Esophagitis overview: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
GERD is believed to be first described and treated by the ancient Egyptians according to the papyrus which was discovered by Edwin Smith at Thebes. The [[esophagus]] itself was named by the ancient Greeks. Friedenwald, and Feldman described the symptoms of GERD in 1925. Robbins and Jankelson used the [[radiological]] procedures to observe GERD in 1926. In 1981, Picus and Frank reported a case of a 16-year-old boy with progressive [[dysphagia]] for 1.5 years, [[endoscopic]] findings were suggestive of multiple 1-mm [[nodular]] filling defects in the [[esophagus]] in an area of [[stricture]] with [[dilatation]] above. The radiology showed a luminal narrowing, wall rigidity, and high circulating [[eosinophil]] count assumed to be a variant of [[eosinophilic]] [[gastroenteritis]]. | |||
==Classification== | ==Classification== | ||
Esophagitis may be classified according to the ''Los Angeles Classification'' into 4 grades. | |||
==Pathophysiology== | ==Pathophysiology== | ||
[[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]]<nowiki/>or [[EoE]]. The documented [[cytokine]] expression profile in the [[esophageal]] [[tissue]] of [[EoE]] 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]]<nowiki/>prolongs the survival of the [[eosinophils]]. The activated [[TH2-cells|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 [[Tumour necrosis factor|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 lymphoma|peripheral T cells.]] Delayed or type- IV [[hypersensitivity]] is the mechanism is involved in the [[Eosinophilic esophagitis|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|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)-α and -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]]<nowiki/>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 [[Mediator|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 molecule|cell-adhesion]] [[molecules]]. The above-mentioned processes lead to tissue remodeling eventually causing an overall [[esophageal]] [[Dysfunctional|dysfunction]].Pathophysiology of reflux esophagitis depends on several mechanisms that lead to the retrograde movement of the acidic content of [[Stomach|the stomach]] to the [[esophagus]]. These mechanisms include transient [[lower esophageal sphincter]] relaxation, hypotensive lower [[esophageal sphincter]], [[Hiatus hernia|hiatal hernia]], and prolonged[[esophageal]] [[acid]] clearance. | |||
==Causes== | ==Causes== | ||
Common causes of esophagitis include [[gastroesophageal reflux disease]], [[Barrett's esophagus]], caustic burns, and chemical injury by either alkaline or acid solutions. Among immuncompromised patients, the most common causes of esophagitis are [[Candidiasis]], ''[[Cytomegalovirus]]'', and ''[[Herpes simplex virus]]'' | |||
==Differentiating {{PAGENAME}} from Other Diseases== | ==Differentiating {{PAGENAME}} from Other Diseases== | ||
Esophagitis must be differentiated from [[gastritis]], [[peptic ulcer]] disease, [[gastroesophageal reflux]] disease, [[acute coronary syndrome]], [[angina pectoris]], [[cholecystitis]], [[biliary colic]], [[pulmonary embolism]] and esophageal perforation, rupture and tears. | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
In the USA and Europe, the prevalence of GERD ranges from low of 10,000 per 100,000 persons to high of 20,000 per 100,000 people. In Asia, the prevalence of GERD is 5,000 per 100,000 people. The [[prevalence]] of EoE is approximately 50-100 per 100,000 individuals worldwide. In the USA, the incidence of GERD is 5,400 per 100,000 persons. In Europe, the incidence of GERD is 840 per 100,000 persons. The [[incidence]] of EoE is approximately 10 per 100,000 individuals worldwide. The prevalence of GERD increases with age. GERD affects all age groups but it affects more the people older than 40 years. Patients of all age groups may develop EoE. Men and women are affected equally by GERD. Males are more commonly affected by EoE than females. There is no racial predilection for GERD. EoE usually affects individuals of the white race. | |||
==Risk Factors== | ==Risk Factors== | ||
Common risk factors in the development of esophagitis are [[immunosuppression]], alcohol use, [[smoking]], [[excessive vomiting]], certain medications, and surgery or [[radiation]] to the chest. | |||
==Screening== | ==Screening== | ||
There is insufficient evidence to recommend routine screening for Esophagitis. | |||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
