Eosinophilic esophagitis natural history: Difference between revisions
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{{Eosinophilic esophagitis}} | {{Eosinophilic esophagitis}} | ||
{{CMG}};{{AE}}{{Ajay}} | |||
==Overview== | ==Overview== | ||
In patients with [[EoE]], symptoms persist over years raising suspicion that a [[Chronic (medical)|chronic]] [[inflammatory process]] is an underlying event responsible for it. The [[Inflammation|inflammatory]] activity is proportional to the density of the [[eosinophilic]] infiltration in the [[esophageal]] tissue. Similar to [[asthma]], [[Eosinophilic esophagitis|EoE]] has [[Chronic (medical)|chronic]] persistent [[eosinophilic]] [[inflammation]] and can eventually lead to [[irreversible]] structural changes of the [[esophagus]] which is called re-modeling of the [[esophagus]]. The [[esophageal]] [[Mucosal|mucosa]] in patients with a longstanding [[EoE]] is characterized by a loss of elasticity. On [[Histology|histologic]] examination of the subepithelial compartments of the [[esophagus]] show an increase in the [[fibrous tissue]]. The endosonographic studies of the [[esophagus]] in patients with [[Eosinophilic esophagitis|EoE]] shows following findings: Thickening of the [[Mucosal|mucosa]], Thickening of the [[Submucosa|submucosal]], and muscularis propria layers. In patients with [[EoE]], the [[Chronic (medical)|chronic]] [[eosinophilic]] inflammation leads to an increased deposition of the [[fibrous connective tissue]] which in turn causes the remodeling of the esophagus hindering the [[esophageal]] transport. | In patients with [[EoE]], symptoms persist over years raising suspicion that a [[Chronic (medical)|chronic]] [[inflammatory process]] is an underlying event responsible for it. The [[Inflammation|inflammatory]] activity is proportional to the density of the [[eosinophilic]] infiltration in the [[esophageal]] tissue. Similar to [[asthma]], [[Eosinophilic esophagitis|EoE]] has [[Chronic (medical)|chronic]] persistent [[eosinophilic]] [[inflammation]] and can eventually lead to [[irreversible]] structural changes of the [[esophagus]] which is called re-modeling of the [[esophagus]]. The [[esophageal]] [[Mucosal|mucosa]] in patients with a longstanding [[EoE]] is characterized by a loss of elasticity. On [[Histology|histologic]] examination of the subepithelial compartments of the [[esophagus]] show an increase in the [[fibrous tissue]]. The endosonographic studies of the [[esophagus]] in patients with [[Eosinophilic esophagitis|EoE]] shows following findings: Thickening of the [[Mucosal|mucosa]], Thickening of the [[Submucosa|submucosal]], and muscularis propria layers. In patients with [[EoE]], the [[Chronic (medical)|chronic]] [[eosinophilic]] inflammation leads to an increased deposition of the [[fibrous connective tissue]] which in turn causes the remodeling of the esophagus hindering the [[esophageal]] transport. The [[complications]] of the [[EoE]] are as follows [[Scarring]] of [[esophagus]]-leading to [[dysphagia]], [[Esophageal]] [[stenosis]]- causing food stuck. [[Tears]] or [[perforation]] during the [[endoscopy]] or [[retching]] leading to [[boerhaave syndrome]]. The prognosis of the EoE is as follows: [[Eosinophilic esophagitis|EoE]] is a relatively newly recognized disease, there is very limited data on the [[causes]], [[Natural history of disease|natural history]], [[prognosis]], [[diagnosis]] and management of these patients. The long-term [[prognosis]] of the [[Eosinophilic esophagitis|EoE]] is unclear but patients [[Diagnose|diagnosed]] with [[Eosinophilic esophagitis|EoE]] have an unaffected [[lifespan]]. Patients should be [[Counseling|counseled]] that although it is a [[Chronic (medical)|chronic]] [[disease]], it is a [[benign]] condition. Patients who are untreated or have discontinued the treatment have progression of their symptoms. The [[EoE]] patients with a narrow [[esophageal]] [[lumen]] are resistant to the [[corticosteroid]] treatment and require many [[esophageal]] [[Endoscopy|endoscopic]] [[Procedure|procedures]]. The [[dysphagia]] is common in patients with increased [[eosinophil]] count in the [[blood]]. The [[Eosinophilic esophagitis|EoE]] is restricted only to the [[esophagus]] sparing the [[stomach]] and the [[duodenum]]. A common concern by patient and their families is what is the chance of that [[Eosinophilic esophagitis|EoE]] may progress to a [[malignancy]] if untreated, [[Eosinophilic esophagitis|EoE]] does not progress into [[metaplasia]] or [[dysplasia]] or [[esophageal cancer]]. | ||
