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Browsing by Subject "Intestinal metaplasia"

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    Changing pattern of cytokeratin 7 and 20 expression from normal epithelium to intestinal metaplasia of the gastric mucosa and gastroesophageal junction
    (Murcia : F. Hernández, 2002) Jovanovic, I.; Tzardi, M.; Mouzas, I.A.; Micev, M.; Pesko, P.; Milosavljevic, T.; Zois, M.; Sgantzos, M.; Delides, G.; Kanavaros, Panagiotis
    It is currently unclear whether intestinal metaplasia at the esophagogastric junction and in the distal esophagus represent a continuum of the same underlying disease process, i.e., gastroesophageal reflux, or constitute different entities with a diff e r e n t pathogenesis. Biopsies below the Z line might show specialized epithelium in some patients and the question is whether this is another form of short segment Barrett’s esophagus or whether it is related to a generalized atrophic process of the stomach. Data from recent studies regarding the expression of cytokeratin CK7 and CK20 in intestinal metaplasia (IM) found at the gastroesophageal junction are conflicting. Prompted by these data we undertook the present study: a) to evaluate the expression of CK7 and CK20 in IM of the gastric cardia and to compare the findings with those in patients with Barrett’s esophagus and IM of the gastric corpus and antrum mucosa; and b) to evaluate the immunophenotype of non-intestinalized cardiac mucosa and to compare it with that of normal gastric epithelium. We studied the expression of CK7 and CK20 on biopsy specimens from patients with long-seg m e n t B a r r e t t ’s esophagus (n=17) and surgical resection and biopsy specimens of gastric cardia (n=15), corpus (n=14) and antrum (n=22) from patients with histological evidence of IM. Eighty-four biopsy specimens from 42 patients (antrum n=15, corpus n=20, cardia n=7) without evidence of IM were studied as a control group. We observed an immunophenotype characterised by diffuse moderate to strong CK7 staining on the surface and crypt epithelium combined with strong CK20 staining on the surface and superficial part of the crypts in 94.1% (16/17) of the cases with long-se g m e n t Barrett’s esophagus, but in none of the 36 cases with IM in distal stomach (antrum and corpus). IM in the gastric cardia expressed the immunophenotype seen in IM of the gastric mucosa in 93.3% (14/15) of the cases. On the other hand, normal cardiac epithelium expressed patchy strong CK7 staining on the surface epithelium and on both, superficial and deep parts of the pits combined with patchy strong CK20 staining on the surf a c e epithelium and superficial pits, a feature permitting distinction of the normal cardiac epithelium from those of the normal gastric antrum and corpus epithelium. We conclude that the expression of cy t o keratins 7 and 20 can be used to distinguish the origin of IM of the gastroesophageal junction. The CK7/20 immunophenotype of IM in the gastric cardia closely resembles that of the IM in the gastric antrum and corpus and is different from IM in long-segment Barrett's esophagus. In contrast, the CK7/20 immunophenotype of the cardiac epithelium is different from that of the gastric antrum and corpus mucosa, suggesting that cardiac epithelium might not be a native normal g a s t r i c epithelium but one that is acquired as a consequence of longstanding inflammation. Changing pattern of CK7 and CK20 expression from normal to intestinalized epithelium suggests that IM arising from cardiac epithelium might have distinctive features.
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    Gastric intestinal metaplasia eleven years after randomized selective proximal vagotomy for peptic ulcer
    (Murcia : F. Hernández, 1993) Rubio, C.A.; Emas, S.; Slezak, P.; Nakano, H.; Kalin, B.
    The presence of intestinal metaplasia (IM) 11 years after selective proximal vagotomy (SPV), selective proximal vagotomy with pyloroplasty (SPV + PP) and selective vagotomy with pyloroplasty (SV + PP) was investigated in 38 consecutive patients. IM was significantly more frequent in SPV than in SV + PP, SPV + PP or in unoperated controls of matching ages. IM occurred more frequently both at an older age (260 years) in SPV and in a larger number of gastric areas than in the other group of patients. Reports in the literature indicate that vagotomy may increase the risk of gastric carcinoma and that IM inay antedate malignant transformation. It would thus appear that patients previously operated with SPV (without pyloroplasty) having IM, should be the group of patients to be enrolled in endocospical surveillance programs for detection of possible cancer development.
