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Gastrointestinal Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Gareth Davies, Chris Black, Keeley Fairbrass
This is an acquired condition due to long-term acid reflux where the stratified squamous epithelium that normally lines the distal oesophagus is replaced by columnar epithelium. This change, where one type of fully differentiated cell replaces another, is called metaplasia. It is a risk factor for oesophageal adenocarcinoma.
Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Sometimes chronic irritation can cause cells to change from one differentiated cell type into another. In general, more delicate cells are replaced with more robust cells that are better able to withstand the irritant. This process, called metaplasia (see Figure 5.7), is usually reversible; if the initiating irritant is removed, cells revert to their original type. Metaplasia usually occurs when stem cells are stimulated to follow a different developmental path, rather than causing a change in already differentiated cells. The immediate consequences of metaplasia are generally not serious. When it occurs in mammals, metaplasia is not a direct cause of cancer. However, metaplastic cells eventually have a higher likelihood of becoming cancerous if the abnormal stimulus is not eliminated. A well-characterized example is the replacement of pseudostratified columnar epithelial cells in the respiratory system with stratified squamous epithelial cells in response to tobacco smoke.
Disorders of Growth and Differentiation
Published in Jeremy R. Jass, Understanding Pathology, 2020
This is the replacement of one differentiated cell type by another. It is seen in situations of chronic inflammation: squamous metaplasia in the respiratory tract in response to tobacco smoke, intestinal metaplasia of the stomach in chronic gastritis, columnar metaplasia of the lower oesophagus in gastro-oesophageal reflux and glandular metaplasia of the chronically inflamed urinary bladder. The extent to which metaplasia is an adaptive phenomenon as opposed to an error in developmental programming is unclear. There is evidence that metaplasia may regress, at least partially, when the causative agent is removed but the change is also associated with an increased risk of cancer. The high frequency and reversibility of metaplasia suggests that genetic mutation is unlikely to be a factor in its aetiology. Epigenetic inactivation of genes, for example by hypermethylation, could explain metaplasia, however.
Endoscopic and clinicopathologic features of early gastric signet ring cell carcinoma ≤20 mm: a retrospective observational study
Published in Scandinavian Journal of Gastroenterology, 2023
Jianing Xu, Jingyi Zhu, Lanhui Lin, Zhiyu Li, Feng Gu, Fangning Wang, Huihong Zhai
Twenty-two cases receiving ESD and surgery were further histologically compared (Table 4). When evaluating the background mucosa, nearly half of the lesions presented with atrophic gastritis in each group. Herein, we showed the endoscopic images of a diminutive GSRCC occurring on non-atrophic background mucosa (Figure 2) and a small GSRCC stemming from atrophic background mucosa (Figure 3). The incidence of intestinal metaplasia in the diminutive, small and intermediate groups was 0%, 66.7% and 62.5%, respectively. Nearly, all the lesions were poorly differentiated or undifferentiated predominant type except two cases (16.7%) presenting with mixed type in the small group. The occurrence of submucosal invasion was positively correlated with larger tumor size without statistical significance. Lymphovascular invasion was only seen in one case (12.5%) in the intermediate group with no case in the other two groups.
Endoscopic scoring system for gastric atrophy and intestinal metaplasia: correlation with OLGA and OLGIM staging: a single-center prospective pilot study in Korea
Published in Scandinavian Journal of Gastroenterology, 2022
Hee Kyong Na, Kee Don Choi, Young Soo Park, Hwa Jung Kim, Ji Yong Ahn, Jeong Hoon Lee, Kee Wook Jung, Do Hoon Kim, Ho June Song, Gin Hyug Lee, Hwoon-Yong Jung
Biopsy specimens were fixed and paraffin-embedded, and each section was stained with hematoxylin and eosin (H&E). Atrophic gastritis and intestinal metaplasia were interpreted by an experienced gastrointestinal pathologist (PYS) who was unaware of the endoscopic scores, using the updated Sydney system. The presence of atrophy was assessed based on findings of shrinking or vanishing of the glands and fibrosis of the lamina propria. The presence of metaplasia was assessed based on findings of intestinal metaplasia or pseudo-metaplasia of the corpus. OLGA and OLGLIM staging were applied according to the OLGA and OLGIM guidelines [7,22,23]. In each of the two areas (the lesser curvature and greater curvature), overall atrophy and metaplasia score expressed the sum of the percentages of atrophy/metaplasia changes and was divided by two [22]. Atrophic gastritis was graded as no, mild (1–30%), moderate (31–60%), or severe (>60%) atrophy of the observed biopsy tissue from the antrum and corpus, respectively [22]. Intestinal metaplasia was graded as non-existent, mild (1–9), moderate (10–29), or severe metaplasia (≥30%) at each antrum and corpus biopsy level, respectively. Stages 0, 1, 2 were placed into the low-risk group whereas stages 3 and 4 were the high-risk group.
Gastric intestinal metaplasia assessment between linked color imaging based on endoscopy and pathology
Published in Scandinavian Journal of Gastroenterology, 2021
Guanpo Zhang, Jin Zheng, Linfu Zheng, Shentong Yu, Chuanshen Jiang, Wulian Lin, Dazhou Li, Lijuan Qu, Wen Wang
At present, there is no consensus on whether intestinal metaplasia is reversible after treatment. One of the reasons for this is the scattered mucosal distribution of intestinal metaplasia, with alternating areas of metaplasia and normal mucosa and mucosa showing different degrees of intestinal metaplasia appearing together. Therefore, follow-up assessments with random biopsy may misjudge the patient’s true intestinal metaplasia level, and the GIM at this part of the stomach may be overestimated or underestimated at different follow-up times. In this regard, Pedro et al. believe that this issue and other questions regarding the effect of interventions on the progression or regression of intestinal metaplasia can be addressed only by observing the total area of intestinal metaplasia (i.e., the range of intestinal metaplasia) [16]. Thus, we believe that future studies assessing whether intestinal metaplasia can be reversed after treatment can use the EGGIM to follow up the entire range of intestinal metaplasia to obtain conclusive answers to these unresolved questions.