Esophagitis pathophysiology: Difference between revisions

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===Pathological Findings===
===Pathological Findings===
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
====Gross Images====
<gallery>
Image:Candida esophagitis 1.jpg|Esophagus: Candida: Gross natural color close up of distal esophagus mucosa, an excellent example of candida esophagitis 
Image:Candida esophagitis 2.jpg|Esophagitis Candida: Gross natural color close-up, an excellent example
</gallery>
<gallery>
Image:Candida esophagitis 3.jpg|Esophagitis Candida: Gross natural color excellent close-up photo case of acute myelomonocytic leukemia
Image:Necrotizing esophagitis 1.jpg|Necrotizing esophagitis and gastritis, sulfuric acid ingested as suicide attempt
</gallery>


====Microscopic Images====
====Microscopic Images====

Revision as of 18:23, 23 January 2018

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

Overview

Eosinophilic esophagitis is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. The eosinophils are absent in an otherwise normal esophagus, the presence of the eosinophils in the esophagus suggests GERD or EoE. The documented cytokine expression profile in the esophageal tissue of EoE patients is that of a TH2 inflammatory response. IL-5 and 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 response leads to the recruitment and activation of Mast cells degranulate and cause tissue damage and repair. Cytokines produced by TH-1 cells are tumor necrosis factor (TNF)-α, Interferon (IFN)-γ, TNF-α is expressed by the epithelial cells of the esophagus whereas the INF-γ is upregulated by the peripheral T cells. Delayed or type- IV hypersensitivity is the mechanism is involved in the EoE rather than the non-IgE. 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. CD34+ myeloid precursor cells in the bone marrow produce eosinophils and then the eosinophils develop granulation and migrate to vascular spaces. The preformed granule proteins of the eosinophils are ECP- Eosinophil Cationic Protein, MBP- 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 IL-5, IL-13, Transforming growth factor (TGF)-α and -β, Chemokines (eotaxins and RANTES), Lipid mediators such as platelet activating factor (PAF) and leukotriene C4. 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 the increase the vascularity. Fibrogenic mediators such as 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 through their involvement in smooth muscles, fibroblasts, and cell-adhesion molecules. The above-mentioned processes lead to tissue remodeling eventually causing an overall esophageal dysfunction.Pathophysiology of reflux esophagitis depends on several mechanisms that lead to the retrograde movement of the acidic content of the stomach to the esophagus. These mechanisms include transient lower esophageal sphincter relaxation, hypotensive lower esophageal sphincterhiatal hernia, and prolongedesophageal acid clearance.

Pathophysiology

Normal physiology of the food motility through the esophagus

Pathogenesis

Esophagitis is defined as inflammation of mucosal layer of esophagus. Based on the etiology of inflammation esophagitis can be discussed under two categories

  • Reflux esophagitis
  • Eosinophilic esophagitis

Reflux Esophagitis

Pathogenesis of reflux esophagitis 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:[2][3]

Eosinophilic Esophagitis

Eosinophilic esophagitis is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. The pathophysiology of the EoE is as follows:[7][8][9][10][11][12][13][14][15][16]

Production of eosinophils

  • TH2 inflammatory cell response play a major role in the production of eosinophils.
  • Activated TH2 response leads to the recruitment and activation of eosinophils and mast cells.
  • T cells (Th2) cell response also stimulates production of IL-5 and IL-13.
  • IL-13 stimulates the epithelial cells of the esophagus 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.
Granule proteins of the eosinophils
ECP Eosinophil Cationic Protein
MBP Major Basic Protein
EPO Eosinophil Peroxidase
EDN Eosinophil Derived Neurotoxin

Role of eosinophils in inflammation

Eosinophils cause inflammation in the EoE patients by the following mechanisms

Gross Pathology


File:File:Eosinophilic esophagitis endo.jpg
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

Microscopic Images

Histopathological Findings: Herpes Esophagitis

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References

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  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.
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  8. 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.
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  13. Straumann A (2012). "Eosinophilic esophagitis: rapidly emerging disorder". Swiss Med Wkly. 142: w13513. doi:10.4414/smw.2012.13513. PMID 22307811.
  14. 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.
  15. Godat S, Moradpour D, Schoepfer A (2011). "[Eosinophilic esophagitis: update 2011]". Rev Med Suisse (in French). 7 (307): 1678–80, 1682. PMID 21987875.
  16. 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.
  17. "Vertical lines in distal esophageal mucosa (VLEM): a true endoscopic manifestation of esophagitis in children? - PubMed - NCBI".
  18. "Fragility of the esophageal mucosa: a pathognomonic endoscopic sign of primary eosinophilic esophagitis? - PubMed - NCBI".
  19. "Eosinophilic esophagitis: red on microscopy, white on endoscopy. - PubMed - NCBI".
  20. "The prevalence and diagnostic utility of endoscopic features of eosinophilic esophagitis: a meta-analysis. - PubMed - NCBI".

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