Gastric duodenal metaplasia in duodenal adenomas

Abstract

Backgound: In cases of known aetiology, gastric duodenal metaplasia (GMD) is a reversible lesion. In cases of unknown aetiology, the fate of GMD remains elusive. GMD was recently found in a duodenal adenoma. Aim: To audit the frequency of GMD occurring in a cohort of duodenal adenomas. Methods: Filed H&E-stained sections from 306 consecutive duodenal adenomas were investigated for the presence of GMD. Results: 68% of the adenomas (n = 208) were from patients with familial adenomatous polyposis (FAP), and the remaining 32% (n = 98) were sporadic. GMD was found in 31.7% (66/208) of the duodenal FAP adenomas and in 59.2% (58/98) of the duodenal sporadic adenomas (p,0.05). The causes for this difference are elusive. Conclusions: As for other metaplasias of the gastrointestinal tract (intestinal metaplasia of the oesophagus and of the stomach, and metaplastic-hyperplastic polyposis of the colon, known to antedate neoplastic transformation), a subset of GMDs of unknown cause might be present in the duodenal mucosa before adenomatous changes ensue. That subset of GMD might have neoplastic proclivity similar to the metaplastic epithelium in other organs of the gastrointestinal tract. The known carcinogenic effect of high concentrations of bile acids and pancreatic juices bathing the duodenal mucosa carrying an irreversible subset of GDM might set aflame the adenomatous neoplastic transformation in these patients.T he normal mucosa of the duodenum is built of absorbing columnar enterocytes and secreting goblet cells. Goblet cells produce acid sialomucins and stain with periodic acidSchiff (PAS), and more specifically with the cationic dye alcian blue.1 The absorbing columnar enterocytes are unable to produce neutral mucins, or sulphomucins under normal conditions.1 In gastric metaplasia in the duodenum (GMD), the luminal aspect of the cytoplasm of absorbing columnar enterocytes has the property of secreting PAS-positive neutral mucins and, occasionally, traces of alcian blue-positive sialomucins.1 GMD is a histologically detectable mucosal change thought to evolve following an abnormally high production of gastric acid triggered by Helicobacter pylori infection.2 When that hypersecretion reaches the duodenum, the enterocytes of the villi react with apical mucin metaplasia to buffer the unwanted low pH of the microenvironment. Recent studies indicate, however, that GMD may be found in the absence of gastric H pylori infection [2][3][4][5][6] in coeliac disease, 7 in Crohn's disease extending to the duodenum 8 and even in the absence of all these conditions. The cause(s) of GMD in the latter group of patients is elusive. Whereas GMD usually disappears following the eradication of the H. pylori, 9 and following a gluten-free diet in patients with coeliac disease, little is known about the evolution of GMD 10 in patients without H. pylori infection and without coeliac disease.Recently, while reviewing duodenal adenomas, 11 we noticed that GMD could be detected in those neoplasias. The purpose of the present study was to inve...

Endoscopic assessment and management of sporadic duodenal adenomas: The results of single centre multidisciplinary management

“…Kim et al[13] found that all of their 17 non ampullary adenomas were dysplastic while a larger series from Japan[14] demonstrated that dysplasia was presented in all 233 non-ampullary adenomas assessed. The rate of low grade dysplasia in non-ampullary adenomas in our series was 73.3%, which was within range (52%-84%) of recently published series[13-15,19], while the rate of low grade dysplasia in our ampullary adenomas (78%) was higher than 53%-66% previously reported[16-18]. The processes responsible for the high rates of dysplasia in SDA are not clear however Rubio[19] suggested that the duodenum of those patients may exhibit gastric duodenal metaplasia and bile acids and pancreatic juices may provide a milieu that encourages the metaplasia to proceed onto the adenoma-carcinoma sequence.…”

“…The rate of low grade dysplasia in non-ampullary adenomas in our series was 73.3%, which was within range (52%-84%) of recently published series[13-15,19], while the rate of low grade dysplasia in our ampullary adenomas (78%) was higher than 53%-66% previously reported[16-18]. The processes responsible for the high rates of dysplasia in SDA are not clear however Rubio[19] suggested that the duodenum of those patients may exhibit gastric duodenal metaplasia and bile acids and pancreatic juices may provide a milieu that encourages the metaplasia to proceed onto the adenoma-carcinoma sequence. It is possible that SDA progress to dysplasia faster than other adenomas in the gastrointestinal tract[19].…”

“…This investigation was undertaken to review multidisciplinary management of SDA and confirms that the majority of SDA are not symptomatic and are found incidentally[ 6 - 9 ]. Endoscopically SDA tend to be large, sessile and located in the second part of the duodenum[ 6 , 10 - 13 ] and this series also confirms that most SDA harbour dysplasia[ 14 - 19 ]. Kim et al[ 13 ] found that all of their 17 non ampullary adenomas were dysplastic while a larger series from Japan[ 14 ] demonstrated that dysplasia was presented in all 233 non-ampullary adenomas assessed.…”

“…Endoscopically SDA tend to be large, sessile and located in the second part of the duodenum[6,10-13] and this series also confirms that most SDA harbour dysplasia[14-19]. Kim et al[13] found that all of their 17 non ampullary adenomas were dysplastic while a larger series from Japan[14] demonstrated that dysplasia was presented in all 233 non-ampullary adenomas assessed.…”

Duodenal Epithelial Polyps: A Clinicopathologic Review

“…2 Clinical Significance and Treatment.-Although in most cases gastric foveolar metaplasia and gastric heterotopia represent benign lesions, some studies have raised the possibility that a subset of them may be preneoplastic and represent a precursor of adenomas and gastric-type adenocarcinomas. 18,19 In fact, in a recent study Matsubara et al 20 identified mutations in GNAS and/or KRAS in 55% of cases with duodenal gastric foveolar metaplasia and 28% of cases with gastric heterotopia. These lesions are usually small and asymptomatic; however, when very large they may cause obstruction or intussusception requiring endoscopic or rarely, surgical excision.…”