was a lipomatous lesion in the submucosal layer, composed of mature adipose tissues. Scattered irregular lobules of Brunner's gland-like structures with well-preserved construction but mildly enlarged nuclei and occasional conspicuous nucleoli of the constituent cells were observed. The resection margin was negative. EMR findings of the duodenal polyp showed a gastric epithelial tumor within a lipoma, a rare histological type that has not been reported previously. This tumor may be classified as a "neoplasm with uncertain malignant potential" in a lipoma, an intermediate category between adenoma and invasive adenocarcinoma. There is no consensus on treatment, and careful follow-up is recommended. This is the first report of a duodenal gastric-type neoplasm with uncertain malignant potential in a lipoma.

Brunner Gland Hamartomas-Uncommon Presentations and Endoscopic Management.

Brunner gland hamartoma (BGH) is a rare condition that requires a high clinical suspicion to diagnose. Large hamartomas may initially present with iron deficiency anemia (IDA) or symptoms suggesting intestinal obstruction. Barium swallow may demonstrate the lesion, but endoscopic evaluation is the acceptable first line management unless a concern for underlying malignancy. The present case report and literature review highlight the uncommon presentations and endoscopic role in large BGHs management. Internists should consider BGH in their differential, especially in patient with occult bleeding, IDA, or obstruction, which can be treated with endoscopic resection of large sized tumors by trained experts.

KRAS G12D mutation in Brunner gland adenoma.

Brunner gland lesions (BGLs) encompass benign proliferations of the homonymous glands and have been designated as hyperplasia, adenoma (BGA), hamartoma or nodule. In general terms, lesions larger than 0.5 cm are considered true neoplasia with unknown malignant potential and unclear pathogenesis. Genetic alterations have seldom been reported in BGL, and include SMAD4/DPC4 and LRIG1, but not KRAS (Kirsten rat sarcoma viral oncogene homologue) to the best of our knowledge.We present the case of a man in his 60s, evaluated for iron deficiency anaemia harbouring a 1.5 cm BGA found by duodenoscopy. Immunohistochemistry failed to reveal microsatellite instability, and next-generation sequencing revealed a KRAS G12D point mutation.

Aquaporins in Glandular Secretion.

Exocrine and endocrine glands deliver their secretory product, respectively, at the surface of the target organs or within the bloodstream. The release of their products has been shown to rely on secretory mechanisms often involving aquaporins (AQPs). This chapter will provide insight into the role of AQPs in secretory glands located within the gastrointestinal tract, including salivary glands, gastric glands, duodenal Brunner's glands, liver, gallbladder, intestinal goblets cells, and pancreas, as well and in other parts of the body, including airway submucosal glands, lacrimal glands, mammary glands, and eccrine sweat glands. The involvement of AQPs in both physiological and pathophysiological conditions will also be highlighted.

Human glycoprotein-2 expressed in Brunner glands - A putative autoimmune target and link between Crohn's and coeliac disease.

Glycoprotein 2 (GP2) is an autoantigen in Crohn's (CD) and coeliac disease (CeD). We assessed GP2-isoform (GP21-4)-expression in intestinal biopsies of paediatric patients with CD, CeD, ulcerative colitis (UC), and healthy children (HC). Transcription of GP21-4 was elevated in proximal small intestine in CeD and CD patients (only GP22/4) compared to jejunum (CeD/CD) and large bowel (CD). CeD patients demonstrated higher duodenal GP22/4-mRNA levels compared to HC/UC patients whereas CD patients showed higher GP24-mRNA levels compared to UC patients. Duodenal synthesis of only small GP2 isoforms (GP23/4) was demonstrated in epithelial cells in patients/HC and in Brunner glands (also large isoforms) with a more frequent apical location in CD/CeD patients. All four GP2 isoforms interacted with gliadin and phosphopeptidomannan. Gliadin digestion improved binding to GP2 isoforms. GP21-4 binding to CeD/CD-related antigens, elevated duodenal GP21-4-mRNA transcription, and GP2-protein secretion in Brunner glands of CeD/CD patients suggest an autoimmune CeD/CD link.