Eosinophilic esophagitis causes: Difference between revisions
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*The causes of [[Eosinophilic esophagitis|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="pmid1">{{cite journal |vauthors=Makar AB, McMartin KE, Palese M, Tephly TR, Famaey JP, Colinet E |title=Formate assay in body fluids: application in methanol poisoning |journal=Biochem Med |volume=13 |issue=2 |pages=117–26 |year=1975 |pmid=1 |doi= |url=}}</ref><ref name="pmid1">{{cite journal |vauthors=Makar AB, McMartin KE, Palese M, Tephly TR, Makar AB, McMartin KE, Palese M, Tephly TR, Makar AB, McMartin KE, Palese M, Tephly TR, Bose KS, Sarma RH, Chow YW, Pietranico R, Mukerji A, Alekseeva IG, Lapina GP, Tulovskaia ZD, Izmaĭlova VN, Smith RJ, Bryant RG, Hendrickson WA, Ward KB, Marniemi J, Parkki MG, Smith RJ, Bryant RG, Wiesmann UN, DiDonato S, Herschkowitz NN, Bose KS, Sarma RH, Hendrickson WA, Ward KB, Thornton JA, Harrison MJ, Chow YW, Pietranico R, Mukerji A, Makar AB, McMartin KE, Palese M, Tephly TR, Maneksha S, Harry TV, Bose KS, Sarma RH, Gulyassy PF, Farrand JR, Gugler HD, Orskov ER, Fraser C, Thornton JA, Harrison MJ, Bose KS, Sarma RH, Maneksha S, Harry TV, Bose KS, Sarma RH, Galliard T, Phillips DR, Matthew JA, Ivanov IuG, Andonian MR, Barrett AS, Vinogradov SN, Bose KS, Sarma RH, Gulyassy PF, Farrand JR, Gugler HD, Orskov ER, Fraser C, Jansen AH, Russell BJ, Chernick V, James NT, Meek GA, Sturges S, Brown M, Sanner T |title=Formate assay in body fluids: application in methanol poisoning |journal=Biochem Med |volume=13 |issue=2 |pages=117–26 |year=1975 |pmid=1 |doi= |url=}}</ref><ref name="pmid1">{{cite journal |vauthors=Makar AB, McMartin KE, Palese M, Tephly TR, Cianferoni A, Spergel J |title=Formate assay in body fluids: application in methanol poisoning |journal=Biochem Med |volume=13 |issue=2 |pages=117–26 |year=1975 |pmid=1 |doi=10.1007/s12016-015-8501-z |url=}}</ref><ref name="pmid1">{{cite journal |vauthors=Makar AB, McMartin KE, Palese M, Tephly TR, Kusunose H, Ohara S |title=Formate assay in body fluids: application in methanol poisoning |journal=Biochem Med |volume=13 |issue=2 |pages=117–26 |year=1975 |pmid=1 |doi= |url=}}</ref><ref name="pmid1">{{cite journal |vauthors=Makar AB, McMartin KE, Palese M, Tephly TR, Liacouras CA, Furuta GT, Hirano I, Atkins D, Attwood SE, Bonis PA, Burks AW, Chehade M, Collins MH, Dellon ES, Dohil R, Falk GW, Gonsalves N, Gupta SK, Katzka DA, Lucendo AJ, Markowitz JE, Noel RJ, Odze RD, Putnam PE, Richter JE, Romero Y, Ruchelli E, Sampson HA, Schoepfer A, Shaheen NJ, Sicherer SH, Spechler S, Spergel JM, Straumann A, Wershil BK, Rothenberg ME, Aceves SS |title=Formate assay in body fluids: application in methanol poisoning |journal=Biochem Med |volume=13 |issue=2 |pages=117–26 |year=1975 |pmid=1 |doi=10.1016/j.jaci.2011.02.040 |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]]. | ||
Revision as of 21:31, 16 December 2017
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Overview
Causes
- The causes of EoE are as follows:[1][1][1][1][1][1]
- 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.