Morfología y repercusiones diagnóstico-terapéuticas de las lesiones preneoplásicas gástricas / Morphology and diagnostic determinants of gastric precancerous conditions

El carcinoma gástrico (CG) de tipo intestinal se origina en un epitelio displásico, que a su vez se desarrolla en medio de una atrofia gástrica (AG) y metaplasia intestinal (MI). La infección por Helicobacter pylori (HP) es la causa más frecuente de AG, causando una pangastritis atrófica multifocal. Entre otras condiciones que producen inflamación crónica de la mucosa gástrica se encuentran también la gastritis autoinmune y la anemia perniciosa. El marco conceptual sobre el cual descansa gran parte de la investigación actual y nuestra comprensión de los cambios que ocurren en la mucosa gástrica se debe a la denominada "cascada de Correa"; quien planteó que la mucosa gástrica crónicamente inflamada, da paso a la AG, que va adquiriendo focos de MI y en dicho epitelio se desarrollará finalmente una displasia (DIS). Se ha acuñado el término lesiones preneoplásicas gástricas (LPG), para referirse a: AG, MI y DIS.Después de la erradicación de HP, se ha demostrado una reducción general de la incidencia de CG; efecto que no es tan claro, cuando la pangastritis por HP ha evolucionado a AG extensa. De tal modo que el efecto de la erradicación de HP medido a través de EC, ha sido poco consistente. La AG grave diagnosticada por histología representa la condición de mayor riesgo. Por otra parte, la MI puede ser de tipo intestinal (delgado-entérica ó incompleta) y la colónica (colónica ó completa) considerándose a esta última, como la variedad de peor pronóstico. El diagnóstico histológico de este tipo de lesiones determina que quien las padece, debe someterse a vigilancia endoscópica. El objetivo de este manuscrito fue resumir la evidencia existente respecto de las LPG, en términos de su caracterización morfológica y sus repercusiones diagnóstico-terapéuticas (significado patológico, graduación del riesgo, vigilancia recomendada; y factores de riesgo).

Gastric carcinoma (GC) of intestinal type, originates from a dysplastic epithelium, which in turn develops in the midst of gastric atrophy (GA) and intestinal metaplasia (IM). Helicobacter pylori (HP) infection is the most frequent cause of GA, causing a multifocal atrophic pangastritis. Among other conditions that produce chronic inflammation of gastric mucosa are also autoimmune gastritis and pernicious anemia. The conceptual framework on which much of current research rests and our understanding of the changes that occur in the gastric mucosa is due to the so-called "Correa waterfall"; who stated that gastric mucosa chronically inflamed, gives way to the GA, which is acquiring foci of IM and in said epithelium a dysplasia (DIS) will eventually develop. The term precancerous conditions (PCC) of the gastric mucosa have been coined to refer to: GA, IM and DIS. After HP eradication, a general reduction in the incidence of GC has been demonstrated; effect that is not so clear, when pangastritis by HP has evolved to extensive GA. Thus, the effect of HP eradication measured through clinical trials has been inconsistent. Severe GA diagnosed represents the highest risk condition. On the other hand, IM can be enteric (grade I), enterocolic (grade II) or colonic (grade III); considering IM III as the variety with the worst prognosis. Histological diagnosis of gastric PCC, determines that the one who suffers them, must undergo endoscopic surveillance. The aim of this manuscript was to update morphological aspects and diagnostic-therapeutic scope of gastric PCC.

Effect of Helicobacter pylori Eradication on Subsequent Dysplasia Development after Endoscopic Resection of Gastric Dysplasia / 대한소화기학회지

BACKGROUND/AIMS: Eradication of Helicobacter pylori reduces the incidence of gastric cancer, and may inhibit gastric dysplasia progression into gastric cancer. The aim of this study was to investigate the effect of eradication of Helicobacter on the incidence of subsequent gastric dysplasia development after endoscopic resection. METHODS: Medical records of patients who underwent endoscopic resection for gastric dysplasia were retrospectively reviewed. Presence of H. pylori was assessed by the Campylobacter-like organism test and histology. The rate of subsequent dysplasia development after endoscopic resection between the eradication group and non-eradication group was compared. RESULTS: Total of 129 patients positive for H. pylori infection were included for analysis. Of these, 85 patients received successful eradication therapy and 44 patients did not receive eradication therapy or failed to achieve successful eradication. Sex, mean age and pathologic grade of dysplasia did not differ between the two groups. In univariate analysis, the grade of intestinal metaplasia (p=0.013) significantly differed between metachronous dysplasia group and non-metachrounous dysplasia group. In multivariate analysis, eradication of H. pylori (p=0.014) was related to reduced incidence of subsequent gastric dysplasia development after endoscopic resection. CONCLUSIONS: Eradication of H. pylori likely has a beneficial effect in preventing the development of subsequent gastric dysplasia, a premalignant lesion of gastric cancer, after endoscopic resection.

Upgrade of Lesions Initially Diagnosed as Low-Grade Gastric Dysplasia upon Forceps Biopsy Following Endoscopic Resection

