Eosinophilic esophagitis causes: Difference between revisions
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==Causes== | ==Causes== | ||
*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="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=27373195a |doi=10.1111/apt.13718 |url=}}</ref> | *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="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=27373195a |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> | ||
*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]]. | ||
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Overview
Causes
- The causes of EoE are as follows:[1][2][2][3]
- 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.
- ↑ 2.0 2.1 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.