==Natural History== | ==Natural History== | ||
*The natural course of primary | *The natural course of primary EoE is as follows:<ref name="pmid24813509">{{cite journal |vauthors=Attwood SE, Furuta GT |title=Eosinophilic esophagitis: historical perspective on an evolving disease |journal=Gastroenterol. Clin. North Am. |volume=43 |issue=2 |pages=185–99 |year=2014 |pmid=24813509 |pmc=4035232 |doi=10.1016/j.gtc.2014.02.010 |url=}}</ref><ref name="pmid28774845">{{cite journal |vauthors=Dellon ES, Hirano I |title=Epidemiology and Natural History of Eosinophilic Esophagitis |journal=Gastroenterology |volume= |issue= |pages= |year=2017 |pmid=28774845 |doi=10.1053/j.gastro.2017.06.067 |url=}}</ref><ref name="pmid24813512">{{cite journal |vauthors=Falk GW |title=Clinical presentation of eosinophilic esophagitis in adults |journal=Gastroenterol. Clin. North Am. |volume=43 |issue=2 |pages=231–42 |year=2014 |pmid=24813512 |doi=10.1016/j.gtc.2014.02.009 |url=}}</ref> | ||
*In patients with | *In patients with EoE, symptoms persist over years raising suspicion that a [[Chronic (medical)|chronic]] [[inflammatory process]] is an underlying event responsible for it. | ||
*The [[Inflammation|inflammatory]] activity is proportional to the density of the [[eosinophilic]] infiltration in the [[esophageal]] tissue. | *The [[Inflammation|inflammatory]] activity is proportional to the density of the [[eosinophilic]] infiltration in the [[esophageal]] tissue. | ||
*Similar to [[asthma]], | *Similar to [[asthma]], EoE has [[Chronic (medical)|chronic]] persistent [[eosinophilic]] [[inflammation]] and can eventually lead to [[irreversible]] structural changes of the [[esophagus]] which is called remodeling of the [[esophagus]]. | ||
*The [[esophageal]] [[Mucosal|mucosa]] in patients with a longstanding | *The [[esophageal]] [[Mucosal|mucosa]] in patients with a longstanding EoE is characterized by loss of elasticity. | ||
* | *[[Histology|Histologic]] examination of the subepithelial compartments of the [[esophagus]] shows an increase in the [[fibrous tissue]]. | ||
*The endosonographic studies of the [[esophagus]] in patients with | *The endosonographic studies of the [[esophagus]] in patients with EoE shows following findings: | ||
**Thickening of the [[Mucosal|mucosa]] | **Thickening of the [[Mucosal|mucosa]] | ||
**Thickening of the [[Submucosa|submucosal]], and muscularis propria layers | **Thickening of the [[Submucosa|submucosal]], and [[Muscularis|muscularis propria]] layers | ||
*In patients with | *In patients with EoE, the [[Chronic (medical)|chronic]] [[eosinophilic]] inflammation leads to an increased deposition of the [[fibrous connective tissue]] which in turn causes the remodeling of the esophagus hindering the [[esophageal]] transport. | ||
==Complications== | ==Complications== | ||
*The [[complications]] of the | *The [[complications]] of the EoE are as follows:<ref name="pmid22040638">{{cite journal |vauthors=Straumann A |title=The natural history and complications of eosinophilic esophagitis |journal=Thorac Surg Clin |volume=21 |issue=4 |pages=575–87 |year=2011 |pmid=22040638 |doi=10.1016/j.thorsurg.2011.09.004 |url=}}</ref><ref name="pmid24117638">{{cite journal |vauthors=Chehade M, Lucendo AJ, Achem SR, Souza RF |title=Causes, evaluation, and consequences of eosinophilic esophagitis |journal=Ann. N. Y. Acad. Sci. |volume=1300 |issue= |pages=110–8 |year=2013 |pmid=24117638 |doi=10.1111/nyas.12243 |url=}}</ref><ref name="pmid23891531">{{cite journal |vauthors=Saillen E, Cellier C, Naneix AL, Canioni D, Bruneval P, Pouchot J, Georgin-Lavialle S |title=[Eosinophilic esophagitis] |language=French |journal=Presse Med |volume=43 |issue=1 |pages=34–8 |year=2014 |pmid=23891531 |doi=10.1016/j.lpm.2013.03.012 |url=}}</ref> | ||
*[[Scarring]] of [[esophagus]] | *[[Scarring]] of [[esophagus]] leading to [[dysphagia]] | ||
*[[Esophageal]] [[stenosis]] | *[[Esophageal]] [[stenosis]] | ||
*[[Tears]] or [[perforation]] during the [[endoscopy]] or [[retching]] leading to [[boerhaave syndrome]]. | *[[Tears]] or [[perforation]] during the [[endoscopy]] or [[retching]] leading to [[boerhaave syndrome]]. | ||
