Inflammatory aetiology of primary oesophageal achalasia: an immunohistochemical and ultrastructural study of Auerbach's plexus

Aim: Achalasia is a disease of the oesophagus characterized by increased lo wer oesophageal sphincter (LOS) tone, absence of LOS relaxation with swallo wing and aperistalsis of the body of the oesophagus. The aetiology and path ogenesis of idiopathic achalasia is still controversial. Methods and results: We examined 16 oesophageal biopsies and one low oesoph agectomy specimen from patients with achalasia. The control group was compo sed of five autopsy cases with no history of oesophageal disorders, three c ases of diffuse oesophageal spasm, one of gastro-oesophageal reflux disease and one patient with oesophageal carcinoma. Sections were immunostained fo r neurofilaments NF70 and NF200, S100 protein and neurone-specific enolase, Biopsies with inflammatory infiltrates, were in addition immunostained wit h antibodies against leucocyte common antigen as well as for CD20, CD43, CD 68 and CD45RO. All biopsies were examined after plastic embedding, and elec tron microscopy (EM) was performed on samples containing autonomic plexus. An inflammatory infiltrate of varying intensity was present along the nerve fascicles and around ganglion cells in 90% of the cases of achalasia, T-ly mphocytes predominated in all these cases. The autonomic nerves showed loss of fibres and degenerative changes which were discernible only by EM. Alth ough there was no convincing neuronal loss or signs of active neuronal dege neration in biopsied cases, the oesophagectomy specimen revealed total abse nce of neurones and significant loss of nerve fibres, The control group sho wed normal plexuses and no inflammation. Conclusion: Degeneration and significant loss of nerve fibres associated wi th predominant T-cell lymphocytic inflammatory infiltrate around the myente ric plexus support the concept for the inflammatory, probably autoimmune, a etiology of autonomic nervous system injury in primary achalasia.