Eosinophilic gastroenteritis after allogeneic bone marrow transplantation.

Abstract

Dear Editor, Eosinophilic gastroenteritis is characterized by symptoms such as abdominal pain, diarrhea, nausea, and marked eosinophilic infiltration into the gastrointestinal tissue. Several reports have shown that eosinophilic gastroenteritis occurred in patients after hematopoietic stem cell transplantation (HSCT) [1–3]. We herein report an adult case with myelodysplastic/ myeloproliferative disease, unclassifiable (MDS/MPD-U) that subsequently developed eosinophilic gastroenteritis after allogeneic bone marrow transplantation (BMT). A 46-year-oldmanwithMDS/MPD-U received azacitidine treatment. Thereafter, he underwent allogeneic BMT from a human leukocyte antigen-matched sibling donor with a conditioning regimen comprising 12 Gy of total body irradiation and high-dose cytarabine because the response to azacitidine was gradually lost. Prophylaxis for graft-versus-host disease (GVHD) consisted of intravenous cyclosporine and shortterm methotrexate. The patient had evidence of grade II acute GVHD of the skin, which required no steroid treatment. On day 122, he developed watery diarrhea with colicky abdominal pain under oral cyclosporine (100 mg/day). A colonoscopic examination revealed mucosal edema, erosion, and shallow ulceration in the cecum to the ascending colon and from the sigmoid colon to the rectum (Fig. 1a). A histological examination of several biopsy specimens of the colon revealed intense infiltration of eosinophils in the lamina propria (Fig. 1b). Based on these findings, the patient was diagnosed with eosinophilic gastroenteritis. His abdominal symptoms were resolved under fasting conditions without any treatment. Follow-up colonoscopy showed complete resolution of the eosinophilic infiltration of random biopsy specimens of the colon. He has not experienced a recurrence of eosinophilic gastroenteritis 1 year after the initial episode. Gastrointestinal complications after allogeneic HSCT can arise due to various causes, such as regimen-related toxicity, GVHD, and infection. In our patient, the histological characteristics of GVHD, such as apoptosis and destruction of crypt epithelial cells, and lymphocyte infiltration of the epithelium and lamina propria, were almost never found in the biopsy specimens of the colon. In addition, the histological findings showed negative immunostaining for cytomegalovirus (CMV). These findings indicated that the diagnosis of intestinal GVHD and CMV colitis could be excluded for our patient. The diagnosis of eosinophilic gastroenteritis is based on the clinical symptoms and histological findings, including eosinophilic infiltration in one or more areas of the gastrointestinal tract, defined as 20 or more eosinophils per high-power field [4]. These findings are compatible with those of our patient. The majority of cases of eosinophilic gastroenteritis have a history of allergy, hypereosinophilia, and elevated serum IgE levels. Therefore, eosinophilic gastroenteritis is closely related to allergic disease [5]. Although our patient and his donor did not have any past history of allergy or hypereosinophilia, the serum IgE level was slightly elevated to 191 IU/mL (upper limit of normal, 173 IU/mL) at the time of the diagnosis of eosinophilic gastroenteritis. In addition, fasting conditions without steroid treatment resulted in improved symptoms in our patient, suggesting that a food allergy might have been associated with the eosinophilic gastroenteritis. This case * Takaaki Konuma tkonuma@ims.u-tokyo.ac.jp