Divergent expression of MUC5AC, MUC6, MUC2, CD10, and CDX-2 in dysplasia and intramucosal adenocarcinomas with intestinal and foveolar morphology: is this evidence of distinct gastric and intestinal pathways to carcinogenesis in Barrett Esophagus?

Dysplasia in Barrett esophagus has been recognized to be morphologically heterogenous, featuring adenomatous, foveolar, and hybrid phenotypes. Recent studies have suggested a tumor suppressor role for CDX-2 in the metaplasia-dysplasia-carcinoma sequence. The phenotypic stability and role of CDX-2 in the neoplastic progression of different types of dysplasias have not been evaluated. Thirty-eight endoscopic mucosal resections with dysplasia and/or intramucosal carcinoma (IMC) arising in Barrett esophagus were evaluated for the expression of MUC5AC, MUC6, MUC2, CD10, and CDX-2. The background mucosa was also evaluated. The results were correlated with morphologic classification and clinicopathologic parameters. Of 38 endoscopic mucosal resections, 23 had IMC and dysplasia, 8 had IMC only, and 7 had dysplasia only. Among dysplastic lesions, 73% were foveolar, 17% were adenomatous, and 10% were hybrid. Twenty of 23 cases with dysplasia and adjacent IMC showed an identical immunophenotype of dysplasia and IMC comprising 16 gastric, 3 intestinal, and 1 mixed immunophenotype. Three cases showed discordance of dysplasia and IMC immunophenotype. These findings suggest that most Barrett-related IMC cases are either gastric or intestinal, with phenotypic stability during progression supporting separate gastric and intestinal pathways of carcinogenesis. CDX-2 showed gradual downregulation of expression during progression in adenomatous dysplasia but not in foveolar or hybrid dysplasia, supporting a tumor suppressor role, at least in the intestinal pathway. CDX-2 was also found to be expressed to a greater degree in intestinal metaplasia compared with nonintestinalized columnar metaplasia. Consistent with CDX-2 as a tumor suppressor, this suggests that nonintestinalized columnar metaplasia may be an unstable intermediate state at risk for neoplastic progression.     

Adenocarcinoma in columnar-lined Barrett's esophagus. Analysis of 13 esophagectomies

From 1977 to 1982, 13 patients with adenocarcinoma arising in the distal esophagus lined by columnar epithelium underwent esophagectomy with detailed analysis of the pathologic specimen. In three patients, microinvasive carcinoma was detected before dysplasia occurred. In five patients, the ectopic mucosa was discontinuous, prolonged cranially by islands of columnar epithelium scattered in the squamous mucosa. Variable degrees of dysplasia were found in the columnar epithelium in seven specimens in areas of intestinal metaplasia. In four patients with high-grade dysplasia, several foci of intramucosal carcinoma were identified. They were scattered over the whole length of the ectopic mucosa. These data strongly suggest that adenocarcinoma develops from dysplasia, the real premalignant lesion. Careful periodic screening must be carried out in patients identified as having Barrett's esophagus. Dysplasia may be detected and located by endoscopy with dye spraying with directed biopsies. Patients with high-grade dysplasia should undergo esophagectomy with resection of the whole ectopic mucosa because they are at high risk for development of carcinoma.     

Gastric foveolar metaplasia with dysplastic changes in Brunner gland hyperplasia: possible precursor lesions for Brunner gland adenocarcinoma

Cases of adenocarcinomas developed in Brunner gland hyperplasia (BGH) have been sporadically reported. Herein, we report the morphologic spectrum of hyperplastic changes culminating into dysplasia and carcinoma in 722 cases of BGH listed in our files. Fifteen of these cases showed dysplastic changes, with 8 graded as low-grade dysplasia, 5 as high-grade dysplasia, 11 as atypical hyperplasia, and 2 as invasive carcinoma, although each frequently coexisted in the same tumor. In two carcinomas, one had high-grade dysplasia in the mucosa, and another had only atypical hyperplasia. Interestingly, hyperplastic glands around dysplastic foci were associated with gastric foveolar metaplasia and papillary configuration in 13 cases, 11 of which showed a gradual increase in nuclear atypism in the transition from metaplastic to dysplastic glands. All of the metaplastic gastric glands showed diffuse and strong immunopositivity for gastric foveolar mucin (MUC5AC). Immunohistochemical profiles also supported the concept of a continuous spectrum in carcinogenesis from gastric foveolar hyperplasia through atypical hyperplasia or dysplasia and eventually to frank adenocarcinoma. The results of our study suggest, therefore, that dysplastic and/or carcinomatous change does occur in BGH, that they form the continuous morphologic spectrum, and that papillary foveolar metaplasia may be a precursor lesion in the process of carcinogenesis with a background of BGH.     

