In the literature, 61 cases of eosinophilic infiltration of the oesophageal mucosa subjected to oesophageal manometric study had been described, and 60.6% of them showed evidence of different types of manometric alterations, mainly with spastic or hypercontractility characteristics. Although six of our cases showed very deficient peristalsis with very low-amplitude or nontransmitted waves, and in another three high-amplitude peristaltic waves were recorded. Motor disorders improved parallel to the disappearance of the eosinophilic infiltration of the mucosa. These data suggest that motor disorders in eosinophilic oesophagitis are a consequence of eosinophil infiltration of the oesophagus and should be considered in the differential diagnosis of dysphagia. These manometric alterations could be considered as primary nonspecific disorders and included in the 'ineffective oesophageal motility' group.

Eosinophilic esophagitis (EE) is a clinical-pathological disorder which is being increasingly diagnosed. It is etiologically associated with hypersensitivity to airborne allergens and/or dietary components. However, immediate hypersensitivity to foods has rarely been proven as the etiologic cause of the disorder. Two patients are presented with a history of rhinoconjunctivitis, allergic asthma, atopic dermatitis and food allergies which are currently under control and who show specific IgE to pulses and chicken respectively. These patients developed acute dysphagia and vomiting immediately after ingesting these foods and following appropriate examination were diagnosed as suffering from EE. The study also showed signs of blood hypereosinophilia while the esophageal manometry revealed a motor disorder characterized by aperistalsis and non-propulsive simultaneous waves affecting the lower two-thirds of the organ composed of smooth muscle. Topical treatment with fluticasone propionate was administered over a period of 3 months, in addition to a diet abstaining from the aforementioned foods and this led to remission of dysphagia and normalization of the endoscopic, histological and manometric studies of the esophagus. This situation remained stable for a considerable length of time after steroid treatment was discontinued, which showed that exposure to foods seemed to be the cause of the esophageal disorder. Similarly, allergies to inhalants and other digestive symptoms which appear upon immediate ingestion of the foods involved would not justify the sudden onset of dysphagia. We offer a pathophysiological explanation for the mechanisms of the disease based on the activation of eosinophils and mast cells by IgE and their ability to disturb the dynamic behavior of the neural and muscle components of the esophageal wall.

Until there is a better understanding of the etiology of that heterogeneous entity, intermediate surveillance is an adequate strategy.