Published online November 1, 2007
PEDIATRICS Vol. 120 Supplement November 2007, pp. S116-S117 (doi:10.1542/peds.2007-0846Z)
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ALLERGY


Allergic Eosinophilic Gastroenteritis With Protein-Losing Enteropathy: Intestinal Pathology, Clinical Course, and Long-term Follow-up

Casey Geaney, MD

Salem, OR

ABSTRACT

Chehade M, Magid MS, Mofidi S, Nowak-Wegrzyn A, Sampson HA, Sicherer SH. J Pediatr Gastroenterol Nutr. 2006;42:516–521

PURPOSE OF THE STUDY. To identify gross and/or histologic distinguishing features of antral and duodenal biopsy specimens as well as clinical response to various treatment regimens in the subset of patients with eosinophilic gastroenteritis (AEG) with protein-losing enteropathy (PLE).

STUDY POPULATION. The experimental group consisted of 6 children with anemia and hypoalbuminemia and biopsy-proven AEG identified retrospectively from a series of 93 patients with AEG who were evaluated at Mount Sinai Medical Center (New York, NY) over a 7.5-year period.

METHODS. Two comparison groups were used in addition to the experimental group. The first included 6 randomly selected patients from the series of 93 patients with AEG without anemia and/or hypoalbuminemia. The second comparison group included 5 patients who presented with symptoms consistent with possible AEG yet normal gross findings and histology after endoscopy. Causes of eosinophilia other than AEG were ruled out. The diagnoses of AEG required the presence of >20 eosinophils per high-power field in antral biopsy specimens and >50 in the duodenum. Hematoxylin/eosin staining and immunohistochemical staining of tryptase were used for identification of eosinophils and mast cells, respectively. The cell count was taken from the high-power field with maximum infiltration.

RESULTS. Various therapies were attempted in the experimental group including oral corticosteroids, cromolyn sodium, 6-mercaptopurine, food-elimination diets, and montelukast. They were, at best, partially or temporarily beneficial. All experimental patients received an exclusive amino acid–based formula diet at some point in their care; this formula was associated with rapid improvement of anemia and hypoalbuminemia as well as clinical symptoms. These patients eventually tolerated the addition of various foods to their diet. In duodenal biopsy specimens, mast cells were significantly increased in patients with AEG and PLE compared with those with AEG only, whereas eosinophil numbers were comparable. This was not seen in the antral samples. Eosinophilia was more prominent in the antrum of patients with AEG and PLE compared with those with AEG only. Patchy duodenal villous blunting was seen in 1 patient with AEG and PLE and 1 with AEG.

CONCLUSIONS. As in the treatment of eosinophilic esophagitis, amino acid–based formulas seem to be the most effective form of therapy. After improvement on an amino acid–based formula diet, many patients eventually tolerate expanded diets. Malabsorption and villous blunting do not seem to be the cause of hypoalbuminemia and anemia in those patients with AEG and PLE. Increased intestinal mast cells seen in the patients with AEG with PLE may be the source of the intestinal protein loss.

REVIEWER COMMENTS. Although the sample size in this study was small, these data provide additional insight into the specific role of mast cells in patients with AEG and PLE.