If left untreated, 20% of patients with GERD may progress to develop [[esophageal stricture]] due to excessive [[acid]] in the [[Esophagus|lower esophagus]]. Complications of GERD include [[barrett's esophagus]], [[Esophagitis|erosive esophagitis]], [[esophageal ulcer]], and [[esophageal]] [[adenocarcinoma]]. Prognosis of GERD is good with the appropriate treatment.The natural course of primary [[Eosinophilic esophagitis|EoE]] is, 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]]. 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]], [[Tears]] or [[perforation]] during the [[endoscopy]] or [[retching]] leading to [[boerhaave syndrome]]. The long-term prognosis of the EoE is unclear but patients diagnosed with EoE have an unaffected lifespan. | |||
==Diagnosis== | ==Diagnosis== | ||
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===History and Symptoms=== | ===History and Symptoms=== | ||
The signs and symptoms of the esophagitis are as follows [[Bad breath|Halitosis]]. [[Chest pain]], in the middle of the chest, often radiating to the back, usually associated with swallowing or soon after a meal. [[Difficulty swallowing|Dysphagia]], [[Painful swallowing|odynophagia]], food getting stuck in the throat. [[Hoarseness]], [[Mouth sores|oral ulcers]], [[Nausea]], [[Sore throat]], [[Vomiting]]. Symptoms of underlying diseases that cause esophagitis include: [[Indigestion]], [[Heartburn|heartburn,]] [[Unpleasant taste in the mouth|metallic taste]], [[Excessive belching]]. | |||
===Physical Examination=== | ===Physical Examination=== | ||
The physical examination usually is not helpful in confirming the diagnosis of uncomplicated esophagitis. However, the examination may reveal other potential sources of chest or abdominal pain. | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
A complete blood count (CBC) is performed in patients with neutropenia or who are immunosuppressed. A CD4 count and HIV test are performed in patients with risk factors for HIV. A collagen workup (eg, antinuclear antibody [ANA], anti-dsDNA) may be performed based on the underlying disease. | |||
=== X-ray === | |||
=== CT === | |||
There are no [[CT scan]] findings associated with esophagitis. However, a [[CT scan]] may be helpful in the diagnosis of complications of esophagitis such as [[tears]], [[perforation]], [[strictures]], etc. | |||
=== MRI === | |||
There are no [[MRI]] findings associated with esophagitis. however, [[MRI]] may be helpful in the diagnosis of complications of esophagitis such as [[tears]], [[perforation]], [[strictures]], etc. | |||
===Imaging Findings=== | ===Imaging Findings=== | ||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
There are no other diagnostic studies associated with esophagitis. | |||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
The mainstay of therapy for reflux esophagitis is acid suppression therapy. Patients with infectious esophagitis are treated with [[antimicrobial]] therapy, whereas patients with eosinophilic esophagitis are treated with [[corticosteroids]]. Supportive therapy for esophagitis includes [[proton pump inhibitors]], topical pain medications (gargled or swallowed), smoking and alcohol cessation, and [[endoscopy]] to remove any lodged pill fragments. | |||
===Surgery=== | ===Surgery=== | ||
Surgical intervention is not recommended for the management of esophagitis. | |||
===Primary prevention=== | |||
There are no established measures for the primary prevention of esophagitis. | |||
=== | === Secondary prevention === | ||
There are no established measures for the secondary prevention of esophagitis. | |||
==References== | ==References== | ||
Revision as of 14:29, 23 January 2018
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Esophagitis Microchapters |
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Esophagitis overview On the Web |
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American Roentgen Ray Society Images of Esophagitis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Esophagitis is a general term for any inflammation, irritation, or swelling of the esophagus. The inflammation can be due to a variety of causes such as gastroesophageal reflux disease, viruses, or chemical injuries.
Historical Perspective
GERD is believed to be first described and treated by the ancient Egyptians according to the papyrus which was discovered by Edwin Smith at Thebes. The esophagus itself was named by the ancient Greeks. Friedenwald, and Feldman described the symptoms of GERD in 1925. Robbins and Jankelson used the radiological procedures to observe GERD in 1926. In 1981, Picus and Frank reported a case of a 16-year-old boy with progressive dysphagia for 1.5 years, endoscopic findings were suggestive of multiple 1-mm nodular filling defects in the esophagus in an area of stricture with dilatation above. The radiology showed a luminal narrowing, wall rigidity, and high circulating eosinophil count assumed to be a variant of eosinophilic gastroenteritis.
Classification
Esophagitis may be classified according to the Los Angeles Classification into 4 grades.
