52-year-old woman with dysphagia.

A 52-year-old woman presented with dysphagia, which started when she was 30 years old. Initially, the dysphagia was intermittent but had progressed to daily occurrences during the past 2 years. She had progessively more difficulty in swallowing solids, but not liquids. The patient described a spasmlike sensation in her chest, which occurred as soon as she started eating; this had become more prominent during the past 6 months. Almost once a week, food would “get stuck” in her esophagus, and she had to regurgitate it to relieve the discomfort. Bread and meat were the usual offenders. The oropharyngeal swallowing mechanism was not compromised. The patient had “heartburn” every week for the past 2 years, which she described as a burning sensation radiating from the lower to the midsternal level; it was relieved with antacids. She denied aspiration, halitosis, neck mass, fevers, night sweats, unexplained weight loss, early satiety, hematemesis, hematochezia, melena, radiation exposure, or caustic injury to her esophagus. Besides the dysphagia, the patient had experienced progressive dyspnea for 4 years, which had been attributed to asthma. The dyspnea was episodic and mostly exertional, but occasionally occurred at rest. There was no clear relationship to environmental allergen exposure. She denied seasonal or food allergies, hay fever, eczema, or dermatitis. The patient had a history of irregular heartbeats associated with benign premature ventricular contractions, but she denied exertional chest pain, diaphoresis, light-headedness, or syncope. Chronic medical issues included megaloblastic anemia due to vitamin B12 deficiency, obesity, hyperlipidemia, migraines, and depression. Surgical history was notable for tonsillectomy, appendectomy, and hysterectomy. She had had a 30-pack-year smoking history but had abstained for the past 8 years and had stopped drinking alcohol 20 years ago. Scheduled medications were nadolol, lovastatin, fluoxetine, and vitamin B12. Medications taken on an as-needed basis were butalbitalaspirin-caffeine, sumatriptan, and carisoprodol. On physical examination, the patient was obese (body mass index, 31.2 kg/m2 [calculated as weight in kilograms divided by height in meters squared]). Vital signs were as follows: blood pressure, 105/67 mm Hg; heart rate, 63 beats/min; and respiratory rate, 18 breaths/min. Findings on cardiac, pulmonary, abdominal, and neurologic examinations were unremarkable. On the patient health questionnaire, she scored a 7 on a maximum of 27 points, suggesting mild depression. Which one of the following is the best initial test to evaluate this patient's dysphagia? Ambulatory pH monitoring Breath test for Helicobacter pylori Esophagogastroduodenoscopy (EGD) Barium swallow study Video swallow study Ambulatory pH monitoring is not helpful in evaluating solid-food dysphagia. It can confirm gastroesophageal reflux disease (GERD) and monitor adequacy of treatment in patients with persistent symptoms despite treatment with acid-suppressing medications. H pylori infection causes heartburn and peptic ulcer disease but does not explain the dysphagia. Esophagogastroduodenoscopy is useful for evaluating dysphagia and is the test of choice in this case because it visualizes the esophageal mucosa, allows evaluation of structural and anatomic defects, and obtains biopsy specimens if clinically indicated. However, subtle lesions such as a small ring or diverticulum may be missed. A barium swallow study might be useful to evaluate oropharyngeal dysphagia, esophageal dysmotility, and structural abnormalities that cause progressive solid-food and liquiddysphagia. A video swallow study allows visualization of the swallowing mechanism, making it useful for evaluation of oropharyngeal dysphagia. On EGD, mucosal changes were consistent with a ringed appearance and longitudinal furrowing. No hiatal hernia or reflux injury was evident at the gastroesophageal junction. The stomach, duodenal bulb, and postbulbar duodenum were normal. On the basis of the symptoms and endoscopic findings, which one of the following is the most likely diagnosis? Pill-induced esophageal injury Esophageal carcinoma Eosinophilic esophagitis (EE) Barrett esophagitis Achalasia The characteristic endoscopic appearance of pill-induced esophageal injury is 1 or more discrete ulcers that range from 1 mm to several centimeters, with a relatively normal surrounding mucosa.1 No ulcers were seen on endoscopy in our patient. There were no infiltrating, ulcerating, excavating, or fungating lesions suggestive of a malignancy. Our patient had longitudinal furrowing with a ringed appearance of the