50 y/o male with duodenal polyp

Clinical History:

A 50 year old man presented with an 8 cm duodenal polyp. Five years ago, he complained of gastric pain and blood in his stool. At endoscopy, he had a 5 cm duodenal polyp, diagnosed as "benign". However, removal of the polyp was delayed for years because a CT scan found a renal cell carcinoma, which was excised. At his recent surgery for the duodenal polyp, a “wet” villous mass was found that abutted the Ampulla of Vater.

Gross:






Microscopic:

Diagnosis:

Hyperplastic polyp of gastric metaplasia / gastric heterotopia

Discussion:

This case demonstrates the presence of mature gastric tissue in the duodenum. Heterotopia is a developmental anomaly, defined as the presence of mature tissue in a location where it is not normally found. Gastric heterotopia has been described in the esophagus (inlet patch), duodenum, gallbladder, Meckel’s diverticulum, and other sites in the bowel. It is associated with diarrhea, obstruction, dyspepsia, ulceration and GI bleeding (Pediatr Dev Pathol 2000;3:277).

Extensive gastric heterotopia of the small intestine resulting in massive gastrointestinal bleeding, bowel perforation, and death: report of a case and review of the literature.

Lambert MP, Heller DS, Bethel C.

Gastric heterotopia of the small intestine is a rare occurrence outside of Meckel's diverticulum and intestinal duplication. The vast majority of cases of gastric heterotopia occur as polypoid or tumorous lesions in the duodenum. These lesions have been associated with clinical symptoms including diarrhea, obstruction, dyspepsia, ulceration, and gastrointestinal bleeding. We present a case of gastric heterotopia that is unique because the lesions occurred as multiple, carpet-like, nonpolypoid areas throughout a large portion of the small intestine. A review of the literature is included.

Grossly, heterotopia usually presents as one or more nodules or sessile polyps. Microscopically, it consists of fundic type mucosa with chief and parietal cells, lined by foveolar epithelium, with a full mucosal thickness, forming a mucosal island. It is rarely associated with gastric type adenomas (Virchows Arch 1999;435:452).

'Pyloric gland-type adenoma' arising in heterotopic gastric mucosa of the duodenum, with dysplastic progression of the gastric type.

Kushima R, Rüthlein HJ, Stolte M, Bamba M, Hattori T, Borchard F.

'Pyloric gland-type adenoma' is a recently described and very rare entity. We report a case of a pedunculated polyp of the duodenal bulb showing the features of pyloric gland-type adenoma. Heterotopic gastric mucosa was found adjacent to the tumour. Immunohistochemically, the tumour cells at the surface of the polyp showed foveolar-type mucin (M1) while most other tumour cells showed deep gastric mucin (M2), displaying a pattern of differentiation similar to the normal gastric mucosa. The polyp also showed villous or papillary structures with disorganization of gastric differentiation and marked increase of proliferating in foci cells. This is the first case of pyloric gland-type adenoma found to arise in heterotopic gastric mucosa of the duodenum, showing dysplastic progression of the gastric type.

Heterotopia differs from metaplasia. Metaplasia is the change from one type of fully differentiated tissue to another fully differentiated tissue, usually due to chronic inflammation. The lower esophagus and duodenal bulb are common sites of gastric metaplasia, which may occur as a protective response to gastric acid. Gastric metaplasia only occupies part of the mucosal thickness, and intermingles with native tissue. It typically is microscopic, and does not present with any gross findings. Histologically, it lacks the specialized cells of fundic type mucosa. It may be important to distinguish gastric metaplasia from heterotopia, because metaplasia is associated with duodenitis and often H. pylori, which may require treatment (Braz J Med Biol Res 2007;40:897, Dig Liver Dis 2002;34:16).

Duodenal gastric metaplasia and Helicobacter pylori infection in patients with diffuse nodular duodenitis.

Li XB, Ge ZZ, Chen XY, Liu WZ

Whether the regression of gastric metaplasia in the duodenum can be achieved after eradication of Helicobacter pylori is not clear. The aim of the present study was to investigate the relationship between H. pylori infection and gastric metaplasia in patients with endoscopic diffuse nodular duodenitis. Eighty-six patients with endoscopically confirmed nodular duodenitis and 40 control patients with normal duodenal appearance were investigated. The H. pylori-positive patients with duodenitis received anti-H. pylori triple therapy (20 mg omeprazole plus 250 mg clarithromycin and 400 mg metronidazole, all twice daily) for one week. A control endoscopy was performed 6 months after H. pylori treatment. The H. pylori-negative patients with duodenitis received 20 mg omeprazole once daily for 6 months and a control endoscopy was performed 2 weeks after treatment. The prevalence of H. pylori infection was 58.1%, and the prevalence of gastric metaplasia was 57.0%. Seventy-six patients underwent endoscopy again. No influence on the endoscopic appearance of nodular duodenitis was found after eradication of H. pylori or acid suppression therapy. However, gastric metaplasia significantly decreased and complete regression was achieved in 15/28 patients (53.6%) 6 months after eradication of H. pylori, accompanied by significant improvement of other histological alterations. Only mild chronic inflammation, but not gastric metaplasia, was found in the control group, none with H. pylori infection in the duodenal bulb. Therefore, H. pylori infection is related to the extent of gastric metaplasia in the duodenum, but not to the presence of diffuse nodular duodenitis.

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

Ciancio G, Nuti M, Orsini B, Iovi F, Ortolani M, Palomba A, Amorosi A, Surrenti E, Ilani SM, Surrenti C.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS:. Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0.>)

(Source: Pathology Outlines Case# 124 by Dr. Nat Pernick)