摘要
Esophageal atresia(EA)is defined as a discontinuity of the lumen of the esophagus repaired soon after birth.Dysphagia is a common symptom in these patients,usually related to stricture,dysmotility or peptic esophagitis.We present 4 cases of patients with EA who complained of dysphagia and the diagnosis of Eosinophilic esophagitis(Eo E)was made,ages ranging from9 to 16 years.Although our patients were on acid suppression years after their EA repair,they presented with acute worsening of dysphagia.Esophogastroduodenoscopy and/or barium swallow did not show stricture and biopsies revealed elevated eosinophil counts consistent with Eo E.Two of 4 patients improved symptomatically with the topical steroids.It is important to note that all our patients have asthma and 3 out of 4 have tested positive for food allergies.One of our patients developed recurrent anastomotic strictures that improved with the treatment of the Eo E.A previous case report linked the recurrence of esophageal strictures in patients with EA repair with Eo E.Once the Eo E was treated the strictures resolved.On the other hand,based on our observation,Eo E could be present in patients without recurrent anastomotic strictures.There appears to be a spectrum in the disease process.We are suggesting that Eo E is a frequent concomitant problem in patients with history of congenital esophageal deformities,and for this reason any of these patients with refractory reflux symptoms or dysphagia(with or without anastomotic stricture)may benefit from an endoscopic evaluation with biopsies to rule out Eo E.
Esophageal atresia (EA) is defined as a discontinuity of the lumen of the esophagus repaired soon after birth. Dysphagia is a common symptom in these patients, usually related to stricture, dysmotility or peptic esophagitis. We present 4 cases of patients with EA who complained of dysphagia and the diagnosis of Eosinophilic esophagitis (EoE) was made, ages ranging from 9 to 16 years. Although our patients were on acid suppression years after their EA repair, they presented with acute worsening of dysphagia. Esophogastroduodenoscopy and/or barium swallow did not show stricture and biopsies revealed elevated eosinophil counts consistent with EoE. Two of 4 patients improved symptomatically with the topical steroids. It is important to note that all our patients have asthma and 3 out of 4 have tested positive for food allergies. One of our patients developed recurrent anastomotic strictures that improved with the treatment of the EoE. A previous case report linked the recurrence of esophageal strictures in patients with EA repair with EoE. Once the EoE was treated the strictures resolved. On the other hand, based on our observation, EoE could be present in patients without recurrent anastomotic strictures. There appears to be a spectrum in the disease process. We are suggesting that EoE is a frequent concomitant problem in patients with history of congenital esophageal deformities, and for this reason any of these patients with refractory reflux symptoms or dysphagia (with or without anastomotic stricture) may benefit from an endoscopic evaluation with biopsies to rule out EoE.
