Eosinophilic Colitis: A Rare Entity

Eosinophilic infiltration of the gastrointestinal tract in association with a recognizable clinical picture is a rare entity that was first described in 1937 by Kaijser (1). Infiltration of the gastrointestinal tract with eosinophils may involve the entire gastrointestinal tract, but usually involves the stomach and small intestine, whereas isolated colonic involvement is limited to sporadic case reports (2–7). Eosinophilic colitis can occur as a component of the inflammatory response in Crohn's disease, ulcerative colitis, parasitic diseases, and milk protein-induced colitis (6–10). Also, eosinophilic infiltration of colonic mucosa is observed in patients with eosinophilic gastroenteritis (EG) (11). CASE REPORT An 8-year old boy was admitted to our hospital with a 10-day history of crampy abdominal pain and bloody diarrhea. During the previous 3 years he was hospitalized several times with a similar clinical picture. He now averaged seven bowel movements a day and occasionally at night. There was no history of weight loss or a change in appetite, and the patient ate a normal diet. He also had asthma. On admission, the patient's physical examination was normal. Abnormal laboratory findings were as follows: erythrocyte sedimentation rate, 26 mm per hour; hemoglobin, 112 g/L; hematocrit, 0.33; red blood cell count, 4.5 × 1012 cells/L; mean corpuscular volume, 73.7 fl; white blood cells, 8.8 × 109 cells/L; eosinophils relative value, 0.17; and eosinophils absolute count, 1,885 × 106 eosinophils/L (normal range, 50–250 × 106 eosinophils/L). Serum immunoglobulin E concentrations were normal. Skin tests (using the prick technique) for possible allergic reactions to multiple inhalant and food antigens were negative. The stool was positive for blood, and negative for bacterial and parasitic enteric pathogens. Esophagogastroduodenoscopy, including histologic features of biopsies from the corpus and antrum of the stomach and from the duodenum and the jejunum, was normal. Colonoscopy revealed diffuse, erythematous, granular, congestive, and friable mucosa with macroscopic changes noted primarily in the sigmoid colon and rectum. Biopsies of colonic mucosa showed edematous and hyperemic lamina propria infiltrated with inflammatory cells, mainly eosinophils (Fig. 1). During the colonoscopy we also examined (and sampled) terminal ileum, which was normal. We initiated therapy with ketotifen, which realized symptomatic improvement.FIG. 1.: Eosinophilic infiltration in colonic mucosa. Eosinophils were observed in the lamina propria. Hematoxylin–eosin, original magnification ×250 before XX% reduction.DISCUSSION There is no universally accepted definition of the still poorly understood condition of eosinophilic gastroenteropathy. Talley et al. (11) defined three criteria: the presence of gastrointestinal symptoms, biopsies showing eosinophilic infiltration of one or more areas of gastrointestinal tract from esophagus to colon, or characteristic radiologic findings with peripheral eosinophilia and no evidence of parasitic or extraintestinal disease. The diagnosis rests on peripheral blood eosinophilia and eosinophilic tissue infiltration with exclusion of the diseases that may mimic EG (10,12). Tissue eosinophilia is not specific for EG (12–14) and can occur as an inflammatory response in various conditions. Some studies suggest that the disease can be patchy, and thus biopsies may miss the diagnosis (6,7,11,13,15,16). Furthermore, the peripheral eosinophilic count seems to be normal in 23 (11) to 40%(12,17) of patients with EG, suggesting that it is not a reliable diagnostic criterion. Blood eosinophilia represents the balance of production and the movement of eosinophils from blood into tissue (12). Eosinophilic gastrointestinal disease is indeed rare (1:100,000), and isolated colonic involvement appears to be very sporadic (2–5,7,18) Because of these reasons, it is not easy to diagnose EG. Furthermore, it is difficult to determine isolated colonic involvement. In our patient, the diagnosis was based on the history, infiltrate of eosinophils in multiple colonic biopsies and peripheral eosinophilia. All biopsy specimens taken from stomach, duodenum, jejunum, and terminal ileum were normal. Histologic features of biopsies from the colon showed typical changes for eosinophilic inflammation. The etiology of the disease is still not defined and it is considered to be idiopathic (13,19). Past history of allergy is reported in one third (10,18,20) to one half (3,11) of all patients with EG, suggesting an allergic basis. (Allergens could be medications, worms, and food proteins.) (2,21–24). The pathogenesis of EG is not clear. Perhaps it is the excessive accumulation of eosinophils, which causes destruction of intestinal epithelium caused by the release of eosinophilic major protein (7,11,25). Our patient has asthma (with no evidence of allergy) and all allergy tests were negative. There is no generally accepted treatment of EG, and the symptoms dictate the therapy. Elimination of the precipitating agent may lead to total resolution of the disorder (2,11,12). Steroids remain the mainstay of therapy, but because of allergic pathogenesis, many authors suggest oral chromoglycate or ketotifen (alone or in combination with steroids) (3,12,20,21). We decided to start with antiallergic therapy, with ketotifen because of the patient's history of asthma, although there was no evidence of allergic etiology. We concluded that EG can affect the colon, but that isolated colonic involvement is very rare. Peripheral eosinophilia may be absent, the disease may be patchy, and thus the diagnosis may be missed. The etiology and pathogenesis are still not known, but steroids or antiallergic medications are effective forms of therapy.