Eosinophilic esophagitis causes: Difference between revisions
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==Causes== | ==Causes== | ||
*The causes of [[Eosinophilic esophagitis|EoE]] are as follows: | *The causes of [[Eosinophilic esophagitis|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]]. | ||
'''EoE contributes to or causes GERD''' | '''EoE contributes to or causes GERD''' | ||
*Various hypotheses have been proposed that EoE contributes to the development of GERD. | *Various [[hypotheses]] have been proposed that [[Eosinophilic esophagitis|EoE]] contributes to the development of [[Gastroesophageal reflux disease|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. | *'''Mucosal barrier'''- [[Eosinophils]] secrete [[Inflammation|inflammatory]] mediators such as [[Vasoactive intestinal peptide|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 | *'''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 [[esophageal]] function contribute to increased [[acid]] exposure due to impaired clearance of [[reflux]] 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 | *'''Cytotoxic effect'''- [[Eosinophil cationic protein]], [[Major basic protein]], and [[Eosinophil peroxidase]] secreted by [[eosinophils]] have a direct [[cytotoxic]] effect on the [[Mucous membrane|mucosa]], rendering the [[esophageal]] [[epithelium]] more susceptible to caustic injury by [[reflux]] [[gastric]] contents. | ||
*'''Epithelial cells and | *'''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. | *'''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''' | ||
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* The pathognomic [[histological]] feature of the [[Gastroesophageal reflux disease|GERD]] is [[Dilation|dilation]] of inter-cellular spaces of the [[esophageal]] [[Squamous epithelium|squamous epithelium.]] | * The pathognomic [[histological]] feature of the [[Gastroesophageal reflux disease|GERD]] is [[Dilation|dilation]] of inter-cellular spaces of the [[esophageal]] [[Squamous epithelium|squamous epithelium.]] | ||
* Increased [[Mucous membrane|mucosal]] [[permeability]] in [[Gastroesophageal reflux disease|GERD]] due to a breach of the [[Mucous membrane|mucosal]] integrity of the [[esophagus]] leads to the penetration of [[allergens]] that may have been [[Swallow|swallowed]] into the | * Increased [[Mucous membrane|mucosal]] [[permeability]] in [[Gastroesophageal reflux disease|GERD]] due to a breach of the [[Mucous membrane|mucosal]] integrity of the [[esophagus]] leads to the [[penetration]] of [[allergens]] that may have been [[Swallow|swallowed]] into the sub-epithelial space, which may then be accessed by [[antigen-presenting cells]]. | ||
* 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 initial step of [[Allergy|allergic]] [[sensitization]] involves [[antigen]] presentation by [[Dendritic cell|dendritic]] cells to [[Naive T cell|naive T cells]] which are transformed to [[antigen]]-specific type 2 T helper ([[TH2-cells|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. | * 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. |
Revision as of 21:13, 15 December 2017
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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 esophageal function contribute to increased acid exposure due to impaired clearance of reflux 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 esophageal epithelium more susceptible to caustic injury by reflux 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
- There is a possibility that GERD may cause EoE.
- The pathognomic histological feature of the GERD is dilation 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 leads to the penetration of allergens that may have been swallowed into the sub-epithelial space, which may 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.