What do we know about the pathogenesis of glandular disease?

There is minimal experimental information regarding the pathogenesis of equine glandular gastric disease (EGGD) [1]. None of the squamous experimental protocols induce EGGD, so it is unlikely that increased acid exposure alone is the cause of EGGD. In man, peptic ulcer disease (PUD) is considered the end result of an imbalance between aggressive gastric luminal factors and defensive mucosal barrier function [2,3]; in horses, it is most likely that weakened mucosal barrier function is the primary cause of EGGD and that acid injury may perpetuate mucosal damage, inhibit epithelial restitution and is required to cause clinical signs ...