Eosinophilic Colitis, Clinical Manifestation an Management

Eosinophilic Colitis, Clinical Manifestation an Management

Eosinophils accumulate in the colons of patients with a variety of disorders, including eosinophilic gastroenteritis, allergic colitis of infancy, infections (including pinworms and dog hookworms), drug reactions, vasculitis (eg, Churg-Strauss syndrome), and IBD.Allergic colitis in infancy (also known as dietary protein–induced proctocolitis of infancy syndrome) is the most common cause of bloody stools in the first year of life. Similar to other EGIDs, these disorders are classified into primary and secondary subtypes . The primary subtype includes the atopic and nonatopic variants, whereas the secondary subtype is divided into 2 groups, one composed of systemic eosinophilic disorders (HES) and the other composed of noneosinophilic disorders.

Eosinophil accumulation in the gastrointestinal tract is a common feature of numerous gastrointestinal disorders, including classic IgE-mediated food allergy, eosinophilic gastroenteritis, allergic colitis, eosinophilic esophagitis (EE), inflammatory bowel disease (IBD), and gastroesophageal reflux disease (GERD). In IBD eosinophils usually represent only a small percentage of the infiltrating leukocytes,11, 19 but their level has been proposed to be a negative prognostic indicator. Primary eosinophilic gastrointestinal disorders (EGIDs; eg, EE, eosinophilic gastritis, eosinophilic gastroenteritis, eosinophilic enteritis, and eosinophilic colitis) are defined as disorders that primarily affect the gastrointestinal tract with eosinophil-rich inflammation in the absence of known causes for eosinophilia (eg, drug reactions, parasitic infections, and malignancy). Patients with EGIDs have a variety of problems, including failure to thrive, abdominal pain, irritability, gastric dysmotility, vomiting, diarrhea, and dysphagia. Evidence in support of the concept that EGIDs arise as a result of the interplay of genetic and environmental factors is accumulating. Notably, a large percentage (approximately 10%) of patients with EGIDs have an immediate family member with an EGID.21 Additionally, several lines of evidence support an allergic cause, including the finding that approximately 75% of patients with EGIDs are atopic, the finding that the severity of disease can sometimes be reversed by institution of an allergen-free diet, and the common finding of mast cell degranulation in tissue specimens. Importantly, our recent models of EGIDs support a potential allergic cause for these disorders. Interestingly, despite the common finding of food-specific IgE in patients with EGIDs, food-induced anaphylactic responses only occur in a minority of patients. Thus EGIDs have properties that fall between pure IgE-mediated food allergy and cellular-mediated hypersensitivity disorders (eg, celiac disease;

In contrast to other EGIDs, eosinophilic colitis is usually a non-IgE–associated disease. Some studies point to a T lymphocyte–mediated process, but the exact immunologic mechanisms responsible for this condition have not been identified.185 In a murine model of oral antigen–induced diarrhea associated with colonic inflammation, colonic T cells have been shown to transfer the disease to naive mice through a STAT6-dependent mechanism.186 It has been reported that allergic colitis of infancy might be an early expression of protein-induced enteropathy or protein-induced enterocolitis syndrome. Cow’s milk and soy proteins are the foods most frequently implicated in allergic colitis of infancy, but other food proteins can also provoke the disease. Interestingly, this condition might more commonly occur in infants exclusively breast-fed and can even occur in infants fed with protein hydrolysate formulas.

Clinical Manifestation

Similar to eosinophilic gastroenteritis, there are a variety of symptoms associated with eosinophilic colitis, depending on the degree and location of tissue involvement. Although diarrhea is a classic symptom, symptoms that can occur independent of diarrhea commonly include abdominal pain, weight loss, and anorexia. There is a bimodal age distribution given the infantile form presented at a mean age at diagnosis of approximately 60 days7 and the other group presenting during adolescence and early adulthood. In infants bloody diarrhea precedes diagnosis by several weeks, and anemia caused by blood loss is not uncommon. The majority of infants affected do not have constitutional symptoms and are otherwise healthy. On endoscopic examination, patchy erythema, loss of vascularity, and lymphonodular hyperplasia are seen mostly localized to the rectum but might extend to the entire colon. Histologic examination often reveals that the overall architecture of the mucosa is well preserved, but there are focal aggregates of eosinophils in the lamina propria, crypt epithelium, and muscularis mucosa and, occasionally, the presence of multinucleated giant cells in the submucosa. No single test is the gold standard for diagnosis, but peripheral blood eosinophilia or eosinophils in the stool are suggestive of eosinophilic colitis.


Treatment of eosinophilic colitis varies, primarily depending on the disease subtype. For example, eosinophilic colitis of infancy is generally a benign disease. On withdrawal of the offending protein trigger in the diet, the gross blood in the stools usually resolves within 72 hours, but occult blood loss might persist longer. Treatment of eosinophilic colitis in older individuals usually requires medical management because IgE-associated triggers are rarely identified. Drugs, such as cromoglycate, montelukast, and histamine receptor antagonists, are generally not successful in the author’s experience. Anti-inflammatory drugs, including aminosalicylates and glucocorticoids (systemic or topical steroids), are commonly used and appear to be efficacious, but careful clinical trials have not been conducted. There are several forms of topical glucocorticoids designed to deliver drugs to the distal colon and rectum, but eosinophilic colitis typically also involves the proximal colon. In severe cases, refractory or dependent on systemic glucocorticoid therapy, intravenous alimentation or immunosuppressive antimetabolite therapy (azathioprine or 6-mercaptopurine) are alternatives.


When eosinophilic colitis presents in the first year of life, the prognosis is very good, with the vast majority of patients being able to tolerate the culprit food or foods by 1 to 3 years of age. Several studies have found an association between allergic colitis and later development of IBD, but this association is controversial. The prognosis for eosinophilic colitis when it develops later in life is more guarded than the infantile subtype. Similar to eosinophilic gastroenteritis, the natural history has not been documented, and this disease is considered to be a chronic waxing and waning disorder. Because eosinophilic colitis can often be a manifestation of other primary disease processes, routine surveillance of the cardiopulmonary systems and regular upper and lower gastrointestinal endoscopy is recommended.

  • Sherman, MP and Cox, KL. Neonatal eosinophilic colitis. J Pediatr. 1982; 100: 587–589
  • Hill, SM and Milla, PJ. Colitis caused by food allergy in infants. Arch Dis Child. 1990; 65: 132–133
  • Odze, RD, Wershil, BK, Leichtner, AM, and Antonioli, DA. Allergic colitis in infants. J Pediatr. 1995; 126: 163–170
  • Liu, LX, Chi, J, Upton, MP, and Ash, LR. Eosinophilic colitis associated with larvae of the pinworm Enterobius vermicularis. Lancet. 1995; 346: 410–412
  • Khoshoo, V, Schantz, P, Craver, R, Stern, GM, Loukas, A, and Prociv, P. Dog hookworm: a cause of eosinophilic enterocolitis in humans. J Pediatr Gastroenterol Nutr. 1994; 19: 448–452
  • Machida, HM, Catto Smith, AG, Gall, DG, Trevenen, C, and Scott, RB. Allergic colitis in infancy: clinical and pathologic aspects. J Pediatr Gastroenterol Nutr. 1994; 19: 22–26
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