Eosinophilic esophagitis

Merves, Jamie; Muir, Amanda B.; Chandramouleeswaran, Prasanna M.; Cianferoni, Antonella; Wang, Mei-Lun; Spergel, Jonathan M.

doi:10.1016/j.anai.2014.01.023

Cited by 34 publications

(33 citation statements)

References 62 publications

(83 reference statements)

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“…IL-4 leads to Th2 lymphocyte survival and induces eotaxin-3 (a key chemoattractant for eosinophils) and the profibrotic factors periostin, collagen, and β-actin [28,61]. IL-5 is the major cytokine responsible for the differentiation, recruitment, activation, and survival of eosinophils [62].…”

Section: Pathogenesismentioning

confidence: 99%

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Eosinophilic Esophagitis and Gastroenteritis

Cianferoni

Spergel

2015

Curr Allergy Asthma Rep

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Eosinophilic gastrointestinal disease (EGID) can be classified as eosinophilic esophagitis (EoE) when the eosinophilia is limited to the esophagus or as eosinophilic gastritis (EG) if it is limited to the gastric tract, eosinophilic colitis (EC) if it is limited to the colon, and eosinophilic gastroenteritis (EGE) if the eosinophilia involves one or more parts of the gastrointestinal tract. EoE is by far the most common EGID. It is a well-defined chronic atopic disease due to a T helper type 2 (Th2) inflammation triggered often by food allergens. EoE diagnosis is done if an esophageal biopsy shows at least 15 eosinophils per high power field (eos/hpf). Globally accepted long-term therapies for EoE are the use of swallowed inhaled steroids or food antigen avoidance. The treatment of EoE is done not only to control symptoms but also to prevent complications such as esophageal stricture and food impaction. EGE cause non-specific gastrointestinal (GI) symptoms and are diagnosed if esophagogastroduodenoscopy (EGD)/colonoscopy show eosinophilia in one or more parts of the GI tract. They are rare diseases with an unclear pathogenesis, and they are poorly defined in terms of diagnostic criteria and treatment. Before initiating treatment of any EGE, it is imperative to conduct a differential diagnosis to exclude other causes of hypereosinophilia with GI localization. EGE are often poorly responsive to therapy and there is no commonly accepted long-term treatment. EG has many characteristics similar to EoE, including the fact that it is often due to a food allergen-driven Th2 inflammation; transcriptome analysis however shows that it is more a systemic disease and has a different gene signature than EoE. EC is a benign form of delayed food allergy in infant and is instead a difficult-to-treat severe inflammatory condition in older children and adults. EC in the latter groups can be a manifestation of drug allergy or autoimmune disease. Overall EGE, EC, and EG are rare and are a diagnosis of exclusion until more common causes of eosinophilia have been excluded.

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Section: Pathogenesismentioning

confidence: 99%

“…In older children: abdominal pain and vomiting 3. In teenagers and adults: dysphagia and food impaction [14,27,28] Symptoms of EoE can be very similar to gastroesophageal reflux disease (GERD), but differently from GERD, they are typically not responsive to maximal dose of proton pump inhibitors (PPI) [14,[27][28][29].…”

Section: Diagnosismentioning

confidence: 99%

Eosinophilic Esophagitis and Gastroenteritis

Cianferoni

Spergel

2015

Curr Allergy Asthma Rep

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“…In a mouse model of EoE, mice that have been genetically modified so they do not express Th2 cytokines, in particular IL-13 or transcriptional factors that determine Th2 switching such as Stat6 or Stat1, are less likely to develop disease [18,21,33]. IL-4 increases Th2-lymphocyte survival and eotaxin-3 secretion from epithelial cells, which in turn significantly promotes eosinophilic migration; in addition, it induces fibroblast to secrete periostin, collagen, and β-actin, therefore promoting local fibrosis [34,35]. IL-5 is the major cytokine responsible for the differentiation, recruitment, and survival of eosinophils [36].…”

Section: Pathogenesismentioning

confidence: 98%

Eosinophilic Esophagitis: A Comprehensive Review

Cianferoni

Spergel

2015

Clinic Rev Allerg Immunol

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“…3 EoE pathophysiology is complex, involving a variety inflammatory cells and cytokines in a non–immunoglobulin E (IgE)-dependent allergic model. 4–6 EoE is primarily caused by the ingestion of one or more food antigens, 7, 8 but may also be triggered by inhaled aeroantigens. 9 EoE and associated complications have a significant impact on patient quality of life 10 and patients with EoE in the United States have an annual health care cost of up to $1.4 billon.…”

Section: Introductionmentioning

confidence: 99%