==Prognosis== | ==Prognosis== | ||
*The prognosis of the EoE is as follows:<ref name="pmid23567357">{{cite journal |vauthors=Dellon ES, Gonsalves N, Hirano I, Furuta GT, Liacouras CA, Katzka DA |title=ACG clinical guideline: Evidence-based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE) |journal=Am. J. Gastroenterol. |volume=108 |issue=5 |pages=679–92; quiz 693 |year=2013 |pmid=23567357 |doi=10.1038/ajg.2013.71 |url=}}</ref><ref name="pmid24703087">{{cite journal |vauthors=Lipka S, Keshishian J, Boyce HW, Estores D, Richter JE |title=The natural history of steroid-naïve eosinophilic esophagitis in adults treated with endoscopic dilation and proton pump inhibitor therapy over a mean duration of nearly 14 years |journal=Gastrointest. Endosc. |volume=80 |issue=4 |pages=592–8 |year=2014 |pmid=24703087 |doi=10.1016/j.gie.2014.02.012 |url=}}</ref><ref name="pmid26608127">{{cite journal |vauthors=Eluri S, Runge TM, Cotton CC, Burk CM, Wolf WA, Woosley JT, Shaheen NJ, Dellon ES |title=The extremely narrow-caliber esophagus is a treatment-resistant subphenotype of eosinophilic esophagitis |journal=Gastrointest. Endosc. |volume=83 |issue=6 |pages=1142–8 |year=2016 |pmid=26608127 |doi=10.1016/j.gie.2015.11.019 |url=}}</ref><ref name="pmid14724818">{{cite journal |vauthors=Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU |title=Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years |journal=Gastroenterology |volume=125 |issue=6 |pages=1660–9 |year=2003 |pmid=14724818 |doi= |url=}}</ref><ref name="pmid19172120">{{cite journal |vauthors=Spergel JM, Brown-Whitehorn TF, Beausoleil JL, Franciosi J, Shuker M, Verma R, Liacouras CA |title=14 years of eosinophilic esophagitis: clinical features and prognosis |journal=J. Pediatr. Gastroenterol. Nutr. |volume=48 |issue=1 |pages=30–6 |year=2009 |pmid=19172120 |doi=10.1097/MPG.0b013e3181788282 |url=}}</ref> | *The prognosis of the EoE is as follows:<ref name="pmid23567357">{{cite journal |vauthors=Dellon ES, Gonsalves N, Hirano I, Furuta GT, Liacouras CA, Katzka DA |title=ACG clinical guideline: Evidence-based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE) |journal=Am. J. Gastroenterol. |volume=108 |issue=5 |pages=679–92; quiz 693 |year=2013 |pmid=23567357 |doi=10.1038/ajg.2013.71 |url=}}</ref><ref name="pmid24703087">{{cite journal |vauthors=Lipka S, Keshishian J, Boyce HW, Estores D, Richter JE |title=The natural history of steroid-naïve eosinophilic esophagitis in adults treated with endoscopic dilation and proton pump inhibitor therapy over a mean duration of nearly 14 years |journal=Gastrointest. Endosc. |volume=80 |issue=4 |pages=592–8 |year=2014 |pmid=24703087 |doi=10.1016/j.gie.2014.02.012 |url=}}</ref><ref name="pmid26608127">{{cite journal |vauthors=Eluri S, Runge TM, Cotton CC, Burk CM, Wolf WA, Woosley JT, Shaheen NJ, Dellon ES |title=The extremely narrow-caliber esophagus is a treatment-resistant subphenotype of eosinophilic esophagitis |journal=Gastrointest. Endosc. |volume=83 |issue=6 |pages=1142–8 |year=2016 |pmid=26608127 |doi=10.1016/j.gie.2015.11.019 |url=}}</ref><ref name="pmid14724818">{{cite journal |vauthors=Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU |title=Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years |journal=Gastroenterology |volume=125 |issue=6 |pages=1660–9 |year=2003 |pmid=14724818 |doi= |url=}}</ref><ref name="pmid19172120">{{cite journal |vauthors=Spergel JM, Brown-Whitehorn TF, Beausoleil JL, Franciosi J, Shuker M, Verma R, Liacouras CA |title=14 years of eosinophilic esophagitis: clinical features and prognosis |journal=J. Pediatr. Gastroenterol. Nutr. |volume=48 |issue=1 |pages=30–6 |year=2009 |pmid=19172120 |doi=10.1097/MPG.0b013e3181788282 |url=}}</ref> | ||
* | *EoE is a relatively newly recognized disease, there is very limited data on the [[causes]], [[Natural history of disease|natural history]], [[prognosis]], [[diagnosis]] and management of these patients. | ||
*The long-term [[prognosis]] of | *The long-term [[prognosis]] of EoE is unclear but patients [[Diagnose|diagnosed]] with EoE have an unaffected [[lifespan]]. | ||
