ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Gastric polyps encompass a wide variety of lesions that most commonly arise from the gastric epithelium. This review focuses on the histologic features, significance, and differential diagnosis of the two most common epithelial polyps: hyperplastic polyps and fundic gland polyps. Hyperplastic polyps are characterized by prominent foveolar hyperplasia, tortuosity, and edema and inflammation of the intervening lamina propria. They are associated with abnormalities of the background gastric mucosa, particularly chronic atrophic gastritis of autoimmune or environmental type. Although they uncommonly undergo neoplastic progression (dysplasia or adenocarcinoma), they denote an increased risk of neoplasia in the surrounding abnormal gastric mucosa. Hyperplastic polyps overlap in their histologic appearance with hamartomas (e.g., juvenile polyps, Peutz-Jeghers polyps, Cowden’s disease) and with more generalized hyperplastic or inflammatory conditions (e.g., Menetrier’s disease). Fundic gland polyps can be sporadic or associated with familial adenomatous polyposis (FAP). FAP-associated polyps occur at earlier ages (including children) and are more frequently multiple. Both sporadic and FAP-associated fundic gland polyps are characterized by ectatic glands lined by attenuated parietal cells, chief cells, and mucus neck cells. The surface epithelium is dysplastic in 25% of FAP-associated fundic gland polyps but only rarely in sporadic polyps. Despite this, the risk of gastric adenocarcinoma does not appear to be significantly increased among Western patients with FAP.

ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Because of the increasing incidence of adenocarcinoma of the gastric cardia, inflammatory processes involving the gastric cardia have become of interest. This article addresses the following major issues: (1) Does the gastric cardia exist as a native structure, or is it a metaplastic mucosa that arises secondary to gastroesophageal reflux? (2) What is the cause or causes of carditis? (3) What is the significance of intestinal metaplasia of the gastric cardia, and can it be distinguished from Barrett’s esophagus? Several recent autopsy studies have found that the gastric cardia exists as a normal structure, although it is extremely small (1–4 mm). However, cardiac-type mucosa, closely resembling the native gastric cardia, can arise in the distal esophagus as a metaplastic phenomenon secondary to gastroesophageal reflux. Biopsy specimens taken near the esophagogastric junction with cardiac-type mucosa are frequently inflamed (so-called carditis). Although some have found this inflammatory process to be closely associated with gastroesophageal reflux disease, others have found it to be a manifestation of aHelicobacter pyloripangastritis. Much of the confusion likely exists because of difficulties in precisely localizing the esophagogastric junction at endoscopy and the presence of histologically similar-appearing cardiac-type mucosae in the distal esophagus and proximal stomach, both of which may be inflamed for different reasons. All available data suggest that there are at least two causes of “carditis.” One form involves inflammation of metaplastic cardiac-type mucosa in the distal esophagus secondary to gastroesophageal reflux, and the second form involves inflammation of the native gastric cardiac mucosa secondary toH. pyloriinfection. The etiology and significance of cardia intestinal metaplasia is controversial. Most available data suggest that intestinal metaplasia of the cardia is secondary to anH. pylori-induced multifocal atrophic gastritis. Recent data suggest the risk of progression of cardia intestinal metaplasia to dysplasia-adenocarcinoma is much lower than that of short- or long-segment Barrett’s esophagus. Immunohistochemical stains for cytokeratins 7 and 20 may be useful in this regard, as there is a reproducible cytokeratin pattern found in Barrett’s esophagus that is typically absent in intestinal metaplasia of the cardia.

ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Infectious causes of esophagitis are most often found in immunocompromised patients. This review discusses in detail the most common causes of esophageal infection—candida, cytomegalovirus, and herpes simplex virus. In addition, ancillary studies and biopsy techniques are also reviewed. Differentiating infectious causes of esophagitis from more common causes of esophagitis such as reflux is best accomplished when the pathologist is equipped with information regarding the immune status of the patient as well as the endoscopic location and appearance of any lesions.

ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

An elderly man complaining of vague abdominal cramping eventually underwent an upper endoscopy that revealed a slightly raised nodular antral lesion. The microscopic evaluation determined a diagnosis of high grade dysplasia. Following the diagnosis he was re-endoscoped and multiple biopsies failed to reveal any additional significant mucosal abnormalities. Another endoscopy at 6 month was also negative. However, a scheduled endoscopy the following year diagnosed a well-differentiated adenocarcinoma. A distal gastrectomy revealed an early gastric adenocarcinoma. The patient is alive and well 3 years after the initial diagnosis. This report emphasizes the diagnostic features of gastric epithelial dysplasia and the clinical significance of this diagnosis. Gastric epithelial dysplasia (GED) is believed to be the penultimate stage of gastric carcinogenesis. Its clinical importance has been underscored since the demonstration of its close association with gastric cancer was established. On this background we review the definition and classification of GED as well as its grading and natural history.

ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

With the increasing incidence of esophageal adenocarcinoma and more aggressive surveillance of patients with Barrett’s esophagus, recognizing and grading dysplasia in this setting is becoming an important issue in daily practice. Criteria for grading dysplasia were published in 1988 and have been recently revisited. Consensus guidelines for clinical management of these patients are emerging together with novel non-invasive therapy. It will become increasingly important for pathologists to attempt to accurately grade these lesions, although there are substantial limitations to this, particularly in assigning grades at the low-grade end of the spectrum.

ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Adenocarcinomas situated near the gastroesophageal junction can be classified as esophageal, cardial or subcardial depending on the anatomic location of the tumor. There is debate about the pathogenesis of adenocarcinoma arising in the proximal stomach/cardia. Do such neoplasms parallel the distal stomach, arising because of chronic gastritis related toHelicobacter pylori? Or are they similar to adenocarcinomas of the distal esophagus, developing in mucosa injured by chronic gastroesophageal reflux. This review describes the molecular profiles of adenocarcinomas at three sites—esophagus, gastroesophageal junction (including gastric cardia) and distal stomach—to see whether junctional neoplasms have a constellation of genetic abnormalities more like those arising in Barrett’s esophagus or those of the stomach. This approach depends on the premise that differences in molecular pathogenesis reflect differences in the inciting insult rather than regional variations in the underlying mucosa. This premise is supported by experience at other sites (e.g., liver) where specific molecular abnormalities are associated with specific etiologic agents, and by the commonality of the precursor lesion (intestinal metaplasia) in the esophagus and stomach, which should largely negate differences of underlying mucosa. The literature indicates that adenocarcinoma of the proximal stomach/cardia demonstrates a pattern of genetic abnormality, which is intermediate between those of distal cancer and Barrett’s-type cancer. Our interpretation is that cardia adenocarcinomas can and do arise as a result of either mechanism. The possibility that both mechanisms may contribute to individual tumors can not be excluded by these data. Pathogenetic mechanisms unique to cardia adenocarcinomas have not been described.

ISSN:1082-9784    

出版商:OVID    

年代:2002

数据来源: OVID