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Asclepius Medical Case Reports  •  Vol 1  •  Issue 1  •  2018 29
INTRODUCTION
Brunner’s gland adenoma, or hamartoma, is a benign
mucosal neoplasm that arises from proximal part of the
duodenum due to exocrine gland hyperplasia.[1]
The
glandular hyperplasia is a result from a loss of leucine-rich
repeats and immunoglobulin-like domains 1 (Lrig1) gene
and an epidermal growth factor receptor (EGFR) ligand
upregulation with an enhanced EGFR signaling.[2]
Her2 and
ErbB are a type of EGFR receptor which has been linked to be
expressed by many malignant and benign cancers. EGFR is
a transmembrane receptor protein which has an intracellular
tyrosine kinase function, and when activated, induces
transcription of genes for synthesis and growth of the cell
cycle, leading to hyperplasia of specific tissue cells. Specific
gene signaling is important in maintaining a balance between
EGFR-mediated cell growth regulation.[3-5]
Lrig1 gene is a
cell cycle regulator that inhibits EGFR and acts as a tumor
suppressor.[2]
Loss of this tumor suppressor causes significant
upregulation of EGFR in duodenal adenoma tissue compared
to the surrounding regular duodenal tissue.[2]
Brunner’s
gland adenoma is rare, with an incidence of 0.01%.[6]
Patients with this lesion are usually asymptomatic but can be
symptomatic if the tumor gets big enough causing possible
upper gastrointestinal bleeding and/or even obstruction.[7]
CASE REPORT
A 60-year-old male was referred to Northside Medical
Center for the evaluation of a mass found in the first part of
the duodenum on esophagogastroduodenoscopy (EGD). He
had undergone endoscopic ultrasound (EUS) and computed
tomography (CT) scan imaging at an outside facility. The
patient presented initially with complaints of epigastric
abdominal pain, postprandial bloating, and hemoccult
positive stools. He underwent an EGD/colonoscopy and EUS
by gastroenterology. Patient had no current symptoms on our
admission; denied nausea, vomiting, diarrhea, constipation,
heartburn, as well as abdominal pain.
Medical history was significant for hypertension,
hyperlipidemia, and gastroesophageal reflux disease for
which he took atorvastatin 20 mg daily, hydrochlorothiazide
25 mg daily, metoprolol tartrate 100 mg daily, omeprazole
40 mg BID, and aspirin 81 mg daily. Laboratory results
revealed a hemoglobin of 14.5 and a hematocrit of 41.4 with
no electrolyte imbalances. Blood urea nitrogen, creatinine,
liver enzymes, and the remainder of laboratory results were
within normal limits.
An EGD under general anesthesia was performed for possible
endoscopic mucosal resection of the polypoid mass in the
CASE REPORT
Brunner’s Gland Adenoma
J. Kyle Phillips MD, Ali Kimyaghalam MD, Eric Trevizo MS, Robert De Vito MS,
Peter De Vito MD
Department of General Surgery, Northside Medical Center, NEOMED, Youngstown, Ohio, USA
ABSTRACT
Brunner’s gland adenoma or hyperplasia is a rare benign mass most commonly found in the proximal part of the duodenum
due to a loss of a cell cycle regulator. This case study was done on a 60-year-old symptomatic male who had a history of
gastroesophageal reflux disease. A Brunner’s gland adenoma may become large enough to cause symptoms of obstruction and
upper gastrointestinal bleeding. The benign lesion successfully underwent endoscopic mucosal resection.
Key words: Brunner gland adenoma, Brunner hyperplasia, Brunner’s adenoma, Brunner’s hamartoma, Brunner’s neoplasm,
Brunneroma, small bowel neoplasm
Address for correspondence:
Ali Kimyaghalam MD, Department of Surgery, Northside Medical Center, USA. E-mail: alik@auamed.net
https://doi.org/10.33309/2638-7700.010111 www.asclepiusopen.com
© 2018 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.