*Patients should be [[Counseling|counseled]] that although it is a [[Chronic (medical)|chronic]] [[disease]], it is a [[benign]] condition. | *Patients should be [[Counseling|counseled]] that although it is a [[Chronic (medical)|chronic]] [[disease]], it is a [[benign]] condition. | ||
*Patients who are untreated or have discontinued the treatment have progression of their symptoms. | *Patients who are untreated or have discontinued the treatment have progression of their symptoms. | ||
* | *EoE patients with a narrow [[esophageal]] [[lumen]] are resistant to the [[corticosteroid]] treatment and require many [[esophageal]] [[Endoscopy|endoscopic]] [[Procedure|procedures]].. | ||
* | *[[dysphagia]] is common in patients with increased [[eosinophil]] count in the [[blood]]. | ||
* | *EoE is restricted only to the [[esophagus]] sparing the [[stomach]] and the [[duodenum]]. | ||
* | *EoE does not progress into [[metaplasia]] or [[dysplasia]] or [[esophageal cancer]]. | ||
==References== | ==References== | ||
Latest revision as of 22:20, 19 December 2017
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Eosinophilic esophagitis natural history On the Web |
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Risk calculators and risk factors for Eosinophilic esophagitis natural history |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ajay Gade MD[2]]
Overview
In patients with EoE, symptoms persist over years raising suspicion that a chronic inflammatory process is an underlying event responsible for it. The inflammatory activity is proportional to the density of the eosinophilic infiltration in the esophageal tissue. Similar to asthma, EoE has chronic persistent eosinophilic inflammation and can eventually lead to irreversible structural changes of the esophagus which is called re-modeling of the esophagus. The esophageal mucosa in patients with a longstanding EoE is characterized by a loss of elasticity. On histologic examination of the subepithelial compartments of the esophagus show an increase in the fibrous tissue. The endosonographic studies of the esophagus in patients with EoE shows following findings: Thickening of the mucosa, Thickening of the submucosal, and muscularis propria layers. In patients with EoE, the chronic eosinophilic inflammation leads to an increased deposition of the fibrous connective tissue which in turn causes the remodeling of the esophagus hindering the esophageal transport. The complications of the EoE are as follows Scarring of esophagus-leading to dysphagia, Esophageal stenosis- causing food stuck. Tears or perforation during the endoscopy or retching leading to boerhaave syndrome. The prognosis of the EoE is as follows: EoE is a relatively newly recognized disease, there is very limited data on the causes, natural history, prognosis, diagnosis and management of these patients. The long-term prognosis of the EoE is unclear but patients diagnosed with EoE have an unaffected lifespan. Patients should be counseled that although it is a chronic disease, it is a benign condition. Patients who are untreated or have discontinued the treatment have progression of their symptoms. The EoE patients with a narrow esophageal lumen are resistant to the corticosteroid treatment and require many esophageal endoscopic procedures. The dysphagia is common in patients with increased eosinophil count in the blood. The EoE is restricted only to the esophagus sparing the stomach and the duodenum. A common concern by patient and their families is what is the chance of that EoE may progress to a malignancy if untreated, EoE does not progress into metaplasia or dysplasia or esophageal cancer.
Natural History
- The natural course of primary EoE is as follows:[1][2][3]
- In patients with EoE, symptoms persist over years raising suspicion that a chronic inflammatory process is an underlying event responsible for it.
- The inflammatory activity is proportional to the density of the eosinophilic infiltration in the esophageal tissue.
- Similar to asthma, EoE has chronic persistent eosinophilic inflammation and can eventually lead to irreversible structural changes of the esophagus which is called remodeling of the esophagus.
- The esophageal mucosa in patients with a longstanding EoE is characterized by loss of elasticity.
- Histologic examination of the subepithelial compartments of the esophagus shows an increase in the fibrous tissue.
