Esophagitis pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
=== Normal physiology of the food motility through the esophagus ===
* The [[esophagus]] is a part of the [[gastrointestinal tract]] which is responsible of moving [[Food|the food]] from the [[mouth]] to the [[rectum]].<ref name="pmid1606845">{{cite journal| author=Stein HJ, DeMeester TR| title=Outpatient physiologic testing and surgical management of foregut motility disorders. | journal=Curr Probl Surg | year= 1992 | volume= 29 | issue= 7 | pages= 413-555 | pmid=1606845 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1606845  }}</ref>
* The esophagus has anti-reflux barrier which prevents the return of the [[acidic]] contentof the [[stomach]] back to the [[esophagus]]. The anti-reflux barrier consists of the [[lower esophageal sphincter]] (LES) and the related part of the [[diaphragm]]. 
* The [[lower esophageal sphincter]] is contracting [[smooth muscle]] at the end of the [[esophagus]] responsible for the food passage to the [[stomach]]. LES has high pressure tone which helps keeping it a strong barrier between the [[esophagus]] and the [[stomach]].
[[Image:GERD.png|350px|thumb|center|Source by:BruceBlaus - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=44923646|]]
 
===Reflux Esophagitis===
* Pathogenesis of GERD depends on various mechanisms that lead to the [[reflux]] of the [[gastric]] [[acidic]] contents into the [[esophagus]].
* Several mechanisms impair the anti-reflux barrier and cause [[esophageal dysmotility]]. These mechanisms include the following:<ref name="pmid11060472">{{cite journal| author=Storr M, Meining A, Allescher HD| title=Pathophysiology and pharmacological treatment of gastroesophageal reflux disease. | journal=Dig Dis | year= 2000 | volume= 18 | issue= 2 | pages= 93-102 | pmid=11060472 | doi=10.1159/000016970 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11060472  }}</ref><ref name="pmid17345925">{{cite journal| author=De Giorgi F, Palmiero M, Esposito I, Mosca F, Cuomo R| title=Pathophysiology of gastro-oesophageal reflux disease. | journal=Acta Otorhinolaryngol Ital | year= 2006 | volume= 26 | issue= 5 | pages= 241-6 | pmid=17345925 | doi= | pmc=2639970 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17345925  }}</ref>
** Transient [[lower esophageal sphincter]] [[Relaxation|relaxations]]
** [[Hypotensive]] [[lower esophageal sphincter]]
** [[Hiatus hernia]]
** Impaired [[esophageal]] [[acid]] clearance
** [[Delayed gastric emptying]] 
==== Transient lower esophageal sphincter relaxations ====
* Transient [[lower esophageal sphincter]] relaxations is considered the main mechanism of GERD development in most of the patients. It occurs alongside a normal LES and more common with [[obesity]]. <ref name="pmid10573376">{{cite journal| author=Fisher BL, Pennathur A, Mutnick JL, Little AG| title=Obesity correlates with gastroesophageal reflux. | journal=Dig Dis Sci | year= 1999 | volume= 44 | issue= 11 | pages= 2290-4 | pmid=10573376 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10573376  }}</ref>
* Distension of the [[stomach]] worsens the case of transient lower esophageal sphincter relaxation. The diaphragm is also affected by the [[sphincter]] relaxation leading to [[diaphragm]] [[inhibition]]. <ref name="pmid10734020">{{cite journal| author=Kahrilas PJ, Shi G, Manka M, Joehl RJ| title=Increased frequency of transient lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia. | journal=Gastroenterology | year= 2000 | volume= 118 | issue= 4 | pages= 688-95 | pmid=10734020 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10734020  }}</ref>
* Some of the GERD patients have [[hypotensive]] [[lower esophageal sphincter]] which leads to retrograde movement of the [[gastric]] content into the [[esophagus]].
==== Hiatal hernia  ====