BACKGROUND/AIMS: Gastric dysplasia is generally accepted to be the precursor lesion of gastric carcinoma. Approximately 25% to 35% of histological diagnoses based on endoscopic forcep biopsies for gastric dysplastic lesions change following endoscopic resection (ER). The aim of this study was to determine the predictive endoscopic features of high-grade gastric dysplasia (HGD) or early gastric cancer (EGC) following ER for lesions initially diagnosed as low-grade dysplasia (LGD) by a forceps biopsy. METHODS: To determine predictive variables for upgraded histology (LGD to HGD or EGC). The lesion size, gross endoscopic appearance, location, and surface nodularity or redness as well as the presence of a depressed portion, Helicobacter pylori infection, and intestinal metaplasia were retrospectively investigated. RESULTS: Among 251 LGDs diagnosed by an initial forceps biopsy, the diagnoses of 100 lesions (39.8%) changed following the ER; 56 of 251 LGDs (22.3%) were diagnosed as HGD, 39 (15.5%) as adenocarcinoma, and 5 (2.0%) as chronic gastritis. In a univariate analysis, large lesions (>15 mm), those with a depressed portion, and those with surface nodularity were significantly correlated with a upgraded histology classification following ER. In a multivariate analysis, a large size (>15 mm; odds ratio [OR], 2.8; 95% confidence interval [CI], 1.46 to 5.43) and a depressed portion in the lesion (OR, 2.7; 95% CI, 1.44 to 5.03) were predictive factors for upgraded histology following ER. CONCLUSIONS: Our study shows that a substantial proportion of diagnoses of low-grade gastric dysplasias based on forceps biopsies were not representative of the entire lesion. We recommend ER for lesions with a depressed portion and for those larger than 15 mm.

A case of recurred gastric dysplasia associated with eosinophilic gastroenteritis / 대한내과학회지

The association of malignant tumors and peripheral eosinophilia or tissue eosinophilic infiltration has been uncommonly described. Moreover, a recent study has demonstrated some gastric cancers can express eosinophilic chemotactic factor. Interestingly, we recently experienced a case of recurrent eosinophilic gastroenteritis with relapsing gastric dysplasia. It is suggested that gastric dysplasia can also produce eosinophilic chemotactic factors and eosinophilic gastroenteritis can develop with recurred dysplasia. In this patient, eosinophilia served as an indicator of disease activity or as a marker. Eosinophilia may represent an important disease marker with prognostic significance and may rarely cause disease on its own.

Diagnostic Significance of the CEA, AgNORs and PCNA in the Gastric Dysplasia and Adenocarcinoma

This study aimed to differentiate gastric mucosal lesions such as the inflammatory gastric mucosa, gastric dysplasia and adenocarcinoma, using the CEA(carcinoembryonic antigen), AgNORS(Nucleolar organizer regions) and PCNA(proliferating cell nuclear antigen) stains. The tissue samples were taken from 30 cases of inflammatory gastric mucosa (19 gastritis and 11 regenerative hyperplasia), 28 cases of gastric dysplasia (9 mild dysplasia, 10 moderate dysplasia and 9 severe dysplasia) and 21 cases of gastric adenocarcinoma. The CEA was expressed in 16 of 21 adenocarcinomas(76%), but in neither inflammatory nor dysplastic gastric mucosae. The mean number of AgNORs per nucleus was 1.54 in inflammatory gastric mucosa, 1.80 in gastric dysplasia, and 1.88 in adenocarcinoma. The number of AgNORs was increased in dysplasia and adenocarcinoma compared to the inflammatory gastric mucosa without statistical significance. The percentage of the PCN A positive cells was 35.2% in inflammatory gastric mucosa, 44.1 % in gastric dysplasia, and 69.0% in gastric adenocarcinoma. The positivity of the PCNA was significantly increased in adenocarcinoma compared to the inflammatory gastric mucosa and dysplasia. In conclusion, the frequency of the CEA positive staining was increased in the gastric adenocarcinoma, and so CEA stain will be able to provide an additive method for the differential diagnosis between severe dysplasia and adenocarcinoma of the stomach.

An Image Analytical Study on the Structural Spectrum of Intestinal Metaplasia-Dysplasia-Carcinoma of the Stomach

Intestinal metaplasia and dysplasia of the stomach have been stressed as precursors of gastric carcinoma of the intestinal type, although their preneoplastic nature is still debated. In this study, the cytomorphometric and cytokinetic spectra of the suggested preneoplastic and neoplastic lesions of the stomach were investigated. From the resected stomachs of early gastric carcinoma of intestinal type, areas of normal, intestinal metaplasia, dysplasia, and carcinoma were selected. They were immunostained for proliferating cell nuclear antigen, counterstained with propidium iodide, and various nuclear parameters were measured by image analysis. Normal and intestinal metaplastic mucosae differed by the localization of proliferation zone, but not by nuclear profile area, circular shape factor, and proliferation index. In dysplasia, proliferation zone covered large parts of the dysplastic area. Nuclear profile area and proliferation index were larger whereas circular shape factor was smaller than in normal or intestinal metaplasia. Carcinomatous lesion had diffuse proliferation activity, the largest nuclear profile area and proliferating index, and circular shape factor in-between those of normal or intestinal metaplasia and dysplasia. The above results showed a structural spectrum among normal of intestinal metaplasia, dysplasia, and carcinoma of intestinal type in cytomorphometric and cytokinetic terms. The structural spectrum raises the possibility that dysplasia of the stomach is a preneoplastic lesion.

A Study on the Cell Kinetics of the Dysplastic Epithelium in the Stomach

This study was designed to evaluate the biological behavior of the dysplastic lesion of the stomach by applying immunohistochemical method for bromodeoxyuridine (BrdUrd). The results obtained were as follows. 1) In most hyperplastic and dysplastic lesions, the proliferative cell zones, loci of BrdUrd-labelled cells, were found in the upper later of the mucosa, whereas they were confined to the neck zone in the normal gastric mucosa. 2) The labelling indices (LIs), percentages of BrdUrd-labelled cells, were 11.0% to 13.6% in the normal gastric mucosa, and were 14.3% to 17.9%, 16.4% to 19.2% and 17.4% to 20.7% in the simple hyperplasia, in the atypical hyperplasia and in the dysplasia, respectively. These findings suggested that proliferative potential in hyperplasia and dysplasia were greater than that in normal gastric mucosa, the higher the grade of dysplasia being, the greater the proliferative potentials.