[Comparison between idiopathic achalasia and achalasia caused by Chagas' disease: a review on the publications about the subject].
BACKGROUND
Although idiopathic achalasia and achalasia caused by Chagas' disease have the same clinical manifestations and treatment, both with destruction of the esophageal myenteric plexus, it is possible that there are differences in the alterations of esophageal motility between the two diseases, caused by different grades of impairment of the excitatory and inhibitory esophageal neurons.


OBJECTIVE
We performed a review of papers with results about the pathophysiology and esophageal motility alterations in idiopathic achalasia and Chagas' disease.


METHODS
We reviewed papers which included data about the characteristics of idiopathic achalasia and Chagas' disease.


RESULTS
Impairment of inhibitory esophageal neurons was shown in the two diseases. The results of the studies of the effects of atropine, edrophonium and botulin toxin suggested that the excitatory innervation is more intensely impaired in Chagas' disease than in idiopathic achalasia, explaining the increase in the lower esophageal sphincter pressure found in achalasia. The patients with Chagas' disease have more circulating muscarinic cholinergic receptor M2 autoantibodies than patient with idiopathic achalasia. The duration of the contractions in the esophageal body is longer in idiophatic achalasia than in Chagas' disease.


CONCLUSIONS
The papers that studied Chagas' disease and idiopathic achalasia, mainly those which studied both diseases with the same methods, suggested that there are different grades of esophageal involvement by the two diseases, mainly the most important involvement of excitatory innervation in Chagas' disease than in idiopathic achalasia.
Dantas
Roberto Oliveira
RO
Departamento de Clínica Médica, Faculdade de Medicina, Universidade de São Paulo, Ribeirão Preto, SP, Brasil. rodantas@fmrp.usp.br
D014355:Chagas Disease / Q000150:complications / Q000503:physiopathology*; D004931:Esophageal Achalasia / Q000209:etiology / Q000503:physiopathology*; D004947:Esophagus / Q000503:physiopathology*; D006801:Humans