esophagus, which is suggestive of EE. Other endoscopic findings of EE include a diminished vascular pattern with mucosal shearing. The mucosa can be thickened yet friable with exudates, described as crepe paper mucosa, and associated with specks, mucosal nodules, and granularity. In severe cases, mucosal rings and esophageal strictures can be present.2,3 In patients with EE, the esophagus can appear to be completely normal on endoscopy.2,3 None of these features are pathognomonic of EE; however, in the appropriate clinical context, the presence of more than 1 of these endoscopic findings is strongly suggestive of EE. The gastroesohageal junction was normal with no signs of ulceration or irregular mucosal margins suggestive of columnar lined esophagus4; thus, Barrett esophagitis is a less likely diagnosis. Endoscopic findings in patients with achalasia include a dilated esophagus that often contains residual food material. During EGD, a diagnosis of EE was entertained. Which one of the following would be the most helpful in diagnosing EE in our patient? Multiple esophageal biopsies White blood cell count with differential Serum IgE level Allergy testing Patient history and EGD appearance are adequate Performing esophageal biopsy is the next step. The sensitivity of finding eosinophilic infiltration can be substantially increased by obtaining several biopsy specimens (at least 6) from the upper two-thirds of the esophagus and fixing the specimens in formalin or paraformaldehyde instead of Bouin fixative.5,6 Peripheral eosinophilia and elevated serum IgE levels are not helpful in the diagnosis of EE because they are insensitive and nonspecific.7 Although EE can be associated with atopic allergies, rhinitis, and asthma, formal allergy testing is not needed to establish the diagnosis. Patient history and EGD appearance are suggestive of but not enough to establish a diagnosis of EE. Multiple biopsy specimens obtained from the upper two-thirds of the esophagus demonstrated hyperplastic squamous esophageal mucosa with greater than 35 intraepithelial eosinophils per high-power field (HPF). Which of one the following is the next best step in management of this patient? Proton pump inhibitor (PPI) Swallowed aerosolized fluticasone Esophageal dilation Oral prednisone Anti-interleukin (IL) 5 antibody treatment Treatment with a PPI is the next step because some patients have clinical and histologic resolution with PPI therapy alone.8 This suggests that GERD may be the underlying cause or exacerbating factor of EE.9,10 GERD may mimic, cause, coexist with, or be exacerbated by EE.11-13 High-dose swallowed aerosolized fluticasone is usually the first line of treatment of EE after a trial of PPI to exclude GERD. Esophageal dilation would not be recommended at this time because it is reserved for patients in whom swallowed fluticasone fails and who have persistent dysphagia that leads to weight loss or who present with food impaction. Oral prednisone is not recommended for mild disease but should be considered in patients with severe refractory disease unresponsive to esophageal dilation. Animal studies have demonstrated the role of IL-5 in the pathogenesis of EE; however, currently, clinical evidence is insufficient to recommend therapy with the humanized monoclonal antibody mepolizumab.14,15 We provided our patient with education on reflux disease. She had not been treated previously with a PPI. Therapy with omeprazole, twice-daily before meals, was initiated; the heartburn resolved completely, and the dysphagia improved substantially. In a 4-week period, the patient had just two 30-second episodes of “meat sticking.” She was able to eat an unlimited diet. Which one of the following is true regarding the natural disease course of and risks associated with EE? Increased risk of esophageal carcinoma Increased risk of eosinophilic gastritis Increased risk of ulcerative colitis Increased risk of recurrent dysphagia Increased risk of esophageal Crohn disease Data on the natural history of EE are scarce. It is not known to be associated with development of esophageal carcinoma, eosinophilic gastritis, ulcerative colitis, or Crohn disease. However, patients with EE are known to have recurrent episodes after treatment and can present with dysphagia, food impaction, or even esophageal strictures that require endoscopic treatment and esophageal dilation.7 At 8 weeks after initiation of oral PPI therapy, our patient reported no solid-food dysphagia and was eating an unlimited diet. We suspect that she has EE with GERD. Because her symptoms completely resolved with PPI therapy, EGD was not repeated and specific therapy for EE was not instituted.