Treatment of Eosinophilic Esophagitis with Inhaled Corticosteroids

Abstract

Eosinophilic esophagitis (EE) is a newly described inflammatory lesion characterized by dense eosinophilic infiltration of the esophagus that occurs in the absence of gastroesophageal reflux (GER), parasitic infection, or other known causes of eosinophilic inflammation (1,2). Clinically, patients have symptoms of dysphagia (most commonly), odynophagia, or chest pain (1,2). Whether EE is a distinct clinical entity or an unusual variant of eosinophilic gastroenteritis is unclear. Although a brisk response to systemic corticosteroid therapy is described (3), multiple courses are often required, with the potential for attendant side-effects. Because steroid inhalers, when used without a spacer (a chamber which, when attached to the inhaler, allows improved delivery of the product to the lungs), deposit a significant portion of the delivered dose to the esophagus (4), we theorized that these devices might provide a route for topical treatment of EE. We report the response of four children with EE treated topically with steroid inhalers. CASE REPORTS Patient 1 A 13-year-old boy with a 5-year history of dysphagia sought treatment. One month before, he had experienced a meat impaction requiring endoscopic removal. At the time of endoscopy, the esophagus was noted to be normal in appearance. No biopsies were performed. A subsequent barium esophagram was normal. He had no history of asthma or allergies (specifically, no food allergies). He was referred to Mayo Clinic for a second evaluation. Results of pertinent laboratory studies showed normal hemoglobin levels and no peripheral eosinophilia. A second endoscopic procedure was performed, and biopsies were performed in the proximal and distal esophagus, antrum, and duodenum. Histologic examination of the esophagus showed dense eosinophilic infiltration (>100 eosinophils per high-power field), consistent with EE. Histologic examination of biopsy specimens obtained from the duodenum and antrum produced normal findings. He was treated with fluticasone (220 µg/puff; four puffs, two times daily for 6 weeks). He was instructed to use the inhaler without a spacer, to swallow after inhalation, and to rinse out his mouth after administration. He experienced a rapid clinical response (within 1 week) with no apparent recurrence 3 months after treatment. Patient 2 A 12-year-old boy came to Mayo Clinic with an 18-month history of chest pain. He had undergone a previous esophagogastroduodenoscopy, which reportedly showed changes consistent with esophagitis, and he had been treated with metoclopramide and ranitidine without improvement. He had a history of asthma and a family history of seasonal allergies. He had no history of food allergies. Results of esophageal manometry and a 24-hour pH probe study were normal. Analysis of peripheral blood smears produced normal findings and no evidence of eosinophilia or anemia. After a month-long course of omeprazole, the patient underwent a second endoscopic examination that showed no mucosal lesions. Histologic specimens obtained from the proximal and distal esophagus showed a dense eosinophilic infiltrate (>50 eosinophils per high-power field) consistent with EE. Findings in analyses of biopsy specimens obtained in the antrum and duodenum were normal. This patient received beclomethasone (42 µg/puff; four puffs, twice daily), and similarly to patient 1, he was instructed on the use of the inhaler without a spacer. Rapid clinical response was observed within 1 week of initiation of therapy. He has used the inhaler three times since the initial diagnosis, but he uses the medication for only 1 week at a time. He has had no symptoms and required no medication for the last 1.5 years. Patient 3 A 13-year-old boy came to the clinic with a 2-year history of dysphagia. He had a history of hypertrophic obstructive cardiomyopathy. He had no history of asthma or allergies (including food allergies) and had a normal complete blood cell count (no anemia or peripheral eosinophilia). Results of a barium esophagram were normal and specifically showed no extrinsic compression. Endoscopic examination showed no mucosal lesions, and the histologic evaluation was consistent with EE. He underwent a 3-month course of oral prednisone and had a prompt symptomatic response. Ten months later, he experienced a meat impaction and again underwent emergency endoscopy. Analysis of biopsy specimens of otherwise normal-appearing mucosa showed recurrence of the dense eosinophilic infiltrate (>100 eosinophils per high-power field) in the proximal and distal esophagus (Fig. 1). Analyses of specimens from the antrum and duodenum produced normal findings.FIG. 1: Dense eosinophilic infiltrate (>100 eosinophils per high-power field) in the proximal and distal esophagus(original magnification 40×).Similar to patient 1, he used fluticasone (220 µg/puff; four puffs, two times daily for 6 weeks). He also experienced a rapid clinical response within 1 week, but approximately 3 months af