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Eosinophilic gastroenteritis (EG) is a rare and heterogeneous condition characterized by patchy or diffuse eosinophilic infiltration of gastrointestinal (GI) tissue, first described by Kaijser in 1937 [1] [2]. Presentation may vary depending on location as well as depth and extent of bowel wall involvement and usually runs a chronic relapsing course. It can be classified into mucosal, muscular and serosal types based on the depth of involvement. [3][4] Any part of the GI tract can be affected, and isolated biliary tract involvement has also been reported[5][6]. The stomach is the organ most commonly affected, followed by the small intestine and the colon [7][8].
Peripheral blood eosinophilia and elevated serum IgE are usual but not universal. The damage to the gastrointestinal tract wall is caused by eosinophilic infiltration and degranulation[9].
As a part of host defense mechanism, eosinophil is normally present in gastrointestinal mucosa, though finding in deeper tissue is almost always pathologic [10]. What triggers such dense infiltration in EG is not clear. It is possible that different pathogenetic mechanisms of disease is involved in several subgroups of patients. Food allergy and variable IgE response to food substances has been observed in some patients which implies role of hypersensitive response in pathogenesis. Many patients indeed have history of other atopic conditions like eczema, asthma etc.
Eosinophil recruitment into inflammatory tissue is a complex process, regulated by a number of inflammatory cytokines. In EG cytokines IL-3, IL-5 and granulocyte macrophage colony stimulating factor (GM-CSF) may be behind the recruitement and activation. They have been observed immunohistochemically in diseased intestinal wall [11]. In addition eotaxin has been shown to have an integral role in regulating the homing of eosinophils into the lamina propria of stomach and small intestine [12]. In the allergic subtype of disease, it is thought that food allergens cross the intestinal mucosa and trigger an inflammatory response that includes mast cell degranulation and recruitment of eosinophils [13].
EG typically presents with a combination of chronic nonspecific GI symptoms which include abdominal pain, nausea, vomiting, diarrhea, weight loss, and abdominal distension. Approximately 80% have symptoms for several years[14]; a high degree of clinical suspicion is often required to establish the diagnosis, as the disease is extremely rare. Occasionally, the disease may manifest itself as an acute abdomen or bowel obstruction[15][16].
Talley et al.[21] suggested 3 diagnostic criteria which is still widely used:
Hypereosinophilia, the hallmark of allergic response, may be absent in up to 20% of patients, but hypoalbuminaemia and other abnormalities suggestive of malabsorption may be present.
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