* A [[Hiatus hernia|hiatal hernia]] occurs as part of the [[stomach]] is dislocated into the [[chest]]. This [[Dislocations|dislocation]] leads to placement of the LES above the [[diaphragm]] impairing the [[acid]] [[Clearance (medicine)|clearance]].<ref name="pmid10443906">{{cite journal| author=Richter J| title=Do we know the cause of reflux disease? | journal=Eur J Gastroenterol Hepatol | year= 1999 | volume= 11 Suppl 1 | issue=  | pages= S3-9 | pmid=10443906 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10443906  }}</ref>
* Increase the exposure of the [[Esophagus|lower esophagus]] due to a [[hiatal hernia]] plays a big role in the pathogenesis of GERD.
==== Impaired mucosal resistance ====
* The [[esophagus]] has pre-[[epithelial]] and [[epithelial]] defensive mechanisms against the [[acidic]] components that can lead to [[esophageal]] [[injury]]. However, these defensive mechanisms are limited and weak to stand against injury in case of excessive acid exposure.
* In case of an excessive increase of the [[noxious]] agents more than the ability of the [[mucosal]] defensive mechanism to eliminate them, [[mucosal]] [[injury]] occurs and GERD develops.
* The [[gastric acid]] leads to erosion of the [[esophageal]] [[Mucosal|mucosa]] and destruction of the intercellular junctions which leads to increase cellular permeability. The increase in the cellular permeability is proved by the [[dilation]] of the intercellular spaces and explains the typical symptoms (e.g, [[heartburn]]) of GERD.
==Associated Conditions==
The most important conditions and diseases associated with GERD include the following: <ref>{{cite journal |author=Morse CA, Quan SF, Mays MZ, Green C, Stephen G, Fass R |title=Is there a relationship between obstructive sleep apnea and gastroesophageal reflux disease? |journal=Clin. Gastroenterol. Hepatol. |volume=2 |issue=9 |pages=761–8 |year=2004 |pmid=15354276 |doi=}}</ref><ref name="pmid17198758">{{cite journal| author=Kasasbeh A, Kasasbeh E, Krishnaswamy G| title=Potential mechanisms connecting asthma, esophageal reflux, and obesity/sleep apnea complex--a hypothetical review. | journal=Sleep Med Rev | year= 2007 | volume= 11 | issue= 1 | pages= 47-58 | pmid=17198758 | doi=10.1016/j.smrv.2006.05.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17198758  }}</ref>
* [[laryngitis]]
* Chronic [[cough]]
* [[pulmonary fibrosis]]
* [[earache]]
* [[asthma]]
* [[sleep apnea|Obstructive sleep apnea]]
===Eosinophilic Esophagitis===
* The [[pathophysiology]] of the EoE is as follows:<ref name="pmid25499460">{{cite journal |vauthors=Malhotra N, Levine J |title=Eosinophilic esophagitis: an autoimmune esophageal disorder |journal=Curr Probl Pediatr Adolesc Health Care |volume=44 |issue=11 |pages=335–40 |year=2014 |pmid=25499460 |doi=10.1016/j.cppeds.2014.10.004 |url=}}</ref><ref name="pmid26051952">{{cite journal |vauthors=Martin LJ, Franciosi JP, Collins MH, Abonia JP, Lee JJ, Hommel KA, Varni JW, Grotjan JT, Eby M, He H, Marsolo K, Putnam PE, Garza JM, Kaul A, Wen T, Rothenberg ME |title=Pediatric Eosinophilic Esophagitis Symptom Scores (PEESS v2.0) identify histologic and molecular correlates of the key clinical features of disease |journal=J. Allergy Clin. Immunol. |volume=135 |issue=6 |pages=1519–28.e8 |year=2015 |pmid=26051952 |pmc=4460579 |doi=10.1016/j.jaci.2015.03.004 |url=}}</ref><ref name="pmid25216976">{{cite journal |vauthors=Lucendo AJ, Arias A, Tenias JM |title=Relation between eosinophilic esophagitis and oral immunotherapy for food allergy: a systematic review with meta-analysis |journal=Ann. Allergy Asthma Immunol. |volume=113 |issue=6 |pages=624–9 |year=2014 |pmid=25216976 |doi=10.1016/j.anai.2014.08.004 |url=}}</ref><ref name="pmid22939463">{{cite journal |vauthors=López-Colombo A |title=[Eosinophilic esophagitis] |language=Spanish; Castilian |journal=Rev Gastroenterol Mex |volume=77 Suppl 1 |issue= |pages=1–3 |year=2012 |pmid=22939463 |doi=10.1016/j.rgmx.2012.07.002 |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="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>
* [[Eosinophilic esophagitis]] is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens.
* Patients presenting with EoE have a history of:
