Eosinophilic esophagitis (EoE) is a chronic, immune-mediated, inflammatory disease that is characterized by eosinophilic infiltration of the esophageal mucosa, resulting in esophageal dysfunction (Table 1).1 The presentation of eosinophils in EoE is frequently accompanied by T-cells, B cells, and mast cells.1 Food and environmental antigens are believed to be the primary provocateurs that cause the inflammatory response and remodeling in patients with EoE.1,2 The exact mechanism behind EoE is still unspecified, but current research supports an immune response mediated by type 2 helper T cells.3
TABLE 1. Diagnostic criteria for eosinophilic esophagitis
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| Presence of esophageal dysfunction |
| Presence of 15 or more eosinophils/HPF from esophageal biopsy |
| Exclusion of GERD |
EoE is a recently recognized disease that was first described as a distinct clinical entity in 1993, with an International Classification of Diseases, Ninth Revision (ICD-9) code not established until 2008.3,4 Since first being described in a 51-year-old patient in 1977, the incidence and prevalence of EoE has increased markedly.3 The prevalence of EoE in Switzerland increased 10-fold between 1989 and 2003.3 The prevalence of EoE in Western countries is estimated to be 43 to 55 per 100,000 inhabitants.1 There is sufficient evidence to suggest that EoE is more common in young adult males; thus age is a predictive factor for EoE in patients who present with dysphagia.1 The Mayo Clinic, in Rochester, Minnesota, found that in outpatients with dysphagia who underwent endoscopy, age younger than 47 years was an independent predictive factor of EoE (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.90-0.98; P =.01).1 In Switzerland, the incidence of EoE in women was demonstrated to be lower in comparison with their male counterparts (relative risk [RR], 0.585; 95% CI, 0.331-1.034; P =.065).1 Furthermore, current epidemiologic studies suggest that EoE may be as common as inflammatory bowel disease.3 With the incidence of EoE increasing, researchers are striving to understand the mechanism behind the increasing prominence of the disease. Some suggest that the increase is directly related to greater recognition of EoE.3 Others have proposed that environmental factors likely play a role in the evolving epidemiology of EoE.5
Patient presentation and history
The EoE patient population is dominated by white males in young adulthood who have a past or current medical history of allergies or atopic conditions such as asthma, hay fever, eczema.2 Along with antigenic exposure, esophageal reflux may play a secondary role in EoE, as some patients have had symptomatic and histologic remission of EoE after proton-pump inhibitor (PPI) therapy.3
The vast majority of patients with EoE present with dysphagia, but a myriad of chief complaints have been associated with EOE. The most common symptoms include food impaction, heartburn, chest pain, vomiting, and abdominal pain.3 Frequently, patients will report alterations to their chewing and eating habits as a result of EoE (ie, eating slowly, extending their neck, and consuming food with substantial amounts of liquid).1 In the pediatric population younger than 2 years of age, feeding disorders and failure to thrive are common presenting symptoms of EoE.1 In children up to 12 years of age, vomiting, nausea, water brash, and heartburn are the most frequent symptoms of EoE.1
Laboratory workup and diagnosis
For clinicians to diagnose EoE, patients must undergo an esophageal endoscopy with biopsy (Figure 1).3 Visual inspection via endoscopy can reveal signs of active inflammation, exudates, furrows, strictures, and tissue-paper mucosa (fragile mucosa).1 Histologic analysis of EoE esophageal biopsies will show 15 or more eosinophils per high-power field (HPF).3 Two to four biopsies should be obtained from both the proximal and distal esophagus.6 In contrast to an EoE esophagus, a typical esophagus has very little to no eosinophil presence, while esophageal biopsies of patients with gastroesophageal reflux disease (GERD) generally have eosinophil counts of 10 or fewer eosinophils per HPF.3 EoE specimens are histologically associated with eosinophilic microabscesses, superficial layering of eosinophils, extracellular eosinophil granules, basal cell hyperplasia, enlarged intercellular spaces, and lamina propria fibrosis.1 Along with endoscopy, barium swallow studies in patients with EoE can reveal small-caliber esophagus, strictures, and concentric rings.2 Allergy testing and evaluation are recommended for all patients presumed to have EoE as a result of the high rate of comorbid atopic conditions such as asthma, eczema, rhinitis, and food and environmental allergies.1 It is recommended that patients undergo both skin-prick testing (SPT) and immunoglobulin E (IgE) serum studies.1 Lastly, pH-monitoring is a useful tool to rule out GERD in patients presenting with esophageal eosinophilia.1
FIGURE 1. Impressions: There was suggestion of feline esophagus and a possible widely patent distal esophgeal ring. Four biopsies taken. Dilatation was performed; normal stomach; normal duodenum.
The typical presentation of EoE on endoscopy shows white exudate that vary in shape and pattern; they can be easily mistaken for candida esophagitis.7 These white lesions are actually very dense populations of eosinophils.7 Esophageal strictures, folds, and furrows are common pathologic findings of EoE.7 Esophageal rings, also known as feline esophagus, are seen in both GERD and EoE, and therefore the importance of biopsy and histological analysis cannot be overemphasized.7 According to Mulder et al, four endoscopic findings are distinctly different between patients with EoE and age-matched patients with GERD. Linear furrows, trachealization, and white papules were significantly associated with EoE while normal endoscopic appearance was found more often in patients with GERD.8
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