Eosinophilic gastroenteritis and colitis

Eosinophils are multifunctional leukocytes, normal constituents of the gastrointestinal tract, except when present in the squamous epithelium of the esophagus. Homeostatic eosinophils reside primarily in the lamina propria of the small intestine and protect against parasites and pathogenic bacteria. These cells are selective in their response to parasites, allowing some to reside in the mucosa, thus regulating the intestinal microbiome and participating in tissue homeostasis.

Eosinophils also modulate the immune response, through the secretion of cytokines that can activate dendritic cells and induce IgA class switching in B cells. In their homeostatic role, eosinophils are evenly and sparsely distributed within the lamina propria and do not form clusters or undergo degranulation.

In the small intestine, eosinophils maintain IgA concentrations by secretory factors that prolong the survival of IgA-secreting plasma cells and induce the production of secretory IgA.

This immunoglobulin is an important first-line defense in the mucosa, preventing the invasion of pathogenic microorganisms by coating them with a hydrophilic envelope that is repelled by the mucosal epithelium, thus allowing expulsion.

Both tissue and peripheral eosinophilia have long been known as evidence of parasite invasion, and as every pathologist knows, when eosinophils predominate in the gastrointestinal mucosa, it is good to keep in mind the principle of “see eosinophils, think parasites.”

Their excessive presence is not beneficial, as in asthma and eosinophilic gastrointestinal disorders, in which eosinophil recruitment is induced by pathogens or allergens, causing epithelial damage

Primary eosinophilic disorders include eosinophilic esophagitis, gastroenteritis and colitis. Gastrointestinal involvement may also be seen in hypereosinophilic syndrome. It is noteworthy that eosinophilic gastroenteritis and colitis are associated with allergic diseases, and patients often have concurrent drug allergy, rhinitis, asthma, sinusitis, dermatitis, food allergy, eczema or urticaria. Autoimmune connective tissue diseases have been reported in patients with eosinophilic gastroenteritis.

The pathogenesis of eosinophilia present in eosinophilic gastroenteritis and colitis is poorly studied. Histopathology is characterized by excessive numbers of eosinophils with signs of degranulation.

The association of allergy and atopy in eosinophilic gastroenteritis and eosinophilic colitis suggests that in some individuals other allergens may also be responsible, since half of the patients with eosinophilic gastritis showed positivity to food allergen or aeroallergen skin sensitivity tests, with increased eosinophil counts in the blood.

In patients with eosinophilic gastroenteritis and increased expression of genes involved in potential operative pathways, a gastric transcriptome was observed, including T-helper-like Immunity driven by interleukins 4, 5 and 13. Some patients with eosinophilic gastrointestinal disorders have a shared autoimmune component without atopy, which could lead to eosinophilia through different immune pathways, indicating the complexity of this disease.

Gastrointestinal dysbiosis could also play a role in the pathophysiology of these disorders. Alterations in the intestinal microbiota have been implicated in allergy, but whether this is a cause or a consequence of the disease is unknown.

Patients with eosinophilic gastroenteritis and eosinophilic colitis usually present with nonspecific gastrointestinal symptoms, with a blood eosinophil count that may be normal. Some studies report that the majority of patients (80%) have at least mild peripheral eosinophilia.

Gastroenteritis and eosinophilic colitis are often associated with esophageal symptoms of reflux disease, dysphagia and other vague symptoms including abdominal pain, nausea, vomiting, failure to thrive, diarrhea and weight loss. More serious conditions have also been observed: ascites, volvulus, intussusception, perforation and obstruction.

The clinical presentation probably depends on the site and the extent and depth of disease in the gastrointestinal tract. Patients with more extensive eosinophilic involvement beyond the mucosa into the muscle may present with obstruction while those with serosal involvement may present with ascites.

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