Years published: 2006, 2009, 2012, 2016, 2019, 2023
NORD gratefully acknowledges Marc E. Rothenberg, MD, PhD, Director of the Division of Allergy and Immunology, and The Cincinnati Center for Eosinophilic Disorders, Professor of Pediatrics, Dave and Denise Bunning Endowed Chair of Allergy and Immunology, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, for assistance in the preparation of this report.
Eosinophilic esophagitis (EoE) is a chronic disorder of the digestive system in which large numbers of a particular type of white blood cell called eosinophils are present in the esophagus. The esophagus is the tube that carries food from the mouth to the stomach. Eosinophils are part of the immune system and play a role in immune regulation and fighting certain infection, and their accumulation is a hallmark of allergic diseases. This condition is characterized by vomiting, stomach or chest pain, failure to thrive (particularly in children), difficulty swallowing and food getting stuck in the throat.
The symptoms of eosinophilic esophagitis are variable, especially in people of different ages. Common symptoms include difficulty swallowing (dysphagia); food getting stuck in the throat (impaction); nausea; vomiting; poor growth; weight loss; stomach pain; poor appetite; and malnutrition. Because of an overlap of these symptoms with gastroesophageal reflux disease (GERD), many patients are initially thought to have GERD, but EoE patients do not typically have GERD upon diagnostic workup. Recently, it has been appreciated that some patients with pronounced esophageal eosinophilia can have complete responses to proton pump inhibitor (PPI) therapy, typically used for the treatment of GERD, but these patients do not typically have GERD but rather EoE that is responsive to PPIs. PPI exert this therapeutic effect by direct action rather than blockade of stomach acid alone. For example, PPIs are also ligands (bind to) the aryl hydrocarbon receptor and this elicits an anti-inflammatory and anti-proliferative effect in the esophagus. PPI responsive esophageal eosinophilia has largely overlapping clinical, histological and molecular characteristics with PPI-resistant esophageal eosinophilia, but entities are referred to as EoE and usage of PPIs is now considered a treatment of EoE. Individuals with eosinophilic esophagitis often have allergic diseases such as asthma or eczema.
Eosinophilic esophagitis is associated with the presence of many eosinophils in the esophagus driven by an immune response to a variety of foods. The production and accumulation of eosinophils may be caused by many factors such as immune hypersensitivity responses to particular foods or environmental proteins (allergens) in some affected individuals. Most individuals with this condition have been found to have an unusually high expression of a particular gene called eotaxin-3. This gene codes for a protein that is important in controlling the accumulation of eosinophils. Eosinophilic esophagitis can run in families but the risk for additional family members is <5% unless they are twins with the EoE patient. Several genes have been identified to contribute to EoE including CAPN14 and TSLP. A fundamental step in the development of EoE is loss of esophageal barrier function which is mediated by loss of anti-proteases such as SPINK7 and desmosomal proteins such as desmoglein-1 and dysregulated expression of the CAPN14 gene product (calpain-14). It is now appreciated that esophageal eosinophilia as well as other pathological features of EoE are driven by a strong cellular response of the adaptive immune system, primarily orchestrated by type 2 helper T cells (Th2 cells). These cells, along with esophageal mast cells, produce high levels of the cytokine interleukin (IL)-13, which is essential in eliciting multiple pathological processes in the esophagus.
The frequency of eosinophilic esophagitis has been estimated to be approximately 1 in 2,000 individuals. This condition has been reported in multiple continents including Europe, Australia and America.
The diagnosis of eosinophilic esophagitis is often delayed because of a lack of awareness of this condition. A small tube is inserted through the mouth into the esophagus (upper endoscopy) and small tissue samples are removed (biopsy) in order to count eosinophils and look for tissue injury and thickening of tissue.
Elevated expression of eotaxin-3 is part of a whole panel of dysregulated genes expressed by the esophagus of EoE patients, termed the “EoE transcriptome” which divides patients into different subgroups, referred to as endotypes.
Many children and adults with EoE show improvement with proton pump inhibitor therapy, as well diet modification so that allergenic food is removed, most commonly milk, egg, soy, wheat, nuts and fish. These foods are sometimes removed all at once or in a gradual manner, starting first with milk. Some affected individuals require a liquid formula diet fed through a feeding tube. Steroid medications are often used to control inflammation. Steroids are typically given by topical delivery by swallowing formulations designed for asthma such as inhaled fluticasone or by using a slurry of liquid budesonide. Additional endoscopies and biopsies are usually necessary to monitor the effectiveness of treatment.
In 2022, a biological agent that blocks the signaling of IL-13 and the related cytokine IL-4, called dupilumab (Dupixent), was approved by the U.S. Food and Drug Administration (FDA) to treat adults and children 12 years and older with EoE. This is the first FDA approved treatment for EoE. Other medicines (e.g., PPIs and steroids) are used as off-label although a swallowed glucocorticoid (budesonide) is now approved in Europe and Canada (under the tradename Jorveza).
Research is underway to develop medications to block the proteins that underly the basic pathogenesis of EoE, as deciphered through the EoE transcriptome. This research has laid the foundation for understanding the key role of IL-13 and clinical studies with antibodies that block this cytokine as well as its receptor (IL-4Ra, which is also shared with IL-4) are at various stages of advanced development. In particular, weekly dupilumab is now approved for the treatment of EoE in patients 12 years and older and is in active investigation for patients between 1-12 years of age. Additional drugs that target IL-13 (such as cendakimab) are at advanced stages of development. Research is being done on the eosinophil growth factor (IL-5 using reslizumab or mepolizumab which are approved for asthma) as well as thymic stromal lymphopoietin (TSLP using tezepelumab which is approved for asthma). Eosinophil depleting antibodies are also now available, including benralizumab (now approved for eosinophilic asthma) as well as lirentelumab (in development). Advances clinical trials with these agents have shown their potent ability to deplete esophageal eosinophils, but these drugs have not yet been demonstrated to provide clinical improvements (in terms of symptoms). These findings draw attention away from eosinophils as the primary culprit cell involved in disease pathogenesis.
A major advance in EoE is the formation of the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR), which is part of the Rare Diseases Clinical Research Network (RDCRN), supported by the National Institute of Health through the National Center for Advancing Translational Science (NCATS). CEGIR is funded by NCATS, the National Institute of Allergy and Infectious Disease (NIAID), the National Institute of Diabetes and Digestive and Kidney Disease (NIDDK), the American Partnership for Eosinophilic Disorders (APFED) and the Campaign Urging Research for Eosinophilic Disorders (CURED). CEGIR aims to improve the lives of individuals with eosinophilic gastrointestinal disease (EGID) through innovative research, clinical expertise and education via collaboration between scientists, health care providers, patients and professional organizations. CEGIR also carries out pilot studies testing new hypotheses concerning EGID. A key mission of CEGIR is to train the next generation of physicians so they have expertise in EGID.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
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