** Elevated [[serum]] [[Immunoglobulin E|IgE]] levels
** Response to interventions such as diet restriction
** History of food [[hypersensitivity]]
* [[Eosinophils]] originate from CD34+ [[myeloid]] precursor cells in the [[bone marrow]], mature to a granulated state and migrate to the [[vascular]] spaces.
* The [[eosinophils]] are absent in an otherwise normal [[esophagus]], the presence of the [[eosinophils]] in the [[esophagus]] suggests [[GERD]] or EoE.
*They tend to be present in all layers of the [[esophagus]] in EoE, but predominate in the [[lamina propria]] and [[Submucosa|submucosal]] regions.
* The documented [[cytokine]] expression profile in the [[esophageal]] [[tissue]] of patients is that of a [[T helper cell|TH2]] [[inflammatory]] response.
* [[IL-5]] and [[Interleukin 13|IL-13]] are produced by the type-2 helper T cells ([[Th2]]) in response to the [[antigenic]] [[proteins]] from the [[food]] or [[inhalation]].
* [[IL-13]] further stimulates the [[epithelial]] cells of the [[esophagus]] to produce large proteins to induce a gene called eotaxin-3, which in turn recruits [[eosinophils]] from the peripheral blood into the tissue.
* [[IL-5]] prolongs the survival of the [[eosinophils]].
*The activated [[TH2-cells|TH2]] response leads to the recruitment and activation of
** '''[[Eosinophils]]'''
** '''[[Mast cells]]'''
* [[Mast cells]] [[degranulate]] and cause tissue damage and repair.
* [[Cytokines]] produced by TH-1 cells are
** '''[[Tumour necrosis factor|Tumor necrosis factor]] (TNF)-α'''
** '''[[Interferon-gamma|Interferon (IFN)-γ]]'''
* [[TNF-α]] is expressed by the [[epithelial cells]] of the [[esophagus]] whereas [[Interferon-gamma|INF-γ]] is upregulated by the [[Peripheral T cells lymphoma|peripheral T cells.]]
* Delayed or type- IV [[hypersensitivity]] is the mechanism is involved in the EoE.
*It is postulated that the EoE-defining [[endoscopic]] and [[histologic]] manifestations are a culmination of the disease process which, may have debilitating long-term effects including [[strictures]] and food impactions in untreated or poorly managed cases of EoE.
* The preformed [[granule]] [[proteins]] of the [[eosinophils]] are
**'''ECP'''- Eosinophil Cationic Protein
**'''MBP'''- [[Major basic protein|Major Basic Protein]]
**'''EPO'''- Eosinophil [[Peroxidase]]
**'''EDN'''- [[Eosinophil]] Derived [[Neurotoxin]]
* Upon the stimulation and the degranulation, the [[eosinophils]] release the [[granule]] [[proteins]] into the tissues.
* [[Eosinophils]] synthesize and release [[cytokines]] such as
**'''[[Interleukin 5|IL-5]]'''
**'''[[Interleukin 13|IL-13]]'''
**'''[[Transforming growth factor]] [[TGF alpha|(TGF)-α]] and [[TGF beta|-β]]'''
**'''[[Chemokines]] (eotaxins and RANTES)'''
**'''Lipid mediators such as platelet activating factor ([[PAF]]) and [[leukotriene]] C4'''
* [[Interleukin 5|IL-5]], [[IL-13]], and [[granulocyte]]-[[macrophage]] colony stimulating factor ([[GM-CSF]]) can cause the [[maturation]] and migration of the [[eosinophils]].
* [[Eosinophils]] cause [[inflammation]] in the EoE patients by the following mechanisms
** [[Angiogenic]] [[molecules]] from the [[eosinophils]] recruits the [[inflammatory]] [[cells]] and increase the [[vascularity]].
** [[Fibrogenic]] [[Mediator|mediators]] such as [[TGF beta|TGF-β1]] and [[matrix]] [[metalloproteinase]] 9 (MMP)-9 causes the [[airway]] remodeling.
** MBP and MMP-9 disrupt the integrity of the [[epithelial cells]] of the [[esophageal|esophagus]] through their involvement in the [[smooth muscles]], [[fibroblasts]], and [[Cell adhesion molecule|cell-adhesion]] [[molecules]].
** The above-mentioned processes lead to tissue remodeling eventually, causing an overall [[esophageal]] [[Dysfunctional|dysfunction]].
**[[TGF-β]] and [[eosinophilic]] [[granule]] [[proteins]] MBP and EPO are the key [[eosinophil]] [[Effector cell|effector]] [[proteins]]. The importance of [[eosinophils]] in mediating tissue [[fibrosis]] is supported by evidence in both [[murine]] and human models.
**These findings not only highlight the importance of targeting [[fibrosis]] reversal in the treatment of EoE, but also underline the importance of [[eosinophils]] in tissue remodeling.
===Gross Pathology===
