Eosinophilic esophagitis

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Eosinophilic esophagitis
Classification and external resources
Eosinophilic esophagitis - very high mag.jpg
Micrograph showing eosinophilic esophagitis. H&E stain.
ICD-10 K20.0
ICD-9 530.13
MeSH D057765
Endoscopic image of esophagus in a case of eosinophilic esophagitis. Concentric rings are termed trachealization of the esophagus.
The barium swallow of the esophagus on the left side shows multiple rings associated with eosinophilic esophagitis.

Eosinophilic esophagitis (eosinophilic oesophagitis), also known as allergic oesophagitis, is an allergic inflammatory condition of the esophagus that involves eosinophiles, a type of white blood cell. Symptoms are swallowing difficulty, food impaction, and heartburn.[1]

Eosinophilic esophagitis (EE) was first described in children but occurs in adults as well. The condition is not well understood, but food allergy may play a significant role.[2]

Symptoms[edit]

EE is associated with oesophageal strictures, and often presents with food impaction, dysphagia, and heartburn. In addition, young children with eosinophilic esophagitis may present with feeding difficulties. It is more common in males, and affects both adults and children.[1]

Pathophysiology[edit]

EE is considered a relatively poorly understood disease of which awareness is rising.[1][3]

EE is characterised by a dense eosinophilic infiltrate into the epithelium of the squamous oesophagus. This is thought to be probably an allergic reaction against ingested food, based on the important role eosinophils play in allergic reactions. Eosinophils are inflammatory cells that release a variety of cytokines which inflame the surrounding oesophageal tissue. This results in symptoms of pain, visible redness on endoscopy, and a natural history that may include stricturisation.[1]

A characteristic set of genes termed the "EE transcriptome" described by Professor Marc Rothenberg MD, PhD, is expressed and distinguishes patients with EE from unaffected individuals or from patients with other forms of esophagitis.[4]

The EE transcriptome has now been developed into a 94 gene panel, called the EE Diagnostic Panel (EDP) which provides a rapid and accurate means to diagnose EE and monitor disease activity.[5]

Genetic & Autoimmune Links[edit]

Many EE patients suffer from concurrent autoimmune and allergic disease. This includes asthma [1] and coeliac disease.[6]

Diagnosis[edit]

The diagnosis of EE is typically made clinicopathologically.[1]

Clinical Findings. