Metaplasia and histopathological lesions of the esophageal mucosa

Authors

DOI:

https://doi.org/10.33448/rsd-v11i2.25778

Keywords:

Esophageal mucosa; Metaplasia; Carcinogenesis.

Abstract

Metaplasia is a reversible adaptive process, which occurs in a cell type that, upon a stimulus, undergoes the replacement of another cell type of similar lineage. Objective: to identify the prevalence of metaplasia in esophageal mucosal samples and evaluate the relationship between metaplasia and histopathological lesions. Method: cross-sectional, retrospective study with a sample of 1953 histopathological reports of the esophageal mucosa. Results: from 1953 reports, 548 (28.1%) had metaplasia, 94 (17.1%) of the intestinal type and of these 35 (6.4%) were focal; 133 (6.8%) had Barrett's esophagus, 414 (75.5%) with gastric ectopia, 21 (1.1%) with dysplasia, 12 (57.1%) with low grade and 9 (42.9 %) high degree and 1427 (73.1%) reports presented esophagitis. The median age group of patients with metaplasia was 45 years (IIQ 34-55), with 289 (51.7%) female and 438 (81.4%) from the capital. Of the reports with metaplasia, 46 (8.2%) had Helicobacter pylori, 30 (5.3%) Barrett's esophagus and 14 (2.6%) had gastric atrophy associated with bacteria, however there was no significant association with H. pylori. The association of metaplasia with esophagitis, eosinophilic esophagitis and adenomatous polyp was statistically significant (p<0.001). Together, we observed a lower risk of metaplasia in the presence of esophagitis (RR: 0.44; 95%CI: 0.36-0.55) and higher in the presence of Eosinophils >=15 eos/CGA (RR: 3.27; 95%CI %: 1.70-6.62). Conclusion: We have no evidence of a relationship between esophageal metaplasia and H.pylori. The absence of esophagitis and the presence of Eosinophils >=15 eos/CGA is associated with an increased risk of metaplastic transformation.

References

Abbas, A. K. et al. (2008). Robbins patologia básica. Elsevier Brasil.

Aceves S. S. (2014). Remodeling and fibrosis in chronic eosinophil inflammation. Digestive diseases (Basel, Switzerland), 32(1-2), 15–21. https://doi.org/10.1159/000357004.

Andreollo, N. A., Beraldo, G. D. C., Alves, I. P. F., Tercioti-Junior, V., Ferrer, J. A. P., Coelho-Neto, J. D. S., & Lopes, L. R. (2018). Pathologic Complete Response (YPT0 YPN0) after chemotherapy and radiotherapy neoadjuvant followed by esophagectomy in the squamous cell carcinoma of the esophagus. ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo), 31.

Casson, A. G., Evans, S. C., Gillis, A., Porter, G. A., Veugelers, P., Darnton, S. J., ... & Hainaut, P. (2003). Clinical implications of p53 tumor suppressor gene mutation and protein expression in esophageal adenocarcinomas: results of a ten-year prospective study. The Journal of thoracic and cardiovascular surgery, 125(5), 1121-1131.

Cook, M. B. (2011). Non-acid reflux: the missing link between gastric atrophy and esophageal squamous cell carcinoma? Am J Gastroenterol. 106: 1930-2. [PMID: 22056574 DOI: 10.1038/ajg.2011.288].

Daly, J. M., Fry, W. A., Little, A. G. et al. (2000). Esophageal cancer: results of an American College of Surgeons Patient Care Evaluation Study. J Am Coll Surg. 190: 562-72.

de Sá, R. C., de Sá, L. K. D. S., Moreno, V. G., de Medeiros Araújo, D. C., & Teston, A. P. M. (2020). Incidência comprobatória de esôfago de barrett (metaplasia) com hipótese de diagnóstico inicial em um laboratório patológico do norte do Paraná. Brazilian Journal of Development, 6(10), 77720-77727.

Degiovani, M et. al, (2019). Existe relação entre o Helicobacter pylori e metaplasia intestinal nas epitelizações colunares curtas até 10 mm no esôfago. 32(4): e1480. DOI: /10.1590/0102-672020190001e1480 distal? https://www.scielo.br/j/abcd/a/Jzwq56NC68yPnmmxqynQRpD/?format=pdf&lang=pt11.

Dolan, K., Walker, S. J., Gosney, J., Field, J. K., & Sutton, R. (2003). TP53 mutations in malignant and premalignant Barrett's esophagus. Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus, 16(2), 83–89. https://doi.org/10.1046/j.1442-2050.2003.00302.x.