Hepatocyte antigen as a marker of intestinal metaplasia

Intestinal metaplasia is a histologic hallmark of Barrett's esophagus and chronic gastritis. Intestinal metaplasia may progress to dysplasia or carcinomas without proper treatment. Most cases of intestinal metaplasia are easily recognized on hematoxylin and eosin-stained sections. However, some cases of intestinal metaplasia may be hard to recognize if they lack the characteristic mucin-producing cells and Paneth cells, or if they are small in size. Recently, keratin 7, keratin 20, and MUC2 expression patterns were reported to be useful in confirming the diagnosis of intestinal metaplasia. We studied hepatocyte (Hep) antigen (a hepatocellular antigen mainly expressing in normal and neoplastic hepatic tissues) in 33 cases of Barrett's esophagus (9 cases associated with esophageal adenocarcinoma) and 13 cases of chronic gastritis associated with intestinal metaplasia and gastric adenocarcinoma. Hep monoclonal antibody recognizes intestinal metaplasia in all cases. We also compared expression of Hep with that of keratin 7, keratin 20, and MUC2 in intestinal metaplasia. The specificity and sensitivity of Hep for intestinal metaplasia were higher than that of keratin 7 and keratin 20, or MUC2. We conclude that Hep may be used as a single diagnostic marker for intestinal metaplasia.     

Adenomatous and foveolar gastric dysplasia: distinct patterns of mucin expression and background intestinal metaplasia

Gastric epithelial dysplasia (GED) can be morphologically categorized into adenomatous (or intestinal) and foveolar (or gastric) types. Although limited genetic differences have been demonstrated between these subtypes, the expression of various mucins has not been systematically evaluated in this context. Endoscopic mucosal resections from 69 cases of GEDs were evaluated for the expression of MUC2, MUC5AC, MUC6, and CD10. The results were correlated with morphologic categorization and clinicopathologic parameters. GED was classified as adenomatous, foveolar, or hybrid (showing features of both types), on the basis of histologic evaluation. The neighboring intestinal metaplasia (IM) was also evaluated. An adenomatous morphology was seen in 45%, hybrid type in 33.3%, and a "pure" foveolar type was seen in 21.7% of the cases. Foveolar GED was often depressed/flat on endoscopy and showed a statistically significant association with high-grade morphology (P = 0.046). Immunohistochemistry confirmed the histologic stratification. The foveolar and hybrid types were more often positive for MUC5AC (P = 0.0001 for both) and negative for CD10 (P = 0.019 and 0.016, respectively) as compared with adenomatous GED. High-grade morphology was associated with MUC5AC expression regardless of the morphologic phenotype (P = 0.026). Foveolar (73.3%) and hybrid (86.9%) GEDs were associated more often with IM showing a retained expression of gastric type mucin than adenomatous GED (29%) (P < 0.01 for both). In contrast, adenomatous type (58.1%) of GED was significantly associated with IM showing a complete intestinal phenotype (CD10+) compared with the foveolar (13.3%) and hybrid types (17.4%) of GED (P = 0.005 for both comparisons). In conclusion, our study indicates that foveolar and adenomatous types of GED have distinct clinicopathologic features, mucin profiles, and association with different types of IM.     

Fundic patch operation in the treatment of esophageal stricture with Barrett's esophagus--a case report

A 66-year-old woman, who had a stricture of the distal esophagus with Barrett's epithelium caused by gastroesophageal reflux, was operated upon by means of the fundic patch method. Preoperative manometric and pH studies revealed that the patient had a cardiac incompetence and a delayed acid clearance of the esophagus. Endoscopic biopsies between 33-35 cm from the incisors, above the gastroesophageal junction, showed columnar metaplasia with a villiform surface, mucous glands, intestinal goblet cells, moderate inflammatory changes and focal mild dysplasia. After the operation, relief of the dysphagia and reflux symptoms were obtained successfully, and an endoscopy done 7 months later demonstrated that the esophageal lumen was adequate enough for passage, and that there was improvement of the esophagitis, though persistent Barrett's esophagus without malignancy still existed. These results indicate that the fundic patch operation with the formation of a mucosal valve and 270 degrees fundoplication is a useful method of choice for benign strictures of the lower esophagus.     