Phillips, et al.: Brunner’s Gland Adenoma
 Asclepius Medical Case Reports  •  Vol 1  •  Issue 1  •  2018
duodenum with possible open laparotomy if necessary. The
lubricated endoscope was introduced, and the oropharynx
was easily intubated with normal length. The Z line was
noted at 38 cm. On entrance of the stomach, the scope was
retroflexed and the cardia appeared normal with no evidence
of a hiatal hernia. The scope was advanced into the antrum,
which appeared normal, then the pylorus was intubated and
the duodenum was traversed. The polypoid mass was well
visualized in the first part of the duodenum appearing to be
at least 4 cm [Figures 1 and 2]. On inspection, the remainder
of the duodenum appeared to be normal. At this time, an
endoscopic mucosal resection was performed. Two pink,
polypoid, and soft rubbery excisions were retrieved using
baskets that measured 1.8 cm × 1.4 cm × 1.2 cm and 2 cm
× 1.4 cm × 0.9 cm. The base of the polypectomy site looked
intact with no residual mass.The scope was retracted back into
the stomach for a second look. The stomach was desufflated
and the scope was removed with a second visualization of the
mucosal surfaces on the way out. At this point, the procedure
was deemed complete and the patient was awakened in stable
condition for further recovery. The patient was placed on a
proton-pump inhibitors BID and clear liquid diet and was
advanced to normal diet on post-operative day 1 and was
subsequently discharged.
Histopathology findings were consistent with chronic
inflammation of the duodenal mucosa and an underlying
polypoid mass of hyperplastic Brunner gland tissue,
consistent with a Brunner’s gland adenoma.
DISCUSSION
Brunner glands are normal submucosal cells that are most
abundant in the proximal duodenum and can extend to the
proximal jejunum.[8]
These glands are made up of secretory
units of epithelial tubules that secrete a protective and
lubricating substance for the duodenum.[9]
The mucous
contains alkaline fluid, to protect the mucosa from gastric
acidic secretions, a glycoprotein, that coats the intestinal
mucosa, and enterogastrone, which inhibits gastric acid
secretion.[8]
It has been postulated that repeated duodenal
mucosal injury either due to acidic gastric secretions or
Helicobacter pylori infections are the cause of Brunner gland
hyperplasia.[10]
Brunner’s adenoma is usually asymptomatic
and found indecently during endoscopy. When the patient
becomes symptomatic, it is usually due to the hamartoma
becoming large enough to cause signs of obstruction and even
hemorrhage.[7]
Only 11% of patients with a case of Brunner’s
adenoma are asymptomatic.[11]
For diagnosis, CT scans seem
to be ineffective unless the mass is large enough to visualize.
The mainstay of diagnosis and treatment, according to
a study in Korea, is to perform and EGD polypectomy of
Brunner’s adenomas. Patients with large adenomas that have
been unsuccessful with EGD or if the size is too large, must
undergo open laparotomy for removal.[12]
Whether to remove
an asymptomatic hamartoma is not clear, their increasing size
may result in complications of obstruction or hemorrhage
as well as a potential for malignant transformation. This is
reason enough for removal.[13]
In conclusion, not only is EGD with endoscopic mucosal
resection a generally safe and low-risk procedure, but studies
have shown also excellent post-operative outcomes with
no reoccurrences with both endoscopic mucosal resection
and open laparotomy for removal.[12]
While it remains
controversial whether an asymptomatic Brunner’s gland
adenoma needs removed, removal of suspected Brunner
adenomas is important to confirm diagnosis and prevent
future complications such as obstruction, bleeding, or
malignant transformation.
REFERENCES
1.	 Michael JO, Kunitake H. Epidemiology, Clinical Features,
and Types of Small Bowel Neoplasms. Available from:
Figure 1: Esophagogastroduodenoscopy (EGD) picture 1
Figure 2: Esophagogastroduodenoscopy (EGD) picture 2
Phillips, et al.: Brunner’s Gland Adenoma
Asclepius Medical Case Reports  •  Vol 1  •  Issue 1  •  2018 31
www.uptodate.com/contents/epidemiology-clinical-
features-and-types-of-small-bowel-neoplasms?search=br
unnersource=search_resultselectedTitle=3~7usage_
type=defaultdisplay_rank=3. [Last accessed on 2018 Jan 05].
2.	 Wang Y, Shi C, Lu Y, Poulin EJ, Franklin JL, Coffey RJ, et al.
Loss of lrig1 leads to expansion of Brunner glands followed
by duodenal adenomas with gastric metaplasia. Am J Pathol
2015;185:1123-34.
3.	 Gotoh N. Feedback inhibitors of the epidermal growth
factor receptor signaling pathways. Int J Biochem Cell Biol
2009;41:511-5.
