Q:

12/8/2013
I read numerous articles on eosinophilic esophagitis after a patient had food bolus impaction requiring 1.5 hours of general anesthesia after 1.5 hours of attempted EGD with conscious sedation to remove it (gastroenterologist said it was the most difficult food bolus he has ever removed). Based on the location of the food bolus (upper mid esophagus), the age 42, history of environmental allergies, and previous episodes of dysphagia the gastroenterologist was suspicious of eosinophilic esophagitis. He went back to the doctor one week after the food bolus was removed for a repeat EGD and biopsies. At the time of the EGD, healing ulcers (present as a result of the food bolus impaction) were present. The biopsy confirmed the presence of a high number of eosinophils. He was treated with 6 weeks of fluticasone. Despite this he had several episodes of dysphagia. He was placed on omeprazole 20mg BID (during this period he did not have any episodes of dysphagia). Repeat EGD did not show eosinophils. My question is could the first biopsy where the eosinophils were present be a false positive on account of the healing ulcer? He does not have heartburn. We've elected not to do any further testing for the time being since he is doing fine and will remain on omeprazole 20mg daily for the next year.

A:

Thank you for your inquiry.

I can well understand why a diagnosis of possible eosinophilic esophagitis was made on the basis of the history. And the findings of eosinophils of course were consistent with such a diagnosis. However, as you can see from the abstracts copied below, the finding of eosinophils is certainly not specific for eosinophilic esophagitis, and the subsequent course, casts some doubt on that condition. I wish I could clarify this issue for you further, but unfortunately the information, in my opinion, does not allow us to make a definitive diagnosis. But since eosinophilic esophagitis, to the best of our knowledge, does not remit, and since the diagnosis is by definition is made by biopsy, the absence of eosinophils on your last biopsy suggests he did not have the condition. Thus, in my opinion, the best one can say is the the diagnosis remains unclear, but does not appear to be eosinophilic esophagitis.

Thank you again for your inquiry.

J Gastrointest Surg. 2003 Nov;7(7):836-42.
Etiology, treatment, and outcome of esophageal ulcers: a 10-year experience in an urban emergency hospital.
Higuchi D, Sugawa C, Shah SH, Tokioka S, Lucas CE.
Source
Department of Surgery, Wayne State University School of Medicine, Detroit, Michigan, USA.
Abstract
Esophageal ulcers are a rare cause of upper gastrointestinal bleeding. This report describes the etiology, treatment, complications, and outcome of esophageal ulcers. An esophageal ulcer is defined as a discrete break in the esophageal mucosa with a clearly circumscribed margin; esophageal ulcers were seen in 88 patients from a total of 7,564 esophagogastroduodenoscopies done by one surgeon at an urban hospital from 1991 to 2001. All hospital reports were reviewed. The etiology of esophageal ulcers included the following: gastrointestinal reflux disease (GERD) (n=58, 65.9%), drug induced (n=20, 22.7%), candidal (n=3, 3.4%), caustic injury (n=2, 2.3%), and herpes simplex virus (HSV), human immunodeficiency virus (HIV), marginal ulcer, foreign body, and unknown etiology (n=1 of each, 1.1%). The mean size of GERD-induced esophageal ulcers and drug-induced esophageal ulcers was 2.78 and 2.92 cm, respectively; 80.3% of GERD-induced esophageal ulcers and 13.8% of drug-induced esophageal ulcers were located in the lower thoracic esophagus. Morbidity (n=44, 50%) included hemorrhage (n=30, 34%), esophageal stricture (n=11, 12.5%), and esophageal perforation (n=3, 3.4%). Nonoperative therapy sufficed in 81 patients (92%). Three patients (3.4%) had a recurrence of esophageal ulcers. Fifteen patients (17.0%) required endoscopic intervention including esophageal dilatation for stricture in 11 patients and endoscopic hemostasis for esophageal bleeding in four patients. Surgery (n=7, 8.0%) was reserved for esophageal stricture and perforation. Two patients (2.3%) died from complications of esophageal ulcers: hemorrhage in one and perforation in one. Three patients died of their primary disease. GERD and drug ingestion are common causes of esophageal ulcers. Midesophageal ulcers have a greater tendency to hemorrhage compared with ulcers at the gastroesophageal junction; this may reflect the etiology. Strictures complicate GERD-induced esophageal ulcers but not drug-induced esophageal ulcers. Esophageal dilatation is an effective treatment for most strictures associated with esophageal ulcers. Esophageal ulcers rarely cause death.

Arch Pathol Lab Med. 2009;133:1087–1095
Update on Esophagitis: Controversial and Underdiagnosed Causes
Amy E. Noffsinger , MD
Abstract
Context: Esophagitis is a common cause of symptoms for which patients seek the advice of a physician. Esophagitis of differing etiologies often demonstrate overlapping histopathologic features, making their distinction difficult. This is especially true in esophageal disorders associated with increased numbers of intraepithelial eosinophils, some of which have just recently been recognized.
Objective: This review discusses the important clinical and pathologic features of the 2 most common disorders associated with esophageal eosinophilic infiltrates—reflux esophagitis and eosinophilic esophagitis—with special emphasis on features that allow the surgical pathologist to distinguish between these disorders. The various forms of drug-induced esophagitis are also discussed because these are frequently underrecognized by pathologists.
Data Sources: Data were extracted from articles identified through PubMed-based research. Histologic figures have been taken from the personal case collection of the author.
Conclusions: Reflux and eosinophilic esophagitis demonstrate overlapping histologic features, which may make their distinction difficult. Drug-induced esophagitis is probably a common phenomenon but is under-recognized by pathologists.

Sincerely,
Phil Lieberman, M.D.

AAAAI - American Academy of Allergy Asthma & Immunology