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    Histopathological features of the gastroesophageal junction: an Eastern view
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Kim, Ahrong; Shin, Nari; Lee, Hyung-Jeong; Jo, Hong-Jae; Kim, Joo-Yeon; Kim, Young-Keum; Park, Do Youn; I, Hoseok; Kim, Gwang Ha
    The definition and features of the gastroesophageal junction (GEJ) and the histopathologic features of the cardiac mucosa remain controversial. Most reports originate from western countries, which have different prevalence of GEJ adenocarcinoma and gastroesophageal reflux disease (GERD) compared to eastern countries. Therefore, we investigated GEJ anatomic and histopathologic features by histological mapping in 30 esophagogastrectomy specimens of middle and lower esophageal squamous cell carcinoma. We measured the lengths of the cardiac mucosa, oxyntocardiac mucosa, and esophageal cardiactype glands. We assessed the presence of intestinal metaplasia, pancreatic acinar cells, Brunner’s-like glands, and submucosal esophageal gland beneath cardiac mucosa and the relationship of these features with age and the circumferential location of cardiac mucosa. The lengths of cardiac mucosa and esophageal cardiac-type glands significantly increased with age (<63 years, 2767.86±734.95 µm vs. ≥63 years, 5453.12±839.52 µm, P=0.025 and <63 years, 1151.78±452.81 µm vs. ≥63 years, 2273.44±321.58 µm, P=0.049, respectively) and the presence of circumferential cardiac mucosa (+, 5731.25±721.57 vs. −, 2625.00±356.00 µm, P=0.007; +, 2425.00±326.13 µm vs. −, 400.00±204.80 µm, P<0.0001 respectively). The presence of intestinal metaplasia and irregular GEJ increased with age and the circumferential location ofcardiac mucosa. The presence of esophageal submucosal glands beneath the cardiac mucosa, pancreatic acinar cells, and Brunner-like glands were seen in 8/30 (26.7%), 15/30 (50%), and 14/30 (46.7%) cases, respectively. These data indirectly suggest that cardiac mucosa originated from the distal esophagus and that the presence of cardiac mucosa may indicate GERD, in accordance with data from Western countries.
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    Mechanisms of regulation of normal and metaplastic intestinal differentiation
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Rodrigues, Jaime P.; David, Leonor; Almeida, Raquel; Barros, Rita; Freitas, Teresa; Ponte, Ana; Sousa, Mafalda; Silva, João Carlos; Carvalho, João
    The gastrointestinal tract is an organized structure originating from the three embryonic germ layers: endoderm, mesoderm and ectoderm. Morphological changes that accompany its formation are relatively well known, although the underlying molecular mechanisms are still poorly defined. Intestinal metaplasia, resulting from an epithelial transdifferentiation process, is considered a precursor lesion of gastric adenocarcinoma, a malignancy with serious consequences in terms of morbidity and mortality worldwide. Similarly to gastrointestinal embryonic development, molecular changes involved in the development of this lesion that recapitulate the intestinal development, out of time and space, are also widely unknown. In this review we present, briefly, the process of formation of the digestive tract, from its embryonic age to adulthood, with emphasis on anterior-posterior patterning and on molecular mechanisms that may play an important role. In addition, we try to establish a parallel and understand what mechanisms can, through their deregulation, originate the metaplastic lesion. Cdx genes appear to be the main regulators of normal intestinal differentiation and also to be largely involved in the metaplastic epithelial transdifferentiation process. However, control of gene expression both during intestinal development and in intestinal metaplasia is complex and seems to depend on several transcription factors. More extensive studies about the mechanisms underlying intestinal metaplasia are needed if we aim to prevent neoplasia development and all its negative consequences in persons at risk.
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    Metaplasia intestinal gástrica. Asociaciones clínico-patológicas e importancia de la secreción de sulfomucinas en un área de bajo riesgo de cáncer gástrico
    (Elsevier, 1991) Martínez Díaz, F.; Ortuño Pacheco, G.; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
    We studied the relationship between the types of entera/ metaplasia, the clinicopathologic parameters (sex, age, location and endoscopic findings) and other abnormalities such as atrophic gastritis, gastric dysplasia and gastric cancer in low risk geographic area. We analized 850 gastric specimens from the "S,. María del Rosell" Hospital and the Department of Pathology of the Medica/ school of Murcia. Our results showed a positive relationship between enteral metaplasia and age (>50 years), antral region, gastric ulcer, atrophic gastritis, gastric dysplasia and gastric adenocarcinoma of intestinal type. Entera/ metaplasia type 111 characterized by the secretion of sulphomucins, although more frequent in the intestinal type of carcinoma ( 3 l .25%) compared with benign lesions ( l 2. 5% ), has no value as screening test due to its low sensitivity (31.25%). However, its high specificity ( 100%) 􀁐uggests that it should be looked for in ali the cases o/intestinal metaplasia in order to select patients at high risk of gastric cancer. -------------------

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