*[[Mucosal]] [[biopsies]] of the [[esophagus]] should be obtained in all patients in whom EoE is a clinical possibility regardless of the [[Endoscopy|endoscopic]] appearance.
*[[Endoscopic]] [[abnormalities]] in patients with EoE are as follows:<ref name="urlTable 3: Proposed classification and grading system for the endoscopic assessment of the esophageal features of eosinophilic esophagitis (<a id=ref-link-section-1 title= href=/articles/#ref44">44</a>)">{{cite web |url=https://www.nature.com/articles/ajg201371/tables/3 |title=Table 3: Proposed classification and grading system for the endoscopic assessment of the esophageal features of eosinophilic esophagitis (<a id=ref-link-section-1 title="" href=/articles/#ref44>44</a>) |format= |work= |accessdate=}}</ref><ref name="urlVertical lines in distal esophageal mucosa (VLEM): a true endoscopic manifestation of esophagitis in children? - PubMed - NCBI">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmed/9199905?dopt=Abstract&holding=npg |title=Vertical lines in distal esophageal mucosa (VLEM): a true endoscopic manifestation of esophagitis in children? - PubMed - NCBI |format= |work= |accessdate=}}</ref><ref name="urlFragility of the esophageal mucosa: a pathognomonic endoscopic sign of primary eosinophilic esophagitis? - PubMed - NCBI">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmed/12612531?dopt=Abstract&holding=npg |title=Fragility of the esophageal mucosa: a pathognomonic endoscopic sign of primary eosinophilic esophagitis? - PubMed - NCBI |format= |work= |accessdate=}}</ref><ref name="urlEosinophilic esophagitis: red on microscopy, white on endoscopy. - PubMed - NCBI">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmed/15383737?dopt=Abstract&holding=npg |title=Eosinophilic esophagitis: red on microscopy, white on endoscopy. - PubMed - NCBI |format= |work= |accessdate=}}</ref><ref name="urlThe prevalence and diagnostic utility of endoscopic features of eosinophilic esophagitis: a meta-analysis. - PubMed - NCBI">{{cite web |url=https://www.ncbi.nlm.nih.gov/pubmed/22610003?dopt=Abstract&holding=npg |title=The prevalence and diagnostic utility of endoscopic features of eosinophilic esophagitis: a meta-analysis. - PubMed - NCBI |format= |work= |accessdate=}}</ref>
**Fixed [[esophageal]] ring which is corrugated
**White [[exudate]]
**Longitudinal furrows
**[[Mucous membrane|Mucosal]] [[pallor]]
**[[Diffuse]] [[esophageal]] narrowing
**[[Mucosal]] fragility leading to [[esophageal]] lacerations during the endoscopy
*However, because these [[Endoscopy|endoscopic]] features have been described in other [[esophageal]] [[disorders]], none can be considered [[pathognomonic]] for EoE.
<gallery>
File:Eosinophilic esophagitis endo.jpg|Endoscopy of the esophagus: Eosinophilic esophagitis <br> Source: Wikimedia
</gallery>
===Histopathology===
*Characteristic features are as follows:
**> 20 eosinophils/0.24 mm2.
**Papillae are elongated
**Papillae reach into the top 1/3 of the epithelial layer
**Basal cell hyperplasia; > 3 cells thick or >15% of epithelial thickness
[[Image:Eosinophilic esophagiits path.jpg|thumb|center|150px|[[H&E]] stain of [[esophagus]] [[biopsy]] showing eosinophilic esophagitis, manifested by an infiltration of [[eosinophils]] in the [[lamina propria]]]]
* The most common cause is [[gastroesophageal reflux disease]] ([[GERD]]). If caused by [[GERD]], the diseases is also called [[reflux esophagitis]].  
* The most common cause is [[gastroesophageal reflux disease]] ([[GERD]]). If caused by [[GERD]], the diseases is also called [[reflux esophagitis]].  
* Other causes of [[esophagitis]] include infections (most commonly [[Candida (genus)|candida]], [[herpes simplex]] and [[cytomegalovirus]]). These infections are typically seen in [[immunocompromised]] people, such as those with [[HIV]].
* Other causes of [[esophagitis]] include infections (most commonly [[Candida (genus)|candida]], [[herpes simplex]] and [[cytomegalovirus]]). These infections are typically seen in [[immunocompromised]] people, such as those with [[HIV]].

