Eosinophilic esophagitis causes: Difference between revisions
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==Causes== | ==Causes== | ||
*The causes of EoE are as follows: | *The causes of EoE are as follows: | ||
*The food and pollen react with the lining of the esophagus, these allergens cause the multiplication of eosinophils in the layers of the esophagus and produce a protein that causes inflammation. | *The food and pollen react with the lining of the [[esophagus]], these [[allergens]] cause the multiplication of eosinophils in the layers of the esophagus and produce a protein that causes inflammation. | ||
*The inflammation further cause scarring, excessive fibrous tissue deposition over the lining of the esophagus eventually leading to dysphagia. | *The inflammation further cause scarring, excessive fibrous tissue deposition over the lining of the esophagus eventually leading to dysphagia. | ||
*The dysphagia can sometimes worsen to cause food impaction and additional symptoms such as chest pain. | *The dysphagia can sometimes worsen to cause food impaction and additional symptoms such as chest pain. | ||
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*'''Remodeling'''- fibrosis and increased thickness of the esophageal wall, eventually leads to an increase in esophageal mural stiffness causing esophageal remodeling. | *'''Remodeling'''- fibrosis and increased thickness of the esophageal wall, eventually leads to an increase in esophageal mural stiffness causing esophageal remodeling. | ||
GERD contributes to or causes EoE | '''GERD contributes to or causes EoE''' | ||
* Counter to the hypothesis of the previous section, it is possible that [[GERD]] could cause EoE. | |||
* The pathognomic [[histological]] feature of the [[Gastroesophageal reflux disease|GERD]] is [[Dilation|dilatation]] of inter-cellular spaces of the [[esophageal]] [[Squamous epithelium|squamous epithelium.]] | |||
The pathognomic histological feature of the GERD is dilatation of inter-cellular spaces of the esophageal squamous epithelium. | |||
Increased mucosal permeability in GERD due to a breach of the mucosal integrity of the esophagus leading to the penetration of allergens that were swallowed into the subepithelial space, which can then be accessed by antigen-presenting cells. | * Increased [[Mucous membrane|mucosal]] [[permeability]] in [[Gastroesophageal reflux disease|GERD]] due to a breach of the [[Mucous membrane|mucosal]] integrity of the [[esophagus]] leading to the penetration of [[allergens]] that were [[Swallow|swallowed]] into the subepithelial space, which can then be accessed by [[antigen-presenting cells]]. | ||
The initial step of allergic sensitization involves antigen presentation by dendritic cells to naive T cells which are transformed to antigen-specific type 2 T helper (TH2) cells. | |||
The thymic stromal lymphopoietin (TSLP) production from the | * The initial step of allergic sensitization involves antigen presentation by [[Dendritic cell|dendritic]] cells to naive T cells which are transformed to antigen-specific type 2 T helper (TH2) cells. | ||
* The [[thymic]] [[stromal]] [[lymphopoietin]] (TSLP) production from the [[esophageal]] [[epithelium]] primes [[esophageal]] [[Mucous membrane|mucosal]] [[basophils]] to secrete [[IL-4]], which promotes the [[Allergy|allergic]] [[sensitization]] process. | |||
==References== | ==References== | ||
Revision as of 16:56, 15 December 2017
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Eosinophilic Esophagitis Microchapters |
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Differentiating Eosinophilic Esophagitis from other Diseases |
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Eosinophilic esophagitis causes On the Web |
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Risk calculators and risk factors for Eosinophilic esophagitis causes |
Overview
Causes
- The causes of EoE are as follows:
- The food and pollen react with the lining of the esophagus, these allergens cause the multiplication of eosinophils in the layers of the esophagus and produce a protein that causes inflammation.
- The inflammation further cause scarring, excessive fibrous tissue deposition over the lining of the esophagus eventually leading to dysphagia.
- The dysphagia can sometimes worsen to cause food impaction and additional symptoms such as chest pain.
EoE contributes to or causes GERD
- Various hypotheses have been proposed that EoE contributes to the development of GERD.
- Mucosal barrier- Eosinophils secrete inflammatory mediators such as VIP (Vasoactive intestinal peptide), PAF (platelet-activating factor), IL-6 which damages the integrity of the mucosal barrier and the smooth muscles of the esophagus.
- Peristalsis- VIP and PAF predisposes a patient to reflux by inducing relaxation of the LES, whereas the IL-6 affects the peristalsis and clearance of the acid, the alterations in oesophageal function contribute to increased acid exposure due to impaired clearance of refluxed contents
- Cytotoxic effect- Eosinophil cationic protein, Major basic protein, and Eosinophil peroxidase secreted by eosinophils have a direct cytotoxic effect on the mucosa, rendering the oesophageal epithelium more susceptible to caustic injury by refluxed gastric contents.
- Epithelial cells and Nerves- the above-mentioned events exposes the epithelial cells and nerves to further acid injury.
- Remodeling- fibrosis and increased thickness of the esophageal wall, eventually leads to an increase in esophageal mural stiffness causing esophageal remodeling.
GERD contributes to or causes EoE
- Counter to the hypothesis of the previous section, it is possible that GERD could cause EoE.
- The pathognomic histological feature of the GERD is dilatation of inter-cellular spaces of the esophageal squamous epithelium.
- Increased mucosal permeability in GERD due to a breach of the mucosal integrity of the esophagus leading to the penetration of allergens that were swallowed into the subepithelial space, which can then be accessed by antigen-presenting cells.
- The initial step of allergic sensitization involves antigen presentation by dendritic cells to naive T cells which are transformed to antigen-specific type 2 T helper (TH2) cells.
- The thymic stromal lymphopoietin (TSLP) production from the esophageal epithelium primes esophageal mucosal basophils to secrete IL-4, which promotes the allergic sensitization process.