Gastric Cardia Intestinal Metaplasia: Biopsy Follow-Up of 85 Patients

Goldstein, Neal S.

doi:10.1038/modpathol.3880198

Cited by 33 publications

(12 citation statements)

References 29 publications

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“…However, not all biopsy specimens with increased chronic inflammation in mucosa from this region contain IM. In one biopsy study of the GEJ region by Goldstein et al, IM was more likely to occur in biopsies that showed high levels of chronic inflammation (60). Their data also suggested that a reduction in chronic inflammation may allow IM to revert to normal in some instances.…”

Section: Pathogenesis Of Intestinal Metaplasia In the Gastroesophageamentioning

confidence: 90%

“…In one study by Goldstein, a reduction in chronic inflammation in serially obtained mucosal biopsies from the GEJ in 85 patients with IM was associated with a lower prevalence rate of IM (60). However, this study was retrospective in design and limited by the potential deleterious effects of sampling error.…”

Section: Natural History and Risk Of Neoplasia Of Intestinal Metaplasmentioning

confidence: 99%

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Unraveling the Mystery of the Gastroesophageal Junction: A Pathologist's Perspective

Odze

2005

Am J Gastroenterology

158

100

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The gastroesophageal junction (GEJ), which is defined as the point where the distal esophagus joins the proximal stomach (cardia), is a short anatomic area that is commonly exposed to the injurious effects of GERD and/or Helicobacter pylori infection. These disorders often lead to inflammation and intestinal metaplasia (IM) of this anatomic region. The true gastric cardia is an extremely short segment (<0.4 mm) of mucosa that is typically composed of pure mucous glands, or mixed mucous/oxyntic glands that are histologically indistinguishable from metaplastic mucinous columnar epithelium of the distal esophagus. In patients with GERD, whether physiologic or pathologic, the length of cardia-type epithelium increases and extends proximally above the level of the anatomic GEJ into the distal esophagus. Columnar metaplasia of the distal esophagus represents a squamous to columnar metaplastic reaction that develops from an esophageal stem cell and may pass through an intermediate phase characterized by the presence of a type of epithelium that possesses a mixture of squamous and columnar features, termed multilayered epithelium. In contrast, IM of the gastric cardia represents a columnar to columnar cell metaplastic reaction that develops from a gastric stem cell located in the deep foveolar compartment of the gastric mucosa. Intestinal metaplasia, particularly the incomplete type, is widely believed to represent the precursor lesion upon which dysplasia and cancer arises. The frequency of IM is probably greater in metaplastic columnar epithelium in the esophagus secondary to GERD, than in cases of true gastric carditis secondary to H. pylori, and may be a reason why there is a higher risk of carcinoma in the former compared to the latter. A variety of clinical, endoscopic, histologic, and histochemical methods can be used to distinguish GERD-induced columnar metaplasia of the distal esophagus from H. pylori-induced inflammation of true gastric cardia, and these are outlined in this review, but further controlled studies are needed to critically evaluate these techniques. Further prospective trials are needed to adequately evaluate the different etiologic and pathogenetic mechanisms and, most importantly, the risk of malignancy in these two conditions.

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Section: Pathogenesis Of Intestinal Metaplasia In the Gastroesophageamentioning

confidence: 90%

Section: Natural History and Risk Of Neoplasia Of Intestinal Metaplasmentioning

confidence: 99%

Unraveling the Mystery of the Gastroesophageal Junction: A Pathologist's Perspective

Odze

2005

Am J Gastroenterology

158

100

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“…In 1994, Genta et al [37] were the first to report that the gastric cardia is involved in H. pylori gastritis, a finding meanwhile confirmed in a number of studies [10,12,13,[33][34][35][38][39][40][41][42][43], also in children [44]. However, there is some variability of H. pylori-infected patients who present with carditis.…”

Section: Carditis In Association With H Pylori Infectionmentioning

confidence: 79%

Carditis at the Interface between GERD and <i>Helicobacter pylori</i> Infection

Peitz

Malfertheiner²

2004

Dig Dis

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Inflammation of the gastric cardia (‘carditis’) is a histological diagnosis. It seems reasonable to transfer histological criteria of the updated Sydney classification from the distal stomach to the cardia as long as a special classification of inflammation of the esophagogastric junction is lacking. The two best characterized causes of carditis are Helicobacter pylori infection and gastroesophageal reflux disease (GERD). However, the causal contribution and interference of these two factors are highly controversial, as is the clinical relevance of carditis in terms of eliciting symptoms or conferring an increased cancer risk. Variability of studies on carditis is based on conflicting concepts of the normal anatomy of the esophagogastric junction. Cardia-type mucosa (CM) apparently exists at birth as a tiny circular area, and extends to a larger area in adulthood. This implies that cardia-type mucosa is largely metaplastic. Metaplastic CM may evolve in the lower esophagus as a consequence of GERD. It is a general phenomenon that H. pylori-induced gastritis also involves the gastric cardia, irrespective whether the cardia is lined by fundus-type mucosa or CM. The contribution of GERD to inflammation of CM in H. pylori-negative individuals is, however, highly controversial. Prevalence of carditis in GERD patients fluctuates between 10 and 97%. Hence, because of its high frequency and low specificity, carditis can currently not be considered as a clinical entity. The role of carditis for the increasing incidence of cancer of the esophagogastric junction requires careful studies that include accurate description of the area with adequate biopsy protocols.

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“…It is the combination of intestinal metaplasia in a biopsy originating in mucosa having endoscopic criteria of Barrett esophagus that allows the unequivocal diagnosis of Barrett esophagus. Whether or not intestinal metaplasia in the gastric cardia has the same significance, biology and clinical implications as in the esophagus is currently a matter of scientific debate [11], but until intestinal metaplasia is shown to have significant precancerous potential, it is important to distinguish the two.…”

Section: When Is a Diagnosis Of Barrett Esophagus Justified?mentioning

confidence: 99%