Acid-induced esophageal shortening in humans: A cause of hiatus hernia?

BACKGROUND: Hiatus hernia and gastroesophageal reflux disease commonly coex ist, and there is pathophysiological evidence that the presence of a hiatus hernia contributes to abnormal acid reflux. However, the cause of hiatus h ernia remains unclear. In an animal model, it has been shown that acute aci d injury to the esophagus results in esophageal shortening, raising the pos sibility that reflux esophagitis per se can contribute to the formation of hiatus hernia by inducing esophageal shortening. AIM: To determine whether luminal acid produces esophageal shortening in hu mans. METHODS: Twelve volunteers were each studied on two occasions, one week apa rt, in a double-blind, crossover trial. The location of the lower esophagea l sphincter (LES), as well as the LES resting pressure and axial length wer e determined at baseline and then again after 20 min of either acid or sali ne perfusion. RESULTS: Acid perfusion did not induce significant changes in resting LES p ressure but resulted in proximal migration of the LES (ie, esophageal short ening) by an average of 0.5 cm, with the largest proximal migration being 1 .8 cm. In contrast, saline perfusion resulted in slight distal migration of the LES (ie, esophageal lengthening). CONCLUSIONS: Intraruminal acid perfusion causes longitudinal axis shortenin g of the esophagus and suggests that gastroesophageal acid reflux may contr ibute to the cause of hiatus hernia.