You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information.
What is Eosinophilic gastroenteritis and explain in detail?
Eosinophilic gastroenteritis (EG or EGE) is a rare and heterogeneous condition characterized by patchy or diffuse eosinophilic infiltration of gastrointestinal (GI) tissue, first described by Kaijser in 1937. 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. Any part of the GI tract can be affected, and isolated biliary tract involvement has also been reported.
The stomach is the organ most commonly affected, followed by the small intestine and the colon.

Signs and symptoms
EG typically presents with a combination of chronic nonspecific GI symptoms which include abdominal pain, diarrhea, occasional nausea and vomiting, weight loss and abdominal distension. Approximately 80% have symptoms for several years; a high degree of clinical suspicion is often required to establish the diagnosis, as the disease is extremely rare. It doesnt come all of a sudden but takes about 3–4 years to develop depending upon the age of the patient. Occasionally, the disease may manifest itself as an acute abdomen or bowel obstruction.
Mucosal EG (25–100%) is the most common variety, which presents with features of malabsorption and protein losing enteropathy. Failure to thrive and anaemia may also be present. Lower gastrointestinal bleeding may imply colonic involvement.
Muscular EG (13–70%) present with obstruction of gastric outlet or small intestine; sometimes as an obstructing caecal mass or intussusception.
Subserosal EG (4.5% to 9% in Japan and 13% in the US) presents with ascites which is usually exudative in nature, abundant peripheral eosinophilia, and has favourable responses to corticosteroids.
Other documented features are cholangitis, pancreatitis, eosinophilic splenitis, acute appendicitis and giant refractory duodenal ulcer.

Pathophysiology
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.As a part of host defense mechanism, eosinophils are normally present in gastrointestinal mucosa, though the finding in deeper tissue is almost always pathologic. 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 recruitment and activation. They have been observed immunohistochemically in diseased intestinal wall.
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.
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.

Diagnosis
Talley et al