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Apport de la biologie moléculaire dans la prise en charge du reflux pharyngo-laryngé: état de l’art

The contribution of molecular biology in the treatment of laryngopharyngeal reflux: a state of art

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Acta Endoscopica

Résumé

Le reflux pharyngo-laryngé (RPL) est actuellement largement mis en cause dans les pathologies laryngées. Le diagnostic et le traitement, calqués sur les méthodes appliquées au reflux gastro-œsophagien, rencontrent de nombreux échecs. Depuis peu, plusieurs auteurs tentent de mettre en évidence les mécanismes d’action propres du RPL au niveau moléculaire. Des pompes H+/K+ ATPase ont été mises en évidence au niveau des glandes sous-muqueuses du larynx humain. D’autre part, l’absence d’anhydrase carbonique au niveau de l’épithélium des cordes vocales chez les patients présentant un RPL pourrait rendre compte de la localisation préférentiellement glottique des atteintes laryngées. Enfin, la présence de pepsine active et d’acides biliaires dans l’épithélium laryngé semble jouer un rôle prépondérant dans la physiopathologie du RPL.

Summary

Today, laryngopharyngeal reflux (LPR) is widely considered as a major cause of laryngeal diseases. Diagnosis and treatment based on the methods used for gastroesophageal reflux disease (GERD) frequently prove to be inefficient. Recently, some authors have been focusing on the specific molecular etiopathology of LPR. They have discovered the presence of H+/K+ ATPase pumps around the submucosa glands of the human larynx. Besides, the lack of carbonic anhydrase in the epithelium of vocal folds in cases of LPR supports the hypothesis according to which reflux-related damages mainly affect the glottic area. Finally, active pepsin and bile acids appear to be strongly involved in inflammation and tumorigenesis related to LPR.

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Desgain, O., Lawson, G., Lévêque, N. et al. Apport de la biologie moléculaire dans la prise en charge du reflux pharyngo-laryngé: état de l’art. Acta Endosc 38, 291–294 (2008). https://doi.org/10.1007/BF02961989

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  • DOI: https://doi.org/10.1007/BF02961989

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