<unk>  <unk>  is an immunoallergic disorder resulting from the interaction between genetics and environmental triggers such as repeated exposure to food and aeroallergens. The documented cytokine expression profile in the esophageal tissue of<unk>  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. Cytokines produced by TH-1 cells are tumor necrosis factor (TNF)-α, Interferon (IFN)-γ. CD34+ myeloid precursor cells in the bone marrow produce eosinophils and then the eosinophils develop granulation and migrate to vascular spaces. Eosinophils cause inflammation in the<unk>  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. The esophageal mucosa in patients with a longstanding<unk>  is characterized by a loss of elasticity. On histologic examination of the subepithelial compartments of the esophagus show an increase in the fibrous tissue. There is no established system for the classification of<unk>  <unk> . The causes of<unk>  include food and pollens.<unk>  must be differentiated from other diseases that cause dysphagia such as reflux esophagitis, esophageal carcinoma, systemic sclerosis, esophageal spasm, pseudoachalasia, stroke, esophageal candidiasis and chagas disease. The incidence<unk>  <unk>  is approximately 10 per 100,000 individuals worldwide. The prevalence of<unk>  is approximately 50-100 per 100,000 individuals worldwide. The risk factors of<unk>  are as follows bimodal age distribution, male gender, cold and dry climate. The history and symptoms of<unk>  <unk> , dysphagia, regurgitation, cough, chest pain, food impaction, upper abdominal pain, vomiting.The complications of the<unk>  includes Scarring of esophagus-leading to dysphagia, Esophageal stenosis, Tears or perforation during the endoscopy or retching leading to boerhaave syndrome.As 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<unk>  is unclear but patients diagnosed with<unk>  have an unaffected lifespan.  Patients who are untreated or have discontinued the treatment have progression of their symptoms. The<unk>  patients with a narrow esophageal lumen are resistant to the corticosteroid treatment and require many esophageal endoscopic procedures. There are no specific diagnostic markers to diagnose the<unk>  patients, however, an increased peripheral<unk> ount is also seen in majority patients. The barium swallow of the esophagus shows multiple rings associated with<unk> , There are no MRI nor CT scan findings associated with<unk> . however, an MRI or a CT scan may be helpful in the diagnosis of complications of<unk>  such as tears, perforation strictures etc. The optimal treatment of<unk>  remains uncertain.  An eight-week course of therapy with topical corticosteroids (fluticasone or budesonide) may be used as the first-line pharmacologic therapy.  Allergen elimination usually leads to improvement in dysphagia and reduction of eosinophil infiltration.  Esophageal dilation of is generally reserved for refractory cases with esophageal stricture.
Eosinophilic esophagitis
CMV esophagitis
Candida esophagitis
Esophageal candidiasis
Barrett's esophagus
Nutcracker esophagus
Atrophic gastritis
Achalasia