4/17/07
Eosinophilic esophagitis update
Summary
Background - There has been increasing interest and recognition of the entity eosinophilic esophagitis (EE) as a possible cause of upper G-I manifestations with previously obscure etiology.Findings - An update on the diagnosis and pathophysiology of EE was presented at a Scripps Clinic conference. The current prevalence of EE in the USA is estimated to be 1 in 10,000. EE is manifested grossly as a patchy inflammatory esophagitis with white patches, long furrows and (after awhile) concentric rings of scar tissue that may obstruct food passage considerably. In about 20% of cases, there are no gross abnormalities seen.
The microscopic picture is characterized by eosinophil accumulation reaching frequencies of over 20/HPF in some areas. There is an increased thickness of the basal zone of the esophageal wall, sometimes with eosinophil micro abscesses.
The presenting symptoms of EE varies with the patient's age. 1) In children less than 2 years old feeding problems predominate; 2) in children ages 2-8 years vomiting after eating is the most common presentation; 3) in older children - abdominal pain and dysphagia are generally the presenting manifestation. Atopic respiratory and skin problems occur in 60% of those with EE.
A major differential diagnosis of EE is with GERD since less prominent eosinophil accumulation can occur in GERD. Esophageal motility abnormalities are common in EE but not the typical reflux pattern in manometry seen in GERD. The problems are more prominent in the distal esophagus in GERD, not in EE. Also, there is increased deposition of eotaxin-3 (a potent Eos chemoattractant) in the esophageal wall in EE but not in GERD.
Food allergy likely plays a pathogenic role in about 60-70% cases of the children EE. This is manifested by positive prick skin tests in most cases. Some groups finds an additional 5-10% of children with EE who have positive patch tests but negative prick skin tests to suspect foods
Editor's Comments
EE is fascinating in several respects, both possibly explaining some previously obscure upper G-I problems and also teaching us about eosinophil-rich inflammatory mechanisms. Avoidance of offending food allergens and oral "soft" steroids (fluticasone, budesonide) have been quite helpful in arresting the progression of EE.