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A pepsina e o cancro da laringe
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O cancro da laringe está classicamente associado ao consumo crónico de tabaco e álcool. Mais recentemente veio a incriminar-se também o Refluxo Laringofaríngeo (RLF) como outro fator etio-patogénico deste cancro.
Os três são, porém, frequentemente indissociáveis, uma vez que o doente com cancro da laringe é, muitas vezes, um fumador crónico que consume álcool. Por sua vez, o álcool e o tabaco promovem o refluxo que potencia o efeito nóxio dos outros. Assim o papel do RLF no desenvolvimento do carcinoma laríngeo não é facilmente individualizável do ponto de vista clínico.
Estudos com pH-metria esofágica com duplo sensor mostram que os doentes com RFL têm episódios de refluxo que ascende ao trato aero-digestivo superior e que, ao inverso da clássica doença de refluxo gastroesofágico (DRGE), ocorre em episódios diurnos e na posição vertical.
O principal constituinte nóxio do refluxo é, indiscutivelmente, a pepsina, enzima que evidencia atividade proteolítica máxima no pH entre 2 e 4 intra-gástrico, mas que mantém ainda atividade, embora decrescente, até a um pH de 6, fora do estômago.
Por sua vez, a mucosa laríngea, ao contrário da esofágica, não possui alguns mecanismos essenciais de defesa contra o refluxo. Mesmo a mucosa esofágica parece ter um limite de tolerância ao mesmo, como se observa no Esófago de Barrett, uma lesão pré-maligna.
O presente trabalho pretende efetuar uma revisão bibliográfica dos conhecimentos mais recentes sobre o papel da pepsina gástrica na etio-patogénese do cancro laríngeo.
Laryngeal cancer is classically associated with chronic cigarette smoking and the consumption of alcohol. More recently, the Laryngopharyngeal Reflux (LPR) has also been incriminated as a causative factor. Clinically the three etio-pathogenic factors seem to have a synergistic effect, as laryngeal cancer patients are frequently chronic smokers and heavy drinkers, and both cigarette smoke and alcohol drinking promote reflux, which in turn potentiates the tissue damage caused by the other two. For this reason, the individual role of LPR in laryngeal cancer pathogenesis goes frequently unrecognized in clinical practice. 24-Hour double-probe pH-metry studies have shown that LPR patients have reflux episodes reaching the upper aero-digestive tract, which typically occur during daytime, in the upright position, a fact that makes LPR a clinically distinctive entity from classic gastro-esophageal reflux disease (GERD). Bearing this in mind, it is the pepsin enzyme that is, undoubtedly, the major culprit in the mucosal tissue damage caused by reflux. It has been shown that the potent enzyme pepsin has maximum proteolytic activity at pH between 2 and 4, as in the stomach milieu, but it does not completely lose its activity at higher pH values, still retaining a significant activity at an extra-gastric pH of 6. The laryngeal mucosa, unlike the esophageal mucosa, lacks some essential defense mechanisms against damage caused by reflux. The esophageal mucosa itself does not seem to possess unlimited resistance to the damaging effects of chronic reflux, as we can see in Barrett’s esophagus, a pre-malignant condition.
Laryngeal cancer is classically associated with chronic cigarette smoking and the consumption of alcohol. More recently, the Laryngopharyngeal Reflux (LPR) has also been incriminated as a causative factor. Clinically the three etio-pathogenic factors seem to have a synergistic effect, as laryngeal cancer patients are frequently chronic smokers and heavy drinkers, and both cigarette smoke and alcohol drinking promote reflux, which in turn potentiates the tissue damage caused by the other two. For this reason, the individual role of LPR in laryngeal cancer pathogenesis goes frequently unrecognized in clinical practice. 24-Hour double-probe pH-metry studies have shown that LPR patients have reflux episodes reaching the upper aero-digestive tract, which typically occur during daytime, in the upright position, a fact that makes LPR a clinically distinctive entity from classic gastro-esophageal reflux disease (GERD). Bearing this in mind, it is the pepsin enzyme that is, undoubtedly, the major culprit in the mucosal tissue damage caused by reflux. It has been shown that the potent enzyme pepsin has maximum proteolytic activity at pH between 2 and 4, as in the stomach milieu, but it does not completely lose its activity at higher pH values, still retaining a significant activity at an extra-gastric pH of 6. The laryngeal mucosa, unlike the esophageal mucosa, lacks some essential defense mechanisms against damage caused by reflux. The esophageal mucosa itself does not seem to possess unlimited resistance to the damaging effects of chronic reflux, as we can see in Barrett’s esophagus, a pre-malignant condition.
Descrição
Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2020
Palavras-chave
Cancro da laringe Refluxo laringofaríngeo Pepsina Otorrinolaringologia