Pyloric gland adenoma: an entity distinct from gastric foveolar type adenoma

Pyloric gland adenoma (PGA) is a rare neoplasm demonstrating gastric epithelial differentiation. In this series, we studied 41 PGAs from 36 patients. We compared them to 28 gastric foveolar type gastric adenomas (GTAs) from 25 patients. PGAs occurred in an older population with a mean age of 73 compared with 48 in GTAs (P<0.001). There was a significant female predominance, particularly for gastric PGAs. Morphologically, PGAs were characterized by closely packed pyloric gland-type tubules with a monolayer of cuboidal to low columnar epithelial cells containing round nuclei and pale to eosinophilic cytoplasm with a ground glass appearance. The cells lacked an apical mucin cap, a feature distinct from GTAs. An immunohistochemical panel of mucin core peptides (MUCs) and CDX2 was performed on a subset of the lesions. All PGAs expressed MUC6 with coexpression of MUC5AC, whereas GTAs expressed predominantly MUC5AC without MUC6. Both lesions lacked CDX2 and MUC2 except in areas of intestinal metaplasia (IM) found in some PGAs. Histologic features consistent with conventional dysplasia were found in 26 (63.4%) PGAs. Using a 2-tier grading system, 5 (12.2%) cases demonstrated low-grade dysplasia whereas 21 (51.2%) cases showed high-grade dysplasia including 5 (12.2%) cases with an associated intramucosal or more deeply invasive adenocarcinoma. This was significantly different from GTAs; all cases showed only low-grade dysplasia (P<0.001). In addition, 60% of gastric PGAs were associated with IM in the surrounding mucosa and 40% of lesions arose in a background of autoimmune gastritis, whereas these 2 conditions were only associated with 1 case (3%) of GTA. In summary, PGA is a distinct entity. Despite its bland histologic appearance, it is much more likely to be accompanied by background IM and autoimmune gastritis and can evolve into invasive adenocarcinoma displaying pyloric gland differentiation.     

Fundic patch operation in the treatment of esophageal stricture with Barrett's esophagus —A case report—

A 66-year-old woman, who had a stricture of the distal esophagus with Barrett's epithelium caused by gastroesophageal reflux, was operated upon by means of the fundic patch method. Preoperative manometric and pH studies revealed that the patient had a cardiac incompetence and a delayed acid clearance of the esophagus. Endoscopic biopsies between 33–35 cm from the incisors, above the gastroesophageal junction, showed columnar metaplasia with a villiform surface, mucous glands, intestinal goblet cells, moderate inflammatory changes and focal mild dysplasia. After the operation, relief of the dysphagia and reflux symptoms were obtained successfully, and an endoscopy done 7 months later demonstrated that the esophageal lumen was adequate enough for passage, and that there was improvement of the esophagitis, though persistent Barrett's esophagus without malignancy still existed. These results indicate that the fundic patch operation with the formation of a mucosal valve and 270° fundoplication is a useful method of choice for benign strictures of the lower esophagus.     

Barrett's esophagus. A surgical entity

During a ten-year period, endoscopy demonstrated acid-peptic esophagitis in 439 patients. Forty of these patients (9.1%) had Barrett's esophagus. Adenocarcinoma was present in the columnar epithelium in 15 (37.5%) of the patients with Barrett's esophagus. Hiatal hernias, with symptoms of heartburn, dysphagia, stricture, and ulceration, were found in more than 75% of the patients with Barrett's esophagus. We developed a treatment algorithm. Patients with symptomatic reflux esophagitis should undergo endoscopy with biopsy. If Barrett's esophagus is diagnosed, an antireflux procedure should be performed, preferably a proximal gastric vagotomy with Nissen's fundoplication. Follow-up examination by endoscopy with biopsy and cytology should be performed every six months. Indications for early esophagectomy include progression of cellular dysplasia, carcinoma in situ, and a non-healing Barrett's ulcer following an antireflux procedure. Our data support an aggressive surgical treatment of patients with Barrett's esophagus.     

