Immunohistochemical Markers for Barrett’s Esophagus and Associations to Esophageal Z-Line Appearance

Wallner, Bengt; Sylvan, Anders; Janunger, Karl-Gunnar; Bozóky, Béla; Stenling, Roger

doi:10.1080/003655201750305404

Cited by 28 publications

(21 citation statements)

References 47 publications

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“…The immunostaining pattern has a strong, diffuse CK7 staining of the surface and glandular epithelium, and weak CK20 staining of the superficial epithelium (18). While these results were confirmed by later reports (1,19), they were not reproducible by others (3,20).…”

contrasting

confidence: 29%

Barrett’s Esophagus and Cardiac Intestinal Metaplasia: Two Conditions within the Same Spectrum

White

Gabril

Ejeckam

et al. 2008

Canadian Journal of Gastroenterology

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BACKGROUND: Immunostaining for cytokeratin 7 (CK7) and cytokeratin 20 (CK20) has a characteristic pattern in Barrett's esophagus (BE), but reports regarding its sensitivity and specificity are inconsistent. Intestinal metaplasia of the gastric cardia (CIM) is histologically similar to BE, but with no abnormal endoscopic findings. OBJECTIVES: To evaluate the sensitivity and specificity of a semiquantitative CK7/CK20 immunostaining pattern for the diagnosis of BE, and to further elucidate the pathogenesis of CIM. METHODS: Tissues were examined by hematoxylin and eosin and periodic acid schiff/alcian blue stains, and then were immunostained with CK7 and CK20 antibodies. Correlations with other clinical parameters were statistically analyzed. RESULTS: When values were revised based on follow-up data and auxiliary testing, all BE cases (100%) displayed the characteristic BE CK7/CK20 immunostaining pattern, compared with 66% of CIM cases. In the subgroup of patients who were endoscopically and immunohistochemistry-positive but histologically negative, all patients except for one had documented BE when clinical history, auxiliary testing and follow-up were evaluated. There were no statistically significant differences between BE and CIM regarding Helicobacter pylori infection or the type of metaplasia (complete versus incomplete). The sensitivity of the CK7/CK20 pattern reached 100% in the subgroup of CIM patients with a history of acid reflux. Of 26 cases of CIM where follow-up was available, four cases (15%) progressed to BE, and one developed dysplasia. All four cases showed the BE pattern of CK7/CK20 staining and were negative for H pylori infection. CONCLUSIONS: A semiquantitative CK7/CK20 pattern can be used to confirm BE even in the absence of histological evidence. The subgroup of CIM with acid reflux may develop into BE and may need closer follow-up.

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contrasting

confidence: 29%

Barrett’s Esophagus and Cardiac Intestinal Metaplasia: Two Conditions within the Same Spectrum

White

Gabril

Ejeckam

et al. 2008

Canadian Journal of Gastroenterology

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“…Ormsby et al found that a BE CK 7/20 staining pattern was highly sensitive and specific for BE compared to gastric IM, and suggested that immunostaining may be useful to differentiate metaplastic columnar epithelium in the esophagus related to BE from chronic gastritis with IM in biopsies from the GEJ region. However, several other workers have not been able to confirm the findings by Ormsby et al, and instead, have shown that the CK 7/20 immunostaining profile in biopsies from the GEJ often show a BE pattern (23,27,90). For instance, in a biopsy study by Glickman et al, patients with long-segment BE, short-segment BE, IM of the GEJ secondary to either H. pylori or GERD, or with a normal gastric antrum, had a BE CK 7/20 staining pattern in 91% of BE cases, 90% of IM of the GEJ cases (regardless of the etiology), and in 14% of gastritis cases secondary to H. pylori (27).…”

Section: Differential Diagnosis Of H Pylori-induced True Gastric Carmentioning

confidence: 46%

“…For instance, in a biopsy study by Glickman et al, patients with long-segment BE, short-segment BE, IM of the GEJ secondary to either H. pylori or GERD, or with a normal gastric antrum, had a BE CK 7/20 staining pattern in 91% of BE cases, 90% of IM of the GEJ cases (regardless of the etiology), and in 14% of gastritis cases secondary to H. pylori (27). Others have also shown mixed results with CK 7/20 immunostaining (13,23,(90)(91)(92).…”

Section: Differential Diagnosis Of H Pylori-induced True Gastric Carmentioning

confidence: 96%

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

Odze

2005

Am J Gastroenterology

155

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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“…Columnar Barrett's epithelium exhibits enterocytic differentiation as evidenced by its expression of proteins associated with intestinal mucosal function, such as sucrase-isomaltase, cytokeratins, and mucins (22)(23)(24)(25). We found that in Barrett's epithelia from which cancer had arisen the predominant change in gene expression was down-regulation of differentiation-specific genes involved in gastrointestinal mucosal functions, such as transport, metabolism, and mucous secretion.…”

Section: Gene Expression In Esophageal Adenocarcinomamentioning

confidence: 76%

Dedifferentiation Precedes Invasion in the Progression from Barrett's Metaplasia to Esophageal Adenocarcinoma

Helm

Enkemann

Coppola

et al. 2005

Clinical Cancer Research

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Purpose: Adenocarcinoma arises in Barrett's esophagus by progression from metaplasia to cancer through grades of dysplasia. Our aim in this exploratory study was to characterize the broad changes in gene expression that underlie this histologic progression to cancer and assess the potential for using these gene expression changes as a marker predictive of malignant progression in Barrett's epithelium. Experimental Design: Microarray analysis was used to obtain individual gene expression profiles from endoscopic biopsies of nine esophageal adenocarcinomas and the Barrett's epithelia from which three of the cancers had arisen. Pooled samples from the Barrett's epithelia of six patients without cancer or dysplasia served as a reference.

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Immunohistochemical Markers for Barrett’s Esophagus and Associations to Esophageal Z-Line Appearance

Abstract: CK7/20 is a feasible marker for Barrett's esophagus. Intestinal metaplasia in different ZAP grades differs regarding expression of immunohistochemical markers.

Cited by 28 publications

References 47 publications

Barrett’s Esophagus and Cardiac Intestinal Metaplasia: Two Conditions within the Same Spectrum

Barrett’s Esophagus and Cardiac Intestinal Metaplasia: Two Conditions within the Same Spectrum

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

Dedifferentiation Precedes Invasion in the Progression from Barrett's Metaplasia to Esophageal Adenocarcinoma

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