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PYLORIC GLAND ADENOMA OF STOMACH: A RARE CASE
Abstract
Pyloric gland adenoma is an uncommon precancerous polypoidal growth. Pyloric gland adenoma of stomach accounts for 2.7% of all gastric polyp. Mostly Pyloric gland adenoma are found in stomach but can be found in other anatomical sites. Pyloric gland adenoma of stomach occur in elderly population and having female predominance. Pyloric gland adenoma of stomach is commonly seen in chronic gastritis patients, autoimmune gastritis but can also occur in some genetic disease like familial adenomatous polyposis and Lynch syndrome. Early identification and therapeutic polypectomy by endoscopically and histopathological evaluation and confirmation of pyloric gland adenoma may reduce the chances of transformation of invasive adenocarcinoma.
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Rationale:
Pyloric gland adenoma (PGA) is often associated with pyloric gland metaplasia. It has high malignant potential but a low clinical diagnosis rate. Therefore, we reported a case of PGA and reviewed the literature to summarize the clinicopathological features of pyloric adenoma.
Patient concerns:
A 62-year-old female underwent gastroscopy due to intermittent acid regurgitation and heartburn, which revealed a 4×6 mm flat, elevated lesion in the greater curvature of the upper gastric body, with depression in the central region and blood scab attachment.
Diagnosis and intervention:
Biopsy revealed gastric adenoma with low-grade intraepithelial neoplasia. The patient was treated with ESD, and pathology showed gastric pyloric gland adenoma with low-grade dysplasia. The cells were positive for MUC6 and MUC5AC immunohistochemically.
Outcomes:
The patient received proton pump inhibitors and gastric mucosal protective agents for one month after ESD. She occasionally presented acid regurgitation and heartburn, with no abdominal pain, abdominal distension, melena, or hematochezia. Follow-up gastroscopy will be reexamined 1 year later.
Lessons:
PGA has nonspecific performance under endoscopy, and its diagnosis mainly depends on pathology. Clinicians need to increase their ability to recognize such lesions and treat them in time to improve the prognosis.
Background:
Pyloric gland adenoma (PGA) is a recently described and rare tumor. Submucosal tumor (SMT)-like PGA is more difficult to diagnose and differentiate from other submucosal lesions.
Case summary:
We present the case of a 69-year-old man with a 10 mm SMT-like elevated lesion with an opening in the upper part of the gastric body, referred to our hospital for further endoscopic treatment. Magnifying endoscopy with narrow-band imaging, endoscopic ultrasonography, and complete endoscopic submucosal dissection were performed on the patient. Histopathological findings revealed tightly packed tubular glands lined with cuboidal or columnar cells that had round-to-oval nuclei containing occasional prominent nucleoli and an eosinophilic cytoplasm similar to that in non-neoplastic gastric pyloric glands. Additionally, immunohistochemical analysis showed positive staining for both mucin 5AC and mucin 6. Therefore, we arrived at the final diagnosis of gastric PGA. Although there was no apparent malignant component in this tumor, PGA has been considered a precancerous disease with a high risk of transformation into adenocarcinoma.
Conclusion:
PGA should be considered when detecting gastric SMT-like lesions. Physicians and pathologists should focus on PGA due to its malignant potential.
Pyloric gland adenoma is a rare neoplasm with a gastric epithelial differentiation. We report 23 cases of pyloric gland adenoma in older persons, with a mean age of 74 years (range 52 - 87 years). They occurred in the esophagus (3 cases), corporal gastric mucosa (7 cases), duodenum (10 cases), gallbladder (2 cases), and choledochus (one case). Histologically, they were characterized by closely packed pyloric gland-type tubules with a monolayer of cuboidal to low columnar epithelial cells containing basally located round nuclei, and a superficial layer of tall, columnar, foveolar-type epithelium. Immunohistochemically, most tumor glands expressed pyloric gland mucin MUC6, whereas MUC5AC was positive in superficial gastric foveolar epithelium, and in a minority of glands. In addition, scattered neuroendocrine cells positive for chromogranin A and/or synaptophysin were seen in all cases. In 3 cases (two cases in the gallbladder and one case in the esophagus), areas of intestinal metaplasia with CK20, CDX2, and MUC2 positivity were found. Focal low-grade dysplasia was found in five cases (21.7%), and diffuse high-grade dysplasia was seen in one adenoma (4.4%), i.e., 6 of 23 PGAs (26.1%) showed dysplastic features. In one esophageal case, an invasive adenocarcinoma was diagnosed. Scattered p53 positive cells were found in all cases. Their number was higher in lesions with low-grade dysplasia and it was substantially increased in adenoma with high-grade dysplasia and in adenocarcinoma. Our molecular genetic results indicate that pyloric gland adenomas neoplastic nature is associated with p53 accumulation, mutations in oncogenes GNAS, KRAS, CTTNB1 and tumor suppressor genes SMAD4, and TP53. Pyloric gland adenoma can evolve into dysplasia and adenocarcinoma.
The prevalence of gastric cancer associated with Lynch syndrome (LS) is highly variable, and the underlying histologic pathway or molecular mechanisms remain unclear. From 1995 to 2012, 15 patients had been treated for both gastric and colonic adenocarcinomas and diagnosed as LS. In all cases, pathologic review, immunohistochemical analysis for mismatch-repair proteins, and microsatellite instability (MSI) tests were performed. To confirm LS, germline mutation tests and multiplex ligation-dependent probe amplification were performed. All gastric and colonic carcinomas were MSI-high and lost expressions of MLH1/PMS2 in 11 (73%) cases and MSH2/MSH6 in 4 (27%) cases. Remarkably, in a patient with LS and germline mutation of MLH1 gene, pyloric gland adenoma (PGA) transformed to adenocarcinoma during follow-up. In 2 additional cases, PGA was found adjacent to advanced gastric cancers. All PGAs in LS patients were MSI-high and lost expression of mismatch-repair proteins (MLH1/PMS2 in 2 cases and MSH2/MSH6 in 1 case), whereas none of the 14 sporadic PGAs was MSI-high or had lost expression of mismatch-repair proteins. On the basis of these observations, although very rare, we suggest the possibility that PGA may be a precursor lesion to gastric adenocarcinoma in LS and that the mismatch-repair deficient pathway of carcinogenesis is involved early in the gastric carcinogenesis pathway.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivitives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/3.0.