Severe gastric dysplasia with intramucosal carcinoma in a 16-year-old male

Gastric dysplasia is a rare adult condition affecting a small area near polyps, ulcers or is an inflammatory process. Adenocarcinoma develops in severe gastric dysplasia, and this process may take 1 year. Mild and moderate dysplasias regress and only a small proportion progresses to severe dysplasia. We report a severe dysplasia in a 16-year-old male with no clinical history of gastric disease with acute and severe upper gastrointestinal bleeding that lowered hemoglobin levels to 2.8 g/dL. Bleeding persisted and subtotal gastrectomy was performed on an emergency basis. At gross examination, bleeding and congestion were found with superficial ulcers. Microscopically, severe dysplasia was observed with intramucosal areas of carcinoma limited to foveolar mucosa. The ulcers were congested and there was no inflammation, no polyps or other alterations in the mucosal layer. Ki-67 and P53 markers were positive, p16 with sporadic positivity. The purpose here is to report an exceptional case because of the young age and extensive and severe dysplasia with areas of intramucosal carcinoma and no previous clinical history. No similar cases of severe dysplasia with carcinoma in situ are reported in the literature.     

Crohn's disease with adenocarcinoma and dysplasia. Macroscopical, histological, and immunohistochemical aspects of two cases

We present two cases of small-bowel adenocarcinoma and dysplasia in patients with longstanding Crohn's disease. In one case, the dysplasia and cancer were exclusively located in the terminal ileum, whereas in the other case, several cancers were found from the ileum toward the transverse colon. In both cases, we found a clinically unsuspected Dukes C1 mucinous adenocarcinoma together with large foci of polypoid villous dysplasia or with multifocal high-grade dysplasia and intramucosal carcinoma. Immunohistochemical staining for carcinoembryonic antigen (CEA) revealed a different staining pattern in various diseased areas. The intensity of CEA staining paralleled the histologic degrees of dysplasia and neoplasia. Cytokeratin expression was disturbed in inflamed mucosa, and it was more pronounced in high-grade dysplasia and invasive carcinoma. We conclude that the presence of dysplasia in an intestinal biopsy of a patient with Crohn's disease should arouse the pathologist's suspicion of carcinoma and force him or her to take multiple sections from strictures and polypoid lesions, especially since the clinical symptoms of a carcinoma may be obscured by the symptoms of inflammatory bowel disease. Immunohistochemical staining with CEA and cytokeratin are useful in the objectivation of dysplasia.     

Cardiac mucosa in the remnant esophagus after esophagectomy is an acquired epithelium with Barrett's-like features

BACKGROUND: The cervical esophagus is normally lined by squamous epithelium and is usually not exposed to gastroesophageal reflux. The aims of this study were, first, to investigate whether cardiac mucosa can be acquired in the remnant cervical esophagus after esophagectomy and cervical esophagogastrostomy and, second, to characterize this mucosa if present. METHODS: The medical records of 100 patients who had undergone esophagectomy with gastric pull-up reconstruction were studied retrospectively to identify those who had biopsies from the cervical esophagus proximal to the gastroesophageal anastomosis during postoperative follow-up. The histopathology and immunohistochemical stains were reviewed to assess similarity to Barrett's mucosa (cytokeratins [CK] 7 and 20 and DAS-1), cellular proliferation (topoisomerase 2alpha), and the potential for dysplasia (cyclo-oxygenase 2 [COX-2] and ornithine decarboxylase [ODC]). RESULTS: Supra-anastomotic biopsies were performed in 20 patients. Cardiac mucosa was present in 10 of 20 (50%) patients in whom biopsies were performed. Four patients had areas of intestinal metaplasia, and dysplasia, and adenocarcinoma developed in 1 patient. The CK7/20 and DAS-1 staining of the columnar mucosa showed a pattern similar to Barrett's mucosa. Topoisomerase 2alpha protein expression was present in 50% of patients with cardiac mucosa. DAS-1 protein was expressed in cervical columnar mucosa but not in normal squamous esophagus mucosa. The cardiac mucosa stained weakly for COX-2 and ODC. CONCLUSIONS: Cardiac mucosa can be acquired. Its expression profile is similar to cardiac mucosa and intestinal metaplasia found in Barrett's esophagus, and different from normal esophageal or gastric mucosa. The development of cardiac mucosa is likely to be related to reflux of acid into the remnant cervical esophagus as the first step in the development of Barrett's esophagus. These findings are applicable to the development of similar changes at the gastroesophageal junction.     

Rapid progression to high-grade dysplasia in Barrett's esophagus after liver transplantation.