4.	 Hanahan D, Weinberg RA. Hallmarks of cancer: The next
generation. Cell 2011;144:646-74.
5.	 Wang Y, Poulin EJ, Coffey RJ. LRIG1 is a triple threat: ERBB
negative regulator, intestinal stem cell marker and tumour
suppressor. Br J Cancer 2013;108:1765-70.
6.	 Stewart ZA, Hruban RH, Fishman EF, Wolfgang CL. Surgical
management of giant brunner’s gland hamartoma: Case report
and literature review. World J Surg Oncol 2009;7:68.
7.	 Rocco A, Borriello P, Compare D, De Colibus P, Pica L,
Iacono A, et al. Large Brunner’s gland adenoma: Case report
and literature review. World J Gastroenterol 2006;12:1966-8.
8.	 Carrie W, Matin A, Syed MA, Levi GS, Carr-Locke DL. When
Brunner glands are not so innocent. Medscape Medscape
Gastroenterol 2012. Available from: http://www.medscape.
com/viewarticle/775988_1. [Last accessed on 2018 June, 08].
9.	 Krause WJ. Brunner’s glands: A structural, histochemical
and pathological profile. Prog Histochem Cytochem
2000;35:259-367.
10.	 Kovacević I, Ljubicić N, Cupić H, Doko M, Zovak M,
Troskot B, et al. Helicobacter pylori infection in patients with
Brunner’s gland adenoma. Acta Med Croatica 2001;55:157-60.
11.	 Walden DT, Marcon NE. Endoscopic injection and
polypectomy for bleeding Brunner’s gland hamartoma: Case
report and expanded literature review. Gastrointest Endosc
1998;47:403-7.
12.	 Gao YP, Zhu JS, Zheng WJ. Brunner’s gland adenoma of
duodenum: A case report and literature review. World J
Gastroenterol 2004;10:2616-7.
13.	 Park JH, Park CH, Park JH, Lee SJ, Lee WS, Joo YE, et al. The
safety and usefulness of endoscopic polypectomy for treatment
of Brunner’s gland adenomas. Korean J Gastroenterol
2004;43:299-303.
How to cite this article: Phillips JK, Kimyaghalam A,
Malliaras G, Trevizo E, De Vito R, De Vito P. Brunner’s
Gland Adenoma. Asclepius Med Case Rep 2018;1(1):29-31

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Brunner’s Gland Adenoma

  • 1. Asclepius Medical Case Reports  •  Vol 1  •  Issue 1  •  2018 29 INTRODUCTION Brunner’s gland adenoma, or hamartoma, is a benign mucosal neoplasm that arises from proximal part of the duodenum due to exocrine gland hyperplasia.[1] The glandular hyperplasia is a result from a loss of leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1) gene and an epidermal growth factor receptor (EGFR) ligand upregulation with an enhanced EGFR signaling.[2] Her2 and ErbB are a type of EGFR receptor which has been linked to be expressed by many malignant and benign cancers. EGFR is a transmembrane receptor protein which has an intracellular tyrosine kinase function, and when activated, induces transcription of genes for synthesis and growth of the cell cycle, leading to hyperplasia of specific tissue cells. Specific gene signaling is important in maintaining a balance between EGFR-mediated cell growth regulation.[3-5] Lrig1 gene is a cell cycle regulator that inhibits EGFR and acts as a tumor suppressor.[2] Loss of this tumor suppressor causes significant upregulation of EGFR in duodenal adenoma tissue compared to the surrounding regular duodenal tissue.[2] Brunner’s gland adenoma is rare, with an incidence of 0.01%.[6] Patients with this lesion are usually asymptomatic but can be symptomatic if the tumor gets big enough causing possible upper gastrointestinal bleeding and/or even obstruction.[7] CASE REPORT A 60-year-old male was referred to Northside Medical Center for the evaluation of a mass found in the first part of the duodenum on esophagogastroduodenoscopy (EGD). He had undergone endoscopic ultrasound (EUS) and computed tomography (CT) scan imaging at an outside facility. The patient presented initially with complaints of epigastric abdominal pain, postprandial bloating, and hemoccult positive stools. He underwent an EGD/colonoscopy and EUS by gastroenterology. Patient had no current symptoms on our admission; denied nausea, vomiting, diarrhea, constipation, heartburn, as well as abdominal pain. Medical history was significant for hypertension, hyperlipidemia, and gastroesophageal reflux disease for which