Background and Aims

Background: Idiopathic achalasia is an esophageal motor disorder, characterized by loss of enteric neurons leading to absence of peristalsis and impaired relaxation of the lower esophageal sphincter (LES). The physiopathology of achalasia is still unknown, although an autoimmune etiology is suspected.
Aim: We aim to determine whether autoantibodies against the autonomic nervous system receptors can explain the enigmatic pathogenesis of achalasia.

Methods

An observational cross-sectional study using an ELISA method designed to identify the level of: 1) Circulating autoantibodies against G protein-coupled receptors of the autonomic nervous system (adrenergic, muscarinic, endothelin and angiotensin receptors). 2) Coexistence autoantibodies including: anti-nuclear antibody (ANA), anti-Ro, anti-La, antibodies to insulin, islet cell autoantibodies (ICA), anti-glutamic acid decarboxylase (anti-GAD), anti-thyroid peroxidase antibody (anti-TPO), anti-thyroid stimulating immunoglobulin (TSI) antibody, anti-gastric parietal cell antibody (GPC), anti-smooth muscle antibody (ASMA), and anti-mitochondrial (AMA). Peripheral blood will be obtained from forty achalasia patients diagnosed by an expert gastroenterologist based on esophageal manometry and upper endoscopy findings. The medical records of each patient will be reviewed. Peripheral blood will also be obtained from forty matched healthy donors (HD) with no diagnosis of achalasia. We will interview HDs in order to discard any history of an autoimmune disease, as well as any symptom suggestive for upper motility disorder.

Results

Pending.

Conclusions

Pending.