Eosinophilic esophagitis causes: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Eosinophilic esophagitis}} | {{Eosinophilic esophagitis}} | ||
{{CMG}};{{AE}}{{Ajay}} | |||
==Overview== | ==Overview== | ||
The causes of [[Eosinophilic esophagitis|EoE]] are 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]]. | |||
==Causes== | ==Causes== | ||
*The causes of EoE are as follows: | *The causes of [[Eosinophilic esophagitis|EoE]] are as follows:<ref name="pmid1">{{cite journal |vauthors=Makar AB, McMartin KE, Palese M, Tephly TR, Kia L, Hirano I |title=Formate assay in body fluids: application in methanol poisoning |journal=Biochem Med |volume=13 |issue=2 |pages=117–26 |year=1975 |pmid=1 |pmc=4948861 |doi=10.1038/nrgastro.2015.75 |url=}}</ref><ref name="pmid27373195">{{cite journal |vauthors=Savarino EV, Tolone S, Bartolo O, de Cassan C, Caccaro R, Galeazzi F, Nicoletti L, Salvador R, Martinato M, Costantini M, Savarino V |title=The GerdQ questionnaire and high resolution manometry support the hypothesis that proton pump inhibitor-responsive oesophageal eosinophilia is a GERD-related phenomenon |journal=Aliment. Pharmacol. Ther. |volume=44 |issue=5 |pages=522–30 |year=2016 |pmid=27373195 |doi=10.1111/apt.13718 |url=}}</ref><ref name="pmid23797116">{{cite journal |vauthors=Straumann A |title=Eosinophilic esophagitis: a bulk of mysteries |journal=Dig Dis |volume=31 |issue=1 |pages=6–9 |year=2013 |pmid=23797116 |doi=10.1159/000347095 |url=}}</ref><ref name="pmid22307811">{{cite journal |vauthors=Straumann A |title=Eosinophilic esophagitis: rapidly emerging disorder |journal=Swiss Med Wkly |volume=142 |issue= |pages=w13513 |year=2012 |pmid=22307811 |doi=10.4414/smw.2012.13513 |url=}}</ref><ref name="pmid21429051">{{cite journal |vauthors=Schoepfer AM, Simon D, Straumann A |title=Eosinophilic oesophagitis: latest intelligence |journal=Clin. Exp. Allergy |volume=41 |issue=5 |pages=630–9 |year=2011 |pmid=21429051 |doi=10.1111/j.1365-2222.2011.03739.x |url=}}</ref><ref name="pmid21987875">{{cite journal |vauthors=Godat S, Moradpour D, Schoepfer A |title=[Eosinophilic esophagitis: update 2011] |language=French |journal=Rev Med Suisse |volume=7 |issue=307 |pages=1678–80, 1682 |year=2011 |pmid=21987875 |doi= |url=}}</ref><ref name="pmid14997131">{{cite journal |vauthors=Potter JW, Saeian K, Staff D, Massey BT, Komorowski RA, Shaker R, Hogan WJ |title=Eosinophilic esophagitis in adults: an emerging problem with unique esophageal features |journal=Gastrointest. Endosc. |volume=59 |issue=3 |pages=355–61 |year=2004 |pmid=14997131 |doi= |url=}}</ref> | ||
*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''' | ||
* | * There is a possibility that [[GERD]] may cause EoE. | ||
* The pathognomic [[histological]] feature of the [[Gastroesophageal reflux disease|GERD]] is [[Dilation| | * 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]] | * 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. | ||
Latest revision as of 19:27, 19 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ajay Gade MD[2]]
Overview
The causes of EoE are 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.
Causes
- The causes of EoE are as follows:[1][2][3][4][5][6][7]
- 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.
References
- ↑ Makar AB, McMartin KE, Palese M, Tephly TR, Kia L, Hirano I (1975). "Formate assay in body fluids: application in methanol poisoning". Biochem Med. 13 (2): 117–26. doi:10.1038/nrgastro.2015.75. PMC 4948861. PMID 1.
- ↑ Savarino EV, Tolone S, Bartolo O, de Cassan C, Caccaro R, Galeazzi F, Nicoletti L, Salvador R, Martinato M, Costantini M, Savarino V (2016). "The GerdQ questionnaire and high resolution manometry support the hypothesis that proton pump inhibitor-responsive oesophageal eosinophilia is a GERD-related phenomenon". Aliment. Pharmacol. Ther. 44 (5): 522–30. doi:10.1111/apt.13718. PMID 27373195.
- ↑ Straumann A (2013). "Eosinophilic esophagitis: a bulk of mysteries". Dig Dis. 31 (1): 6–9. doi:10.1159/000347095. PMID 23797116.
- ↑ Straumann A (2012). "Eosinophilic esophagitis: rapidly emerging disorder". Swiss Med Wkly. 142: w13513. doi:10.4414/smw.2012.13513. PMID 22307811.
- ↑ Schoepfer AM, Simon D, Straumann A (2011). "Eosinophilic oesophagitis: latest intelligence". Clin. Exp. Allergy. 41 (5): 630–9. doi:10.1111/j.1365-2222.2011.03739.x. PMID 21429051.
- ↑ Godat S, Moradpour D, Schoepfer A (2011). "[Eosinophilic esophagitis: update 2011]". Rev Med Suisse (in French). 7 (307): 1678–80, 1682. PMID 21987875.
- ↑ Potter JW, Saeian K, Staff D, Massey BT, Komorowski RA, Shaker R, Hogan WJ (2004). "Eosinophilic esophagitis in adults: an emerging problem with unique esophageal features". Gastrointest. Endosc. 59 (3): 355–61. PMID 14997131.