he took atorvastatin 20 mg daily, hydrochlorothiazide 25 mg daily, metoprolol tartrate 100 mg daily, omeprazole 40 mg BID, and aspirin 81 mg daily. Laboratory results revealed a hemoglobin of 14.5 and a hematocrit of 41.4 with no electrolyte imbalances. Blood urea nitrogen, creatinine, liver enzymes, and the remainder of laboratory results were within normal limits. An EGD under general anesthesia was performed for possible endoscopic mucosal resection of the polypoid mass in the CASE REPORT Brunner’s Gland Adenoma J. Kyle Phillips MD, Ali Kimyaghalam MD, Eric Trevizo MS, Robert De Vito MS, Peter De Vito MD Department of General Surgery, Northside Medical Center, NEOMED, Youngstown, Ohio, USA ABSTRACT Brunner’s gland adenoma or hyperplasia is a rare benign mass most commonly found in the proximal part of the duodenum due to a loss of a cell cycle regulator. This case study was done on a 60-year-old symptomatic male who had a history of gastroesophageal reflux disease. A Brunner’s gland adenoma may become large enough to cause symptoms of obstruction and upper gastrointestinal bleeding. The benign lesion successfully underwent endoscopic mucosal resection. Key words: Brunner gland adenoma, Brunner hyperplasia, Brunner’s adenoma, Brunner’s hamartoma, Brunner’s neoplasm, Brunneroma, small bowel neoplasm Address for correspondence: Ali Kimyaghalam MD, Department of Surgery, Northside Medical Center, USA. E-mail: alik@auamed.net https://doi.org/10.33309/2638-7700.010111 www.asclepiusopen.com © 2018 The Author(s). This open access article is distributed under a Creative Commons Attribution (CC-BY) 4.0 license.
  • 2. Phillips, et al.: Brunner’s Gland Adenoma Asclepius Medical Case Reports  •  Vol 1  •  Issue 1  •  2018 duodenum with possible open laparotomy if necessary. The lubricated endoscope was introduced, and the oropharynx was easily intubated with normal length. The Z line was noted at 38 cm. On entrance of the stomach, the scope was retroflexed and the cardia appeared normal with no evidence of a hiatal hernia. The scope was advanced into the antrum, which appeared normal, then the pylorus was intubated and the duodenum was traversed. The polypoid mass was well visualized in the first part of the duodenum appearing to be at least 4 cm [Figures 1 and 2]. On inspection, the remainder of the duodenum appeared to be normal. At this time, an endoscopic mucosal resection was performed. Two pink, polypoid, and soft rubbery excisions were retrieved using baskets that measured 1.8 cm × 1.4 cm × 1.2 cm and 2 cm × 1.4 cm × 0.9 cm. The base of the polypectomy site looked intact with no residual mass.The scope was retracted back into the stomach for a second look. The stomach was desufflated and the scope was removed with a second visualization of the mucosal surfaces on the way out. At this point, the procedure was deemed complete and the patient was awakened in stable condition for further recovery. The patient was placed on a proton-pump inhibitors BID and clear liquid diet and was advanced to normal diet on post-operative day 1 and was subsequently discharged. Histopathology findings were consistent with chronic inflammation of the duodenal mucosa and an underlying polypoid mass of hyperplastic Brunner gland tissue, consistent with a Brunner’s gland adenoma. DISCUSSION Brunner glands are normal submucosal cells that are most abundant in the proximal duodenum and can extend to the proximal jejunum.[8] These glands are made up of secretory units of epithelial tubules that secrete a protective and lubricating substance for the duodenum.[9] The mucous contains alkaline fluid, to protect the mucosa from gastric acidic secretions, a glycoprotein, that coats the intestinal mucosa, and enterogastrone, which inhibits gastric acid secretion.[8] It has been postulated that repeated duodenal mucosal injury either due to acidic gastric secretions or Helicobacter pylori infections are the cause of Brunner gland hyperplasia.