Endoscopic procedures are the gold standard in identifying, monitoring and treating gastrointestinal system lesions. The evaluation of benign, precancerous and malignant characteristics of these lesions requires good endoscopic inspection and precise pathological examination. Pyloric gland adenoma is a rare precancerous lesion defined in recent years and herein is reviewed in the present case along with the literature.
An 80‐year‐old woman found to have a gastric tumor by endoscopy was referred to our hospital for further examination and treatment. Helicobacter pylori eradication therapy was successfully performed 10 years ago. Conventional endoscopy revealed a 20‐mm flat elevated lesion in the greater curvature of the middle gastric body. (Fig. 1a). Magnifying endoscopy with narrow band imaging (M‐NBI) revealed an irregular microvascular architecture, including closed‐loop vessels with repeated irregular anastomoses (Fig. 1b).
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Aims:
There is limited information regarding the clinicopathologic and immunohistochemical characteristics of gastric pyloric gland adenomas (PGAs).
Methods and results:
Sixty seven cases of gastric PGA from 57 patients were analyzed. PGAs occurred with similar frequency in men and women (47.4% and 52.6%, respectively) with a mean age of 66 years. Most presented in the gastric body/fundus (67.2%). Fifteen cases (22.4%) developed in a background of autoimmune gastritis (AIG), whereas normal mucosa was seen in 35.8%. Only 16.4% (11 cases) developed in patients with a genetic predisposition, most commonly familial adenomatous polyposis. Low-grade lesions had a mean size of 1.5 cm, while PGAs with high-grade dysplasia (HGD) or adenocarcinoma had a mean size of 3.5 cm (p < 0.001) and more commonly showed tubulovillous architecture (50.0% versus 25.6% in low-grade dysplasia; p = 0.040). Most PGAs (61.2%) co-expressed MUC5AC and MUC6 (mixed type), which was significantly associated with HGD or adenocarcinoma (p = 0.013). AIG was also associated with HGD (p = 0.027), but genetic predisposition did not correlate with the grade of dysplasia (p = 0.793). The recurrence rate of PGA was similar for high- (11.8%) and low-grade lesions (7.4%) (p = 0.624).
Conclusions:
The risk of HGD increases with the size of PGA, tubulovillous architecture, and the presence of AIG as well as mixed immunophenotype. Since the overall local recurrence rate is less than 10%, PGAs may be treated conservatively, but they should be completely excised if possible, particularly if they are large or show high-grade features. This article is protected by copyright. All rights reserved.
Pyloric gland adenomas are rare neoplasms of the gastrointestinal tract. Gastric pyloric gland adenomas have been shown to arise in chronically damaged mucosa. The neoplastic glands have gastric pyloric gland differentiation and have a tightly packed organization with occasional cystic dilatation. The individual cells are cuboidal to columnar, with eosinophilic to amphophilic cytoplasm and either no apical mucin cap or a poorly formed apical mucin cap. The nuclei are round to oval, with occasional prominent nucleoli. Immunohistochemically, the neoplastic cells label with markers of gastric pyloric gland differentiation, including MUC6 and MUC5AC. There is limited information regarding the natural history of pyloric gland adenomas, but clinical series have described adenocarcinomas in association with gastric pyloric gland adenomas. The ideal clinical management is adequate sampling of the lesion to investigate for high-grade dysplasia and/or invasive cancer and recommendation to clinical colleagues to investigate the background mucosa for the etiology of chronic gastritis as well as potential additional neoplastic lesions. This review will focus on gastric pyloric gland adenomas.
Pyloric gland adenomas (PGAs) are uncommon to rare and are found mostly in the stomach but in a number of other anatomical sites as well. They were recognised years ago by European and Japanese colleagues whereas North American pathologists learned to diagnose them more recently. They are associated with conditions that result in pyloric metaplasia, the prototype of which is autoimmune gastritis. Since the latter is more common in women and men, gastric PGA has a striking female predominance. There appear to be differences in the distribution of PGA in various populations. Herein we review PGA and note similarities and differences in their distribution in our institutions in Germany and the USA and review their morphological appearance, immunolabelling profile, and preliminary genetic data on these unusual lesions.
Patients with familial adenomatous polyposis (FAP), an autosomal dominant cancer predisposition syndrome caused by mutations in the APC gene, develop neoplasms in both the upper and lower gastrointestinal (GI) tract. To clarify the upper GI tract lesions in FAP patients in a tertiary care setting, we reviewed specimens from 321 endoscopies in 66 patients with FAP. Tubular adenomas in the small bowel were the most common neoplasms (present in 89% of patients), although only 1 patient developed invasive carcinoma of the small bowel. Several types of gastric neoplasms were identified-65% of patients had at least 1 fundic gland polyp, and 23% of patients had at least 1 gastric foveolar-type gastric adenoma. Pyloric gland adenomas were also enriched, occurring in 6% of patients-this is a novel finding in FAP patients. Despite the high frequency of gastric neoplasms, only 1 patient developed carcinoma in the stomach. The very low frequency of carcinoma in these patients suggests that current screening procedures prevent the vast majority of upper GI tract carcinomas in patients with FAP, at least in the tertiary care setting.