Abstract: Eosinophilic esophagitis is characterised for a dense infiltration of the esophagus by eosinophilic leukocytes. The disease's origin is a local reaction to different antigens of which the patient presents previous sensitization, acquired by digestive, inhaled or even epicutaneous exposure. The esophagus contains different cellular types resident in its structure, with capability to participate in the capture, processing and antigens' presentation to T lymphocytes, which could initiate a T helper 2-type immunological response mostly mediated by interleukin-5, with a possible T helper 1-type component. Local production of immunoglobulin E could also participate in the pathophysiology of eosinophilic esophagitis, and for this reason, this disease can be considered a mixed-humoural and cell-mediated immunological disturbance. Studies directed to identificate responsible allergens must consider test for determine immunoglobulin E-mediated reactions as well as cell-mediated hyper-responsiveness responses. Main symptom of eosinophilic esophagitis are dysphagia and esophageal food impactations, which are conditioned by endoscopic alterations and motor disturbances objectively demonstrated by manometric recorders. Eosinophil and mast cell's activation and degranulation against responsible antigens cause damage over esophageal epithelium and dynamic disturbances over neuromuscular components in esophageal wall. Therapies proposed for eosinophilic esophagitis include control of antigen exposition, endoscopic dilation of stenosis and drugs with antieosinophilic effect; in this group topical steroids can be outlined for the capacity of them to restore the histology and the esophageal motility in parallel to vanishment of inflammation.
Abstract: Eosinophilic esophagitis (EE) is an emerging disease caused by dense infiltration of the esophageal epithelium by eosinophilic leucocytes. It is originated from local hypersensitivity to food or airborne allergens. Although the physiopathologic mechanisms of the illness have not been fully discovered, EE is a loss of immunologic tolerance by the esophagus, meaning that it should be considered as an active immunologic organ. In our study, we investigated the immunologic capacity of the epithelium using immunohistochemistry and stereology, to determine the cellular density of eosinophils, T and B lymphocytes, Langerhans cells, mast cells, and cells manufacturing immunoglobulin E in endoscopic biopsies of patients with EE (taken before and after topical treatment with fluticasone propionate) compared with normal individuals and patients suffering from gastroesophageal reflux disease (GERD). We have observed that the density of eosinophils in EE is 300 times greater than in normal conditions and it is only in this disease where eosinophils show signs of activation and degranulation (positivity to major basic protein immunostaining). The number of T intraepithelial lymphocytes also significantly rose in EE, compared with other entities, where CD8 cells were predominant. However, the human esophagus is deficient in B lymphocytes and we only found intraepithelial plasma cells that excreted immunoglobulin E in EE. Under normal conditions mast cells exist in the thickness of the epithelium that are slightly higher in GERD and multiply in density by 17 in EE. Langerhans cells did not show any significant variation in density under the different tested conditions. After topical treatment with steroids, the density of the different cell components fell to similar levels to GERD. Using our study, we can conclude that the human esophagus may contribute to the development of local immunologic responses as it contains all the necessary cell components. EE represents growth of this esophageal capacity and its pathogeny could respond to mixed cellular and humoral mechanisms.
Abstract: OBJECTIVE: To describe the manometric findings detected in adult patients with dysphagia that were diagnosed of eosinophilic oesophagitis, and to compare with the cases of eosinophilic infiltration of the oesophagus reported in the literature. PATIENTS AND METHODS: We present 12 adult patients diagnosed as suffering from this disorder in our department in a 1.5-year period, according to histological criteria and discarding any other cause of eosinophilic infiltration of the oesophagus. Stationary oesophageal manometry using a hydropneumocapillary perfusion system was performed in every case. The recommendations of the Spanish Group of Digestive Motility were followed for the interpretation of the results. In seven patients who presented motor disorder in manometric evaluation, treatment with steroid oesophageal lavage using fluticasone propionate was carried out and these patients were subsequently re-evaluated. RESULTS: All patients were young predominantly men, and the first endoscopic examination showed regular concentric stenosis or a 'ring oesophagus'. Six patients had a severe nonspecific oesophageal motor disorder characterized by up to 80% of nontransmitted or very low-amplitude waves in the lower two-thirds of the organ. Three patients presented a manometric disturbance characterized by hyperkinetic peristaltic waves in distal oesophageal third. One patient had an alteration of the oesophageal motor dynamics characterized by 80% of deglutory complexes formed by a primary simultaneous wave in the two lower oesophageal thirds followed by a secondary peristaltic wave in 50% of cases that had a normal duration and amplitude. The remaining two patients had normal oesophageal motility. The upper oesophageal sphincter showed no alterations, and the manometric evaluation of the lower oesophageal sphincter tone proved normal in 10 patients, with slight hypotension in two cases. In seven of the nine patients who presented an oesophageal motor disorder, treatment with steroid oesophageal lavage using fluticasone propionate was administered and a new oesophageal manometry was performed afterwards, in which the motor disorder was clearly improved as soon as dysphagia, endoscopic lesions and histopathologic alteration disappeared. DISCUSSION: 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.
Abstract: 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.