Revision as of 18:19, 8 January 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

Overview

Pathophysiology

Normal physiology of the food motility through the esophagus

Reflux Esophagitis

Transient lower esophageal sphincter relaxations

  • Transient lower esophageal sphincter relaxations is considered the main mechanism of GERD development in most of the patients. It occurs alongside a normal LES and more common with obesity. [4]
  • Distension of the stomach worsens the case of transient lower esophageal sphincter relaxation. The diaphragm is also affected by the sphincter relaxation leading to diaphragm inhibition. [5]

Hiatal hernia

Impaired mucosal resistance

  • The esophagus has pre-epithelial and epithelial defensive mechanisms against the acidic components that can lead to esophageal injury. However, these defensive mechanisms are limited and weak to stand against injury in case of excessive acid exposure.
  • In case of an excessive increase of the noxious agents more than the ability of the mucosal defensive mechanism to eliminate them, mucosal injury occurs and GERD develops.
  • The gastric acid leads to erosion of the esophageal mucosa and destruction of the intercellular junctions which leads to increase cellular permeability. The increase in the cellular permeability is proved by the dilation of the intercellular spaces and explains the typical symptoms (e.g, heartburn) of GERD.

Associated Conditions

The most important conditions and diseases associated with GERD include the following: [7][8]

Eosinophilic Esophagitis

  • Patients presenting with EoE have a history of:

Gross Pathology

  • Endoscopy of the esophagus: Eosinophilic esophagitis Source: Wikimedia

    Endoscopy of the esophagus: Eosinophilic esophagitis
    Source: Wikimedia


Histopathology

  • Characteristic features are as follows:
    • > 20 eosinophils/0.24 mm2.
    • Papillae are elongated
    • Papillae reach into the top 1/3 of the epithelial layer
    • Basal cell hyperplasia; > 3 cells thick or >15% of epithelial thickness
H&E stain of esophagus biopsy showing eosinophilic esophagitis, manifested by an infiltration of eosinophils in the lamina propria



Pathological Findings

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Gross Images

  • Esophagus: Candida: Gross natural color close up of distal esophagus mucosa, an excellent example of candida esophagitis

    Esophagus: Candida: Gross natural color close up of distal esophagus mucosa, an excellent example of candida esophagitis

  • Esophagitis Candida: Gross natural color close-up, an excellent example

    Esophagitis Candida: Gross natural color close-up, an excellent example

  • Esophagitis Candida: Gross natural color excellent close-up photo case of acute myelomonocytic leukemia

    Esophagitis Candida: Gross natural color excellent close-up photo case of acute myelomonocytic leukemia

  • Necrotizing esophagitis and gastritis, sulfuric acid ingested as suicide attempt

    Necrotizing esophagitis and gastritis, sulfuric acid ingested as suicide attempt

Microscopic Images

  • Herpes esophagitis 100 x

    Herpes esophagitis 100 x

  • Herpes esophagitis 400 x

    Herpes esophagitis 400 x

  • Herpes esophagitis 600 x

    Herpes esophagitis 600 x

  • Reflux esophagitis 100 x

    Reflux esophagitis 100 x

  • Reflux esophagitis 400 x

    Reflux esophagitis 400 x

  • Necrotizing esophagitis and gastritis, sulfuric acid ingested as suicide attempt