Gammon, M. D., Schoenberg, J. B., Ahsan, H., Risch, H. A., Vaughan, T. L., Chow, W. H., Rotterdam, H., West, A. B., Dubrow, R., Stanford, J. L., Mayne, S. T., Farrow, D. C., Niwa, S., Blot, W. J., & Fraumeni, J. F., Jr (1997). Tobacco, alcohol, and socioeconomic status and adenocarcinomas of the esophagus and gastric cardia. Journal of the National Cancer Institute, 89(17), 1277–1284. https://doi.org/10.1093/jnci/89.17.1277.

Henrik Simán, J., Forsgren, A., Berglund, G., Florén, C. H. (2001) Helicobacter pylori infection is associated with a decreased risk of developing oesophageal neoplasms. Helicobacter;6(4):310-6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11843963.

INCA. (2021). Como surge o câncer? Instituto Nacional do Câncer. https://www.inca.gov.br/como-surge-o-cancer.

Instituto Nacional de Câncer (2011). ABC do câncer: abordagens básicas para o controle do câncer / Instituto Nacional de Câncer. Rio de Janeiro. Inca. 128 p. : il

Kusters, J. G., Van Vliet, A. H. M. & Kuipers, E. J. (2006) Patogênese da infecção por Helicobacter pylori. Clinical Microbiology Reviews, 19, 449-90. http://dx.doi.org/10.1128/CMR.00054-05 http://www.ncbi.nlm.nih.gov/pubmed/16847081.

Lv, J., Guo, L., Liu, J. J., Zhao, H. P., Zhang, J., & Wang, J. H. (2019). Alteration of the esophageal microbiota in Barrett's esophagus and esophageal adenocarcinoma. World journal of gastroenterology, 25(18), 2149.

Sales, K. M. S., Silva, W. S., Carvalho, G. P. S. de, Fonseca, A. M. L., Silva, G. P. O., Viaggi, T. C., Aragão, B. C., Fonseca, A. M. R., Braga, A. F. L. da R., Chagas, A. M. B., Guimarães, B. M. de A., Trindade, L. M. D. F., & Lima, F. S. de. (2021). Achados endoscópicos em portadores de sintomas dispépticos. Research, Society and Development, 10(13), e562101321619. https://doi.org/10.33448/rsd-v10i13.21619.

Siewert, J. R., Stein, H. J., Feith, M., Bruecher, B. L., Bartels, H., & Fink, U. (2001). Histologic tumor type is an independent prognostic parameter in esophageal cancer: lessons from more than 1,000 consecutive resections at a single center in the Western world. Annals of surgery, 234(3), 360–369. https://doi.org/10.1097/00000658-200109000-00010.

Souza R. F. (2002). Molecular and biologic basis of upper gastrointestinal malignancy--esophageal carcinoma. Surgical oncology clinics of North America, 11(2), 257–viii. https://doi.org/10.1016/s1055-3207(02)00003-0.

Steiner, S. J., Kernek, K. M., & Fitzgerald, J. F. (2006). Severity of basal cell hyperplasia differs in reflux versus eosinophilic esophagitis. Journal of pediatric gastroenterology and nutrition, 42(5), 506–509. https://doi.org/10.1097/01.mpg.0000221906.06899.1b.

Terry, P., Lagergren, J., Ye, W., Nyrén, O., & Wolk, A. (2000). Antioxidants and cancers of the esophagus and gastric cardia. International journal of cancer, 87(5), 750–754.

Vaughan, T. L., Davis, S., Kristal, A., & Thomas, D. B. (1995). Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 4(2), 85–92.

Xie, F-J. et al. (2013). Helicobacter pylori infection and esophageal cancer risk: an updated meta-analysis. World journal of gastroenterology: WJG. 19(36), 6098.

Zhang, Y. (2013). Epidemiology of esophageal cancer. World journal of gastroenterology: WJG. 19(34), 5598.

Published

25/01/2022

How to Cite

MOURA, E. R. .; SOUZA, G. B. V. de .; TRINDADE, Y. T. D. .; SANTANA NETO, D. J. de .; MOREIRA, L. G. .; SILVA, W. S. .; BARRETO, Íkaro D. de C. .; SILVA, D. F. da .; MEURER, L.; TRINDADE, L. M. D. F. . Metaplasia and histopathological lesions of the esophageal mucosa. Research, Society and Development, [S. l.], v. 11, n. 2, p. e29711225778, 2022. DOI: 10.33448/rsd-v11i2.25778. Disponível em: https://www.rsdjournal.org/index.php/rsd/article/view/25778. Acesso em: 13 jul. 2024.

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Section

Health Sciences