[10] Brunner’s adenoma is usually asymptomatic and found indecently during endoscopy. When the patient becomes symptomatic, it is usually due to the hamartoma becoming large enough to cause signs of obstruction and even hemorrhage.[7] Only 11% of patients with a case of Brunner’s adenoma are asymptomatic.[11] For diagnosis, CT scans seem to be ineffective unless the mass is large enough to visualize. The mainstay of diagnosis and treatment, according to a study in Korea, is to perform and EGD polypectomy of Brunner’s adenomas. Patients with large adenomas that have been unsuccessful with EGD or if the size is too large, must undergo open laparotomy for removal.[12] Whether to remove an asymptomatic hamartoma is not clear, their increasing size may result in complications of obstruction or hemorrhage as well as a potential for malignant transformation. This is reason enough for removal.[13] In conclusion, not only is EGD with endoscopic mucosal resection a generally safe and low-risk procedure, but studies have shown also excellent post-operative outcomes with no reoccurrences with both endoscopic mucosal resection and open laparotomy for removal.[12] While it remains controversial whether an asymptomatic Brunner’s gland adenoma needs removed, removal of suspected Brunner adenomas is important to confirm diagnosis and prevent future complications such as obstruction, bleeding, or malignant transformation. REFERENCES 1. Michael JO, Kunitake H. Epidemiology, Clinical Features, and Types of Small Bowel Neoplasms. Available from: Figure 1: Esophagogastroduodenoscopy (EGD) picture 1 Figure 2: Esophagogastroduodenoscopy (EGD) picture 2
  • 3. Phillips, et al.: Brunner’s Gland Adenoma Asclepius Medical Case Reports  •  Vol 1  •  Issue 1  •  2018 31 www.uptodate.com/contents/epidemiology-clinical- features-and-types-of-small-bowel-neoplasms?search=br unnersource=search_resultselectedTitle=3~7usage_ type=defaultdisplay_rank=3. [Last accessed on 2018 Jan 05]. 2. Wang Y, Shi C, Lu Y, Poulin EJ, Franklin JL, Coffey RJ, et al. Loss of lrig1 leads to expansion of Brunner glands followed by duodenal adenomas with gastric metaplasia. Am J Pathol 2015;185:1123-34. 3. Gotoh N. Feedback inhibitors of the epidermal growth factor receptor signaling pathways. Int J Biochem Cell Biol 2009;41:511-5. 4. Hanahan D, Weinberg RA. Hallmarks of cancer: The next generation. Cell 2011;144:646-74. 5. Wang Y, Poulin EJ, Coffey RJ. LRIG1 is a triple threat: ERBB negative regulator, intestinal stem cell marker and tumour suppressor. Br J Cancer 2013;108:1765-70. 6. Stewart ZA, Hruban RH, Fishman EF, Wolfgang CL. Surgical management of giant brunner’s gland hamartoma: Case report and literature review. World J Surg Oncol 2009;7:68. 7. Rocco A, Borriello P, Compare D, De Colibus P, Pica L, Iacono A, et al. Large Brunner’s gland adenoma: Case report and literature review. World J Gastroenterol 2006;12:1966-8. 8. Carrie W, Matin A, Syed MA, Levi GS, Carr-Locke DL. When Brunner glands are not so innocent. Medscape Medscape Gastroenterol 2012. Available from: http://www.medscape. com/viewarticle/775988_1. [Last accessed on 2018 June, 08]. 9. Krause WJ. Brunner’s glands: A structural, histochemical and pathological profile. Prog Histochem Cytochem 2000;35:259-367. 10. Kovacević I, Ljubicić N, Cupić H, Doko M, Zovak M, Troskot B, et al. Helicobacter pylori infection in patients with Brunner’s gland adenoma. Acta Med Croatica 2001;55:157-60. 11. Walden DT, Marcon NE. Endoscopic injection and polypectomy for bleeding Brunner’s gland hamartoma: Case report and expanded literature review. Gastrointest Endosc 1998;47:403-7. 12. Gao YP, Zhu JS, Zheng WJ. Brunner’s gland adenoma of duodenum: A case report and literature review. World J Gastroenterol 2004;10:2616-7. 13. Park JH, Park CH, Park JH, Lee SJ, Lee WS, Joo YE, et al. The safety and usefulness of endoscopic polypectomy for treatment of Brunner’s gland adenomas. Korean J Gastroenterol 2004;43:299-303. How to cite this article: Phillips JK, Kimyaghalam A, Malliaras G, Trevizo E, De Vito R, De Vito P. Brunner’s Gland Adenoma. Asclepius Med Case Rep 2018;1(1):29-31