Pathophysiology
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 GERDor 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-5prolongs 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 leukotrieneC4. IL-5, IL-13, and granulocyte-macrophage colony stimulating factor (GM-CSF) can cause the maturation and migration of the eosinophils. Eosinophilscause 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 sphincter, hiatal hernia, and prolongedesophageal acid clearance.
Causes
Common causes of esophagitis include gastroesophageal reflux disease, Barrett's esophagus, caustic burns, and chemical injury by either alkaline or acid solutions. Among immuncompromised patients, the most common causes of esophagitis are Candidiasis, Cytomegalovirus, and Herpes simplex virus
Differentiating Esophagitis overview from Other Diseases
Esophagitis must be differentiated from gastritis, peptic ulcer disease, gastroesophageal reflux disease, acute coronary syndrome, angina pectoris, cholecystitis, biliary colic, pulmonary embolism and esophageal perforation, rupture and tears.
Epidemiology and Demographics
In the USA and Europe, the prevalence of GERD ranges from low of 10,000 per 100,000 persons to high of 20,000 per 100,000 people. In Asia, the prevalence of GERD is 5,000 per 100,000 people. The prevalence of EoE is approximately 50-100 per 100,000 individuals worldwide. In the USA, the incidence of GERD is 5,400 per 100,000 persons. In Europe, the incidence of GERD is 840 per 100,000 persons. The incidence of EoE is approximately 10 per 100,000 individuals worldwide. The prevalence of GERD increases with age. GERD affects all age groups but it affects more the people older than 40 years. Patients of all age groups may develop EoE. Men and women are affected equally by GERD. Males are more commonly affected by EoE than females. There is no racial predilection for GERD. EoE usually affects individuals of the white race.
Risk Factors
Common risk factors in the development of esophagitis are immunosuppression, alcohol use, smoking, excessive vomiting, certain medications, and surgery or radiation to the chest.
Screening
There is insufficient evidence to recommend routine screening for Esophagitis.
Natural History, Complications, and Prognosis
If left untreated, 20% of patients with GERD may progress to develop esophageal stricture due to excessive acid in the lower esophagus. Complications of GERD include barrett's esophagus, erosive esophagitis, esophageal ulcer, and esophageal adenocarcinoma. Prognosis of GERD is good with the appropriate treatment.The natural course of primary EoE is, 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. 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, Tears or perforation during the endoscopy or retching leading to boerhaave syndrome. The long-term prognosis of the EoE is unclear but patients diagnosed with EoE have an unaffected lifespan.
Diagnosis
Diagnostic Criteria
History and Symptoms
The signs and symptoms of the esophagitis are as follows Halitosis. Chest pain, in the middle of the chest, often radiating to the back, usually associated with swallowing or soon after a meal. Dysphagia, odynophagia, food getting stuck in the throat. Hoarseness, oral ulcers, Nausea, Sore throat, Vomiting. Symptoms of underlying diseases that cause esophagitis include: Indigestion, heartburn, metallic taste, Excessive belching.
Physical Examination
The physical examination usually is not helpful in confirming the diagnosis of uncomplicated esophagitis. However, the examination may reveal other potential sources of chest or abdominal pain.
Laboratory Findings
A complete blood count (CBC) is performed in patients with neutropenia or who are immunosuppressed. A CD4 count and HIV test are performed in patients with risk factors for HIV. A collagen workup (eg, antinuclear antibody [ANA], anti-dsDNA) may be performed based on the underlying disease.
X-ray
CT
There are no CT scan findings associated with esophagitis. However, a CT scan may be helpful in the diagnosis of complications of esophagitis such as tears, perforation, strictures, etc.
MRI
There are no MRI findings associated with esophagitis. however, MRI may be helpful in the diagnosis of complications of esophagitis such as tears, perforation, strictures, etc.
Imaging Findings
Other Diagnostic Studies
There are no other diagnostic studies associated with esophagitis.
Treatment
Medical Therapy
The mainstay of therapy for reflux esophagitis is acid suppression therapy. Patients with infectious esophagitis are treated with antimicrobial therapy, whereas patients with eosinophilic esophagitis are treated with corticosteroids. Supportive therapy for esophagitis includes proton pump inhibitors, topical pain medications (gargled or swallowed), smoking and alcohol cessation, and endoscopy to remove any lodged pill fragments.
Surgery
Surgical intervention is not recommended for the management of esophagitis.
Primary prevention
There are no established measures for the primary prevention of esophagitis.
Secondary prevention
There are no established measures for the secondary prevention of esophagitis.