There is an increased incidence of malignancies in transplant recipients. Accelerated progression from a premalignant lesion to carcinoma has been reported in transplant recipients with skin cancer and colon cancer. Whereas Barrett's esophagus is a common premalignant condition in the normal population, rapid progression to severe dysplasia or carcinoma has not been widely reported in transplant recipients. We report on a liver transplant recipient who developed rapid progression from Barrett's esophagus without dysplasia to high-grade dysplasia within 9 months after transplantation.     

Intracholecystic Papillary-Tubular Neoplasms (ICPN) of the Gallbladder (Neoplastic Polyps, Adenomas, and Papillary Neoplasms That Are ≥1.0 cm): Clinicopathologic and Immunohistochemical Analysis of 123 Cases

The literature on the clinicopathologic characteristics of tumoral intraepithelial neoplasms (neoplastic polyps) of the gallbladder (GB) is fairly limited, due in part to the variability in definition and terminology. Most reported adenomas (pyloric gland type and others) were microscopic and thus regarded as clinically inconsequential, whereas papillary in situ carcinomas have been largely considered a type of invasive adenocarcinoma under the heading of "papillary adenocarcinomas." In this study, 123 GB cases that have a well-defined exophytic preinvasive neoplasm measuring ≥1 cm were analyzed. The patients were predominantly female (F/M=2:1) with a mean age of 61 y and a median tumor size of 2.2 cm. Half of the patients presented with pain, and in the other half the neoplasm was detected incidentally. Other neoplasms, most being gastrointestinal tract malignancies, were present in 22% of cases. Gallstones were identified in only 20% of cases. Radiologically, almost half were diagnosed as "cancer," roughly half with polypoid tumor, and in 10% the lesion was missed. Pathologic findings: (1) The predominant configuration was papillary in 43%, tubulopapillary in 31%, tubular in 26%. (2) Each case was assigned a final lineage type on the basis of the predominant pattern (>75% of the lesion) on morphology, and supported with specific immunohistochemical cell lineage markers. The predominant cell lineage could be identified as biliary in 50% (66% of which were MUC1), gastric foveolar in 16% (all were MUC5AC), gastric pyloric in 20% (92% MUC6), intestinal in 8% (100% CK20; 75% CDX2; 50%, MUC2), and oncocytic in 6% (17% HepPar and 17% MUC6); however, 90% of cases had some amount of secondary or unclassifiable pattern and hybrid immunophenotypes. (3) Of the cases that would have qualified as "pyloric gland adenoma," 21/24 (88%) had at least focal high-grade dysplasia and 18% had associated invasive carcinoma. Conversely, 8 of 47 "papillary adenocarcinoma"-type cases displayed some foci of low-grade dysplasia, and 15/47 (32%) had no identifiable invasion. (4) Overall, 55% of the cases had an associated invasive carcinoma (pancreatobiliary type, 58; others, 10). Factors associated significantly with invasion were the extent of high-grade dysplasia, cell type (biliary or foveolar), and papilla formation. Among systematically analyzed invasive carcinomas, tumoral intraepithelial neoplasia was detected in 6.4% (39/606). (5) The 3-year actuarial survival was 90% for cases without invasion and 60% for those associated with invasion. In contrast, those associated with invasion had a far better clinical outcome compared with pancreatobiliary-type GB carcinomas (3-yr survival, 27%), and this survival advantage persisted even with stage-matched comparison. Death occurred in long-term follow-up even in a few noninvasive cases (4/55; median 73.5 mo) emphasizing the importance of long-term follow-up. In conclusion, tumoral preinvasive neoplasms (≥1 cm) in the GB are analogous to their pancreatic and biliary counterparts (biliary intraductal papillary neoplasms, pancreatic intraductal papillary mucinous neoplasms, and intraductal tubulopapillary neoplasms). They show variable cellular lineages, a spectrum of dysplasia, and a mixture of papillary or tubular growth patterns, often with significant overlap, warranting their classification under 1 unified parallel category, intracholecystic papillary-tubular neoplasm. Intracholecystic papillary-tubular neoplasms are relatively indolent neoplasia with significantly better prognosis compared with pancreatobiliary-type GB carcinomas. In contrast, even seemingly innocuous examples such as those referred to as "pyloric gland adenomas" can progress to carcinoma and be associated with invasion and fatal outcome.     

