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Abstract(s)
A primeira referência à entidade que hoje conhecemos por Esófago de Barrett
remonta a 1906 1, quando Tileston descreveu uma “úlcera do esófago distal, sobrejacente ao
cárdia, com aspectos macro e microscópicos sobreponíveis aos da úlcera gástrica”. Porém, a
metaplasia colunar do esófago, também conhecida como metaplasia ou Esófago de Barrett
(EB), ainda hoje é motivo de controvérsia, estando o seu estudo longe de ser um capítulo
encerrado.
É conhecida a relação estreita entre o EB e o refluxo gastroesofágico prolongado 2,3 e
um dos motores impulsionadores da investigação nesta área é o facto de se tratar de uma
condição pré-maligna, associada à biopatogenia do adenocarcinoma (ADC) do esófago. 3,4 Esta
é a neoplasia cuja incidência, apesar de baixa, mais cresceu nas últimas décadas, no mundo
ocidental 5, tendo um prognóstico sombrio, com uma sobrevivência aos 5 anos inferior a 20%.
6 A sequência metaplasia displasia carcinoma, descrita por Haggitt em 1978 4, traduz a
evolução do EB para ADC do esófago. Porém, nem todos os casos de metaplasia colunar do
esófago evoluem para ADC e, neste ponto, tornou-se evidente que o fenótipo intestinal é o
indicador major de risco de transformação maligna. 7-9 Para além deste tipo epitelial,
caracterizado pela presença de células caliciformes, foram identificados nos segmentos
metaplásicos outros 2 epitélios habitualmente presentes no estômago: o juncional 10 ou
cárdico 11 e o fúndico-atrófico 10 ou oxíntico-cárdico 11. Segundo Chandrasoma 11, a
substituição metaplásica do epitélio pavimentoso normal do esófago progride de acordo com a
sequência: mucosa de tipo cárdico oxíntico-cárdico intestinal. 12
Tendo em conta esta evolução temporal, e conhecendo a instabilidade do EB, seria de
considerar a hipótese de a metaplasia intestinal (MI) aumentar com o tempo de doença. Neste
contexto, no decorrer da elaboração da monografia surgiu a necessidade de explorar um
pouco mais o comportamento da relação dos dois tipos epiteliais metaplásicos (intestinal e
não intestinal), tendo em conta a duração do refluxo, pelo que desenvolvi um estudo
retrospectivo longitudinal observacional com uma amostra de doentes com Esófago de Barrett
seguidos no Instituto Português de Oncologia de Lisboa, procurando avaliar a percentagem de
metaplasia intestinal em 3 momentos distintos da evolução de cada doente, sua correlação
com a duração dos sintomas de refluxo e extensão dos segmentos metaplásicos. Não foi
testemunhada a progressão da MI, mas também não se verificou uma diminuição da mesma, o
que corrobora a estabilidade deste fenótipo.
The first reference of what we know today as Barrett’s Esophagus dates from 1906, when Tileston describes an "ulcer of the distal esophagus, overlying the cardia, with macro and microscopic aspects similar to those of gastric ulcer." However, the esophagus’ columnar metaplasia, also known as Barrett’s metaplasia or Barrett's esophagus (BE), is still matter of controversy, and its study is far from being a closed chapter. There is a known close relationship between EB and prolonged gastroesophageal reflux2,3, and one of the central drivers of research in this area is that it is a premalignant condition associated with esophagus’ adenocarcinoma (ADC). 3,4 This is a cancer whose incidence, although low, most increase, in the western word, over the past decades 5 ; it has a poor prognosis, with a 5 years’ survival less than 20%. 6 The sequence metaplasia → dysplasia → carcinoma, described by Haggitt in 1978 4 , reflects the evolution of the BE to esophagus’ ADC. However, not all cases of esophagus’ columnar metaplasia evolve to ADC, and, at this point, it became apparent that the intestinal phenotype is the major risk for malignant transformation. 7-9 Apart from this epithelial type, characterized by the presence of goblet cells, there were identified two other metaplastic segments usually present in the stomach: junctional 10 or cardiac 11 and gastric atrophic fundic 10 or oxyntocardiac 11. According Chandrasoma11, replacing normal squamous epithelial metaplasia of the esophagus progresses through the sequence: cardiac type mucosa → oxyntocardiac type → intestinal metaplasia. Given this evolution, and knowing the instability of the BE, it would be to consider the hypothesis that intestinal metaplasia (IM) increase with duration of disease. In this context, during the preparation of the monograph, came the need to explore the behavior of the two metaplastic epithelial types (intestinal and non-intestinal), taking into account the duration of reflux, so, I developed a retrospective longitudinal observational study with Barrett's esophagus patients followed in the Portuguese Oncology Institute of Lisbon, attempting to assess the percentage of intestinal metaplasia in three distinct moments of each patient, the correlation with the duration of reflux symptoms and extent of the metaplastic segment. It was neither observed the progression of IM, nor a decrease of it, which confirms the stability of this phenotype.
The first reference of what we know today as Barrett’s Esophagus dates from 1906, when Tileston describes an "ulcer of the distal esophagus, overlying the cardia, with macro and microscopic aspects similar to those of gastric ulcer." However, the esophagus’ columnar metaplasia, also known as Barrett’s metaplasia or Barrett's esophagus (BE), is still matter of controversy, and its study is far from being a closed chapter. There is a known close relationship between EB and prolonged gastroesophageal reflux2,3, and one of the central drivers of research in this area is that it is a premalignant condition associated with esophagus’ adenocarcinoma (ADC). 3,4 This is a cancer whose incidence, although low, most increase, in the western word, over the past decades 5 ; it has a poor prognosis, with a 5 years’ survival less than 20%. 6 The sequence metaplasia → dysplasia → carcinoma, described by Haggitt in 1978 4 , reflects the evolution of the BE to esophagus’ ADC. However, not all cases of esophagus’ columnar metaplasia evolve to ADC, and, at this point, it became apparent that the intestinal phenotype is the major risk for malignant transformation. 7-9 Apart from this epithelial type, characterized by the presence of goblet cells, there were identified two other metaplastic segments usually present in the stomach: junctional 10 or cardiac 11 and gastric atrophic fundic 10 or oxyntocardiac 11. According Chandrasoma11, replacing normal squamous epithelial metaplasia of the esophagus progresses through the sequence: cardiac type mucosa → oxyntocardiac type → intestinal metaplasia. Given this evolution, and knowing the instability of the BE, it would be to consider the hypothesis that intestinal metaplasia (IM) increase with duration of disease. In this context, during the preparation of the monograph, came the need to explore the behavior of the two metaplastic epithelial types (intestinal and non-intestinal), taking into account the duration of reflux, so, I developed a retrospective longitudinal observational study with Barrett's esophagus patients followed in the Portuguese Oncology Institute of Lisbon, attempting to assess the percentage of intestinal metaplasia in three distinct moments of each patient, the correlation with the duration of reflux symptoms and extent of the metaplastic segment. It was neither observed the progression of IM, nor a decrease of it, which confirms the stability of this phenotype.
Description
Keywords
Metaplasia colunar do esófago Metaplasia colunar do esófago - Factores de risco Esófago de Barrett Metaplasia intestinal Adenocarcinoma do esófago
Citation
Publisher
Universidade da Beira Interior