Incidental finding of Brunner Gland Hyperplasia in a case of Gastric Adenocarcinoma.
Brunner gland hyperplasia first described by swiss physician Johann Conrad brunner. The main function of these glands is to produce a mucus rich alkaline secretion in order to protect the duodenum from the acidic content of chyme (which is introduced into the duodenum from the stomach), provide an alkaline condition for intestinal enzymes, lubrication of intestinal walls and for better absorption.
They also secrete urogastrone which inhibits parietal and chief cells of the stomach from secreting excess acid and their digestive enzymes.
CASE HISTORY: A 70year old male patient presented with pain abdomen, vomiting and past history revealed on and off bouts of hematemesis and history of black colored stools. Routine investigations showed microcytic hypochromic anemia, renal parameters and liver function tests were within normal limits. Computerized tomography of lungs and liver showed no focal lesion or organomegaly. computerized tomography of abdomen showed diffuse wall thickening stomach partially distended along greater curvature average diameter measuring 1.6cm and kidney showed bilateral multiple renal cortical cysts.
Endoscopy revealed nodular ulcerative mass lesion involving 3/4th of the circumference noted in distal body of stomach along the incisura not involving pylorus. Endoscopic biopsy bits revealed presence of gastric adenocarcinoma and patient underwent distal gastrectomy, specimen was sent to our pathology department for histological examination. Gross examination of distal gastrectomy specimen measured 11x 5x1cm, cut section showed an ulcerative lesion in the stomach 3 cm away from pylorus. Histopathological sections showed moderately differentiated adenocarcinoma of the stomach, Infiltrating the submucosa and muscularis mucosa to a depth of 5mm.proximal duodenum showed ulcerated duodenal mucosa with lobular proliferation of brunner glands in the submucosa and few of the glands were cystically dilated. There was no evidence of dysplasia or H. pylori infection.
DISCUSSION: Brunner gland hyperplasia accounts for 10.6% of all benign duodenal tumors. Common age incidence is 5 th or 6th decade with equal gender distribution. 70% of brunner gland hyperplasia is seen in proximal duodenum duodenal bulb (Posterior wall) and 26 % are seen in second Part of duodenum and 4% in other parts. Mostly these are pedunculated. They commonly Present with bleeding or obstruction. (2) The etiology of Brunner gland hyperplasia is unknown. (2)
Most of the cases measure less than 1cm in size and called hyperplasia. Some of the cases measure more than 1cm in size and are called adenoma or brunneroma and few cases show presence of fat and muscle. (3)
In 1934 Feyrter classified brunner gland hyperplasia into 3 types (1) diffuse nodular hyperplasia (2) circumscribed nodular hyperplasia (3) adenomatous hyperplasia/ glandular adenoma.
Brunneroma or polypoid hamartoma is rare. (4) Usually it presents as asymptomatic abdominal pain vague discomfort nausea or bloating. Brunner gland hyperplasia is associated with Chronic renal failure, chronic pancreatitis, duodenitis, peptic ulcer. (5,6)
Brunner gland hyperplasia is an infrequently encountered polypoidal lesion in the proximal duodenum. (7) Differential diagnosis is leiomyoma, polypoid adenoma, aberrant pancreatic tissue, malignancy. Brunner gland hyperplasia is not fatal and patients remain asymptomatic, except for bleeding or obstruction or intussusception. (8) Use of endoscopic sonography will be helpful to visualize sub mucosal lesions of duodenum with brunner gland hyperplasia showing characteristic cobble stone pattern whereas hamartomas show variable echogenicity. (9) These lesions can also occur at ampulla of vater, though very rare should be considered in the differential diagnosis of mass lesions at ampulla. (10)
CONCLUSION: Benign lesions of the duodenum are very rare and exact prevalence cannot be assessed because many of these are asymptomatic. Brunner gland hyperplasia or adenomas are still rarer and pose diagnostic challenge. They are usually asymptomatic but can present with rare complications like bleeding, hemorrhagic shock or obstruction. Hence awareness of this entity and entertaining this in differential diagnosis is needed. Hence we present this case for its rarity and clinical significance.
(1.) A Costa-Pinho, J Pinto-de-sousa, M Baptista et al. Brunner's gland hyperplasia, an unusual cause of hemorrhagic shock. Oxford Journal's medicine, Journal of Surgical Case Reports, Volume 2011, Issue 5 > pp.2.
(2.) Levine JA, Burgart LJ, Balls KP, Wang KK. Brunner's gland hamartomas, clinical presentation and pathological features of 27 cases. AMJ Gastroenterol 1995 Feb; 90 (2), 290-4.
(3.) Chong KC, Cheah WK, Lenzi JE, Goh PM. Benign duodenal tumors. Hepatogastroenterology. 20Q0sep-Oct; 47(35):1298-300.
(4.) Feyrter F uber-wucharungerder Brunnerschen Drusen. Virchows Arch 1938; 293: 509-26.
(5.) Refcrao YP, Zhu JS, Zhang WJ. Brunner's gland adenoma of the duodenum- A case report and literature review. World J gastroenterol 2004; 10:2616-7.
(6.) Zollinger RM Jr. Primary neoplasms of the small intestine. Am J Surg 1986, 151:654-8.
(7.) Ajaz Ahmed Malik, Mohd Lateef Wani et al. Brunner's gland hyperplasia: An unusual cause of gastrointestinal bleeding. Turk J gastroenterol 2011; 22 (4): 419-421.
(8.) Chattopadhyay P, Kundu AK, Bhattacharyya S, Bandyopadhyay A. Diffuse nodular hyperplasia of Brunners glands Presenting as upper gastrointestinal hemorrhage. Singapore Med J 2008, 49:81-3.
(9.) Patel ND, Levy AD, Mehrotra AK, Sobin LH. Brunner's gland hyperplasia and hamartoma; imaging features with clinicopathologic correlation. Am J Roentgenol 2006; 187:715-22.
(10.) Janes SEJ, Zaitoun AM, Catton JA, Aithal GP, Beckingham. Brunner's gland hyperplasia at the ampulla of vater. J Postgrad med 2006; 52: 38-40.
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[1.] Neelala Neelaveni
[2.] Anunayi Jeshtadi
[3.] L. Aruna
[4.] C. H. Sreedevi
[5.] V. Vijaya Sreedhar
PARTICULARS OF CONTRIBUTORS:
[1.] Assistant Professor, Department of Pathology, Osmania General Hospital and Medical College.
[2.] Associate Professor, Department of Pathology, Osmania General Hospital and Medical College.
[3.] Assistant Professor, Department of Pathology, Osmania General Hospital and Medical College.
[4.] Senior Resident, Department of Pathology, Osmania General Hospital and Medical College.
[5.] Professor and HOD, Department of Pathology, Osmania General Hospital and Medical College.
NAME ADDRESS EMAIL ID OF THE CORRESPONDING AUTHOR:
Dr. Neelala Neelaveni, Flat No. 201, Vijaya Krishna Residency, Kalyanpuri, Uppal, Hyderabad--39.
Date of Submission: 05/02/2014.
Date of Peer Review: 06/02/2014.
Date of Acceptance: 14/02/2014.
Date of Publishing: 27/02/2014.
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|Title Annotation:||CASE REPORT|
|Author:||Neelaveni, Neelala; Jeshtadi, Anunayi; Aruna, L.; Sreedevi, C.H.; Sreedhar, V. Vijaya|
|Publication:||Journal of Evolution of Medical and Dental Sciences|
|Date:||Mar 3, 2014|
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