In 2013, a 52-year-old female presented to the gastroenterology outpatient clinic with dysphagia for both solids and liquids. She reported since 1998 some severe episodes of dysphagia with an unpleasant feeling of bolus transit stop at the level of the mid esophagus associated to sialorrhoea, spontaneously reverted without the need for a therapeutic endoscopy. Comorbidities included carotid atherosclerosis on ASA, homozygosis for MTHFR gene mutation and atopy with prick test positivity for sensibilization to cat epithelium with oculorhinitis manifestations but not bronchospastic reactions. At the beginning of symptoms, in 1998, upper endoscopy showed regular esophageal canalization, a small hiatal hernia, the absence of esophageal and duodenal mucosa lesions and the presence of a juxtapyloric mucosal erosion. Mucosal biopsies for standard histological evaluation were not collected. It was performed only a rapid test for Helicobacter pylori, which resulted positive and the patient underwent eradication treatment with success. Thereafter, some courses of PPI were prescribed to treat symptom relapse. 
Abdominal and thoracic examination were unremarkable. Routine laboratory tests were normal. Videofluoroscopic swallowing study and esophageal transit evaluation did not reveal the presence of structural or functional alterations: in particular, the transit of liquid, semi-solid and solid boluses were normal. Esophageal manometry detected normal progression of the peristaltic waves, but wave amplitude was much increased (> 300 mmHg) together with a mild hypertensive LES (32 mmHg). 
She underwent upper endoscopy showing normal esophageal, gastric and duodenal mucosa. Gastric and duodenal histology were unremarkable but a significant esophageal infiltrate at distal, medium and proximal esophagus, with eosinophilic counts of 169, 58 and 29 cells per high-power field, respectively, was shown.
A diagnosis of EoE was done and prednisone 25 mg/day (0.5 mg/kg body weight) per 2 weeks followed by a gradual tapering in 6 weeks was prescribed. The patient experienced a complete clinical remission for 2 years. Due to the occurrence of reflux-related symptoms, in particular moderate heartburn and mild regurgitation, two courses of 4-week PPI were prescribed. 
In 2018, she experienced a flare of symptoms. A videofluoroscopic swallowing study and esophageal transit evaluation was repeated. The presence of mildly spiculed esophageal profile was evident (Figure 1(Fig. 1)). Upper endoscopy showed mucosal rings, furrows and exudates along the esophagus (Figure 2(Fig. 2)). Esophageal histology confirmed the presence of a significant intraepithelial eosinophilic infiltrate, with eosinophilic count of 60/HPF. Accordingly, the patient begun a 12-week period of budesonide 9 mg/die associated to pantoprazole 40 mg/die, tapered to budesonide 6 mg/die associated to pantoprazole 40 mg/die for further 12 weeks. The complete recovery of symptoms induced the reduction of budesonide dosage at 3 mg/day for another 12-week period. To minimize side effects, a maintaining treatment with 12-week period of budesonide alternated with 12-week period of PPI was prescribed and still ongoing, with complete absence of dysphagia and resolution of endoscopic esophageal signs.