    Necrotizing esophagitis and gastritis, sulfuric acid ingested as suicide attempt

Histopathological Findings: Herpes Esophagitis

{{#ev:youtube|bJME-CJvHfs}}

References

  1. ↑ Stein HJ, DeMeester TR (1992). "Outpatient physiologic testing and surgical management of foregut motility disorders". Curr Probl Surg. 29 (7): 413–555. PMID 1606845.
  2. ↑ Storr M, Meining A, Allescher HD (2000). "Pathophysiology and pharmacological treatment of gastroesophageal reflux disease". Dig Dis. 18 (2): 93–102. doi:10.1159/000016970. PMID 11060472.
  3. ↑ De Giorgi F, Palmiero M, Esposito I, Mosca F, Cuomo R (2006). "Pathophysiology of gastro-oesophageal reflux disease". Acta Otorhinolaryngol Ital. 26 (5): 241–6. PMC 2639970. PMID 17345925.
  4. ↑ Fisher BL, Pennathur A, Mutnick JL, Little AG (1999). "Obesity correlates with gastroesophageal reflux". Dig Dis Sci. 44 (11): 2290–4. PMID 10573376.
  5. ↑ Kahrilas PJ, Shi G, Manka M, Joehl RJ (2000). "Increased frequency of transient lower esophageal sphincter relaxation induced by gastric distention in reflux patients with hiatal hernia". Gastroenterology. 118 (4): 688–95. PMID 10734020.
  6. ↑ Richter J (1999). "Do we know the cause of reflux disease?". Eur J Gastroenterol Hepatol. 11 Suppl 1: S3–9. PMID 10443906.
  7. ↑ Morse CA, Quan SF, Mays MZ, Green C, Stephen G, Fass R (2004). "Is there a relationship between obstructive sleep apnea and gastroesophageal reflux disease?". Clin. Gastroenterol. Hepatol. 2 (9): 761–8. PMID 15354276.
  8. ↑ Kasasbeh A, Kasasbeh E, Krishnaswamy G (2007). "Potential mechanisms connecting asthma, esophageal reflux, and obesity/sleep apnea complex--a hypothetical review". Sleep Med Rev. 11 (1): 47–58. doi:10.1016/j.smrv.2006.05.001. PMID 17198758.
  9. ↑ Malhotra N, Levine J (2014). "Eosinophilic esophagitis: an autoimmune esophageal disorder". Curr Probl Pediatr Adolesc Health Care. 44 (11): 335–40. doi:10.1016/j.cppeds.2014.10.004. PMID 25499460.
  10. ↑ Martin LJ, Franciosi JP, Collins MH, Abonia JP, Lee JJ, Hommel KA, Varni JW, Grotjan JT, Eby M, He H, Marsolo K, Putnam PE, Garza JM, Kaul A, Wen T, Rothenberg ME (2015). "Pediatric Eosinophilic Esophagitis Symptom Scores (PEESS v2.0) identify histologic and molecular correlates of the key clinical features of disease". J. Allergy Clin. Immunol. 135 (6): 1519–28.e8. doi:10.1016/j.jaci.2015.03.004. PMC 4460579. PMID 26051952.
  11. ↑ Lucendo AJ, Arias A, Tenias JM (2014). "Relation between eosinophilic esophagitis and oral immunotherapy for food allergy: a systematic review with meta-analysis". Ann. Allergy Asthma Immunol. 113 (6): 624–9. doi:10.1016/j.anai.2014.08.004. PMID 25216976.
  12. ↑ López-Colombo A (2012). "[Eosinophilic esophagitis]". Rev Gastroenterol Mex (in Spanish; Castilian). 77 Suppl 1: 1–3. doi:10.1016/j.rgmx.2012.07.002. PMID 22939463.
  13. ↑ 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.
  14. ↑ Straumann A (2013). "Eosinophilic esophagitis: a bulk of mysteries". Dig Dis. 31 (1): 6–9. doi:10.1159/000347095. PMID 23797116.
  15. ↑ Straumann A (2012). "Eosinophilic esophagitis: rapidly emerging disorder". Swiss Med Wkly. 142: w13513. doi:10.4414/smw.2012.13513. PMID 22307811.
  16. ↑ 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.
  17. ↑ Godat S, Moradpour D, Schoepfer A (2011). "[Eosinophilic esophagitis: update 2011]". Rev Med Suisse (in French). 7 (307): 1678–80, 1682. PMID 21987875.
  18. ↑ 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.
  19. ↑ "Vertical lines in distal esophageal mucosa (VLEM): a true endoscopic manifestation of esophagitis in children? - PubMed - NCBI".
  20. ↑ "Fragility of the esophageal mucosa: a pathognomonic endoscopic sign of primary eosinophilic esophagitis? - PubMed - NCBI".
  21. ↑ "Eosinophilic esophagitis: red on microscopy, white on endoscopy. - PubMed - NCBI".
  22. ↑ "The prevalence and diagnostic utility of endoscopic features of eosinophilic esophagitis: a meta-analysis. - PubMed - NCBI".

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