Karzinom des ösophagogastralen Übergangs und Barrett-Ösophagus

From a clinical and biological point of view, the term "adenocarcinoma of the esophagogastric junction" (AEG) encompasses several distinct tumor entities. The topographic anatomic classification into adenocarcinoma of the distal esophagus (AEG I), true carcinoma of the cardia (AEG II), and subcardiac gastric cancer (AEG III) also reflects differences regarding the pathogenesis of these tumors and is increasingly accepted worldwide. Associated Barrett's esophagus, which usually develops as a consequence of chronic gastroesophageal reflux, can be documented in practically all patients with AEG I tumors and constitutes the most important precancerous lesion. A metaplasia-dysplasia-carcinoma sequence has been confirmed for these tumors. Barrett's esophagus is thus considered a model for studies on carcinogenesis and the prevention of esophageal adenocarcinoma. Its pathogenetic role in AEG II and III tumors must, however, be discussed differently. Our own experience shows that pathogenetic mechanisms similar to those in AEG I tumors may be present in up to 30% of tumors classified as AEG II. The majority of AEG II tumors, however, show morphologic, biologic and pathogenetic similarities with AEG III tumors and proximal gastric cancer.     

Duplication cyst of the stomach with respiratory epithelium in adult: an uncommon finding. Report of case and review of literature

Gastrointestinal duplication is a congenital rare disease entity. Duplication cyst of the stomach with pseudo stratified columnar ciliated epithelium is extremely rare. The very appearance of a gastric duplication cyst in an adult can present a diagnostic dilemma. In majority of reported cases, the diagnosis is established during surgical exploration. We report on a 34 year-old female patient suffering from repeated episodes of epigastric pain and gastroesophageal reflux. Abdominal computed tomography and endoscopic ultrasound demonstrated a intramural lesion attached to the gastric fundus, suggestive of gastrointestinal stromal tumor (GIST). At exploratory laparotomy a non-communicating cyst, was found along the greater curvature of the stomach in the esophagogastric transition. The lesion was excised along with an adjacent sleeve of the stomach and esophagus wall because shared muscular layer with the stomach and esophagus. The final pathologic examination revealed that the inner wall of the cyst was lined by a pseudostratified columnar ciliated epithelium (respiratory type) and, in part, columnar and gastric foveolar epithelium. Even though a panel of imaging modalities is available, it is still difficult to obtain a preoperative diagnosis. Duplication cyst can be mistaken for a soft tissue tumor of the gastrointestinal tract. There is no therapeutic algorithm. Surgical treatment is recommended for symptomatic cases.     

Barrett's esophagus and antireflux surgery: a study of a series of 26 patients]

STUDY AIM: The aim of this study was to report the results of a retrospective series of 26 patients with Barrett's esophagus treated by antireflux surgery. PATIENTS AND METHODS: From 1979 to 1998, 21 men and five women (mean age: 53 years) with histologically proven Barrett's esophagus underwent an antireflux procedure. The mean length of Barrett's epithelium was 5.9 cm for 19 patients (73.1%). Six patients (23.1%) had tongue lesions of Barrett's epithelium, and one (3.8%) had ectopic gastric mucosa. None of the patients had a preoperative esophageal biopsy that revealed high-grade dysplasia or carcinoma. Laparotomy was performed in 17 cases and laparoscopy in nine cases. Preoperative endoscopic local treatment with argon coagulation was performed in one patient. RESULTS: Clinical mean follow-up was 78 months and endoscopic mean follow-up was 59.3 months. No increase in the length of the Barrett's epithelium was observed. Seven patients (27%) had complete or partial regression (among them three patients with tongue lesions and one patient preoperatively treated by argon). No patients developed high-grade dysplasia or carcinoma. CONCLUSION: Regression of Barrett's esophagus is possible but not frequent and unpredictable after antireflux procedure. However, endoscopic and histological surveillance should be continued postoperatively.     

Common characteristics of jejunal heterotopic gastric tissue in children: a case report with review of the literature

An 11-year-old boy underwent laparotomy for intermittent intussusceptions because of a polypoid lesion located in the proximal jejunum. The polypoid lesion was diagnosed as heterotopic gastric mucosa (HGM). Jejunal HGM is a very rare entity, and review of the literature revealed common characteristics in children with this pathologic condition. The usual presenting age is about 14 years, and the common clinical picture is intermittent intussusceptions. Jejunal HGM is usually polypoid and predominantly located within a few centimeters distal to ligament of Treitz. The aforementioned characteristics should suggest jejunal HGM be included in the differential diagnosis of jejunal polypoid lesions in children.