- The endosonographic studies of the esophagus in patients with EoE shows following findings:
- Thickening of the mucosa
- Thickening of the submucosal, and muscularis propria layers
- In patients with EoE, the chronic eosinophilic inflammation leads to an increased deposition of the fibrous connective tissue which in turn causes the remodeling of the esophagus hindering the esophageal transport.
Complications
- The complications of the EoE are as follows:[4][5][6]
- Scarring of esophagus leading to dysphagia
- Esophageal stenosis
- Tears or perforation during the endoscopy or retching leading to boerhaave syndrome.
Prognosis
- The prognosis of the EoE is as follows:[7][8][9][10][11]
- EoE is a relatively newly recognized disease, there is very limited data on the causes, natural history, prognosis, diagnosis and management of these patients.
- The long-term prognosis of EoE is unclear but patients diagnosed with EoE have an unaffected lifespan.
- Patients should be counseled that although it is a chronic disease, it is a benign condition.
- Patients who are untreated or have discontinued the treatment have progression of their symptoms.
- EoE patients with a narrow esophageal lumen are resistant to the corticosteroid treatment and require many esophageal endoscopic procedures..
- dysphagia is common in patients with increased eosinophil count in the blood.
- EoE is restricted only to the esophagus sparing the stomach and the duodenum.
- EoE does not progress into metaplasia or dysplasia or esophageal cancer.
References
- ↑ Attwood SE, Furuta GT (2014). "Eosinophilic esophagitis: historical perspective on an evolving disease". Gastroenterol. Clin. North Am. 43 (2): 185–99. doi:10.1016/j.gtc.2014.02.010. PMC 4035232. PMID 24813509.
- ↑ Dellon ES, Hirano I (2017). "Epidemiology and Natural History of Eosinophilic Esophagitis". Gastroenterology. doi:10.1053/j.gastro.2017.06.067. PMID 28774845.
- ↑ Falk GW (2014). "Clinical presentation of eosinophilic esophagitis in adults". Gastroenterol. Clin. North Am. 43 (2): 231–42. doi:10.1016/j.gtc.2014.02.009. PMID 24813512.
- ↑ Straumann A (2011). "The natural history and complications of eosinophilic esophagitis". Thorac Surg Clin. 21 (4): 575–87. doi:10.1016/j.thorsurg.2011.09.004. PMID 22040638.
- ↑ Chehade M, Lucendo AJ, Achem SR, Souza RF (2013). "Causes, evaluation, and consequences of eosinophilic esophagitis". Ann. N. Y. Acad. Sci. 1300: 110–8. doi:10.1111/nyas.12243. PMID 24117638.
- ↑ Saillen E, Cellier C, Naneix AL, Canioni D, Bruneval P, Pouchot J, Georgin-Lavialle S (2014). "[Eosinophilic esophagitis]". Presse Med (in French). 43 (1): 34–8. doi:10.1016/j.lpm.2013.03.012. PMID 23891531.
- ↑ Dellon ES, Gonsalves N, Hirano I, Furuta GT, Liacouras CA, Katzka DA (2013). "ACG clinical guideline: Evidence-based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE)". Am. J. Gastroenterol. 108 (5): 679–92, quiz 693. doi:10.1038/ajg.2013.71. PMID 23567357.
- ↑ Lipka S, Keshishian J, Boyce HW, Estores D, Richter JE (2014). "The natural history of steroid-naïve eosinophilic esophagitis in adults treated with endoscopic dilation and proton pump inhibitor therapy over a mean duration of nearly 14 years". Gastrointest. Endosc. 80 (4): 592–8. doi:10.1016/j.gie.2014.02.012. PMID 24703087.
- ↑ Eluri S, Runge TM, Cotton CC, Burk CM, Wolf WA, Woosley JT, Shaheen NJ, Dellon ES (2016). "The extremely narrow-caliber esophagus is a treatment-resistant subphenotype of eosinophilic esophagitis". Gastrointest. Endosc. 83 (6): 1142–8. doi:10.1016/j.gie.2015.11.019. PMID 26608127.
- ↑ Straumann A, Spichtin HP, Grize L, Bucher KA, Beglinger C, Simon HU (2003). "Natural history of primary eosinophilic esophagitis: a follow-up of 30 adult patients for up to 11.5 years". Gastroenterology. 125 (6): 1660–9. PMID 14724818.
- ↑ Spergel JM, Brown-Whitehorn TF, Beausoleil JL, Franciosi J, Shuker M, Verma R, Liacouras CA (2009). "14 years of eosinophilic esophagitis: clinical features and prognosis". J. Pediatr. Gastroenterol. Nutr. 48 (1): 30–6. doi:10.1097/MPG.0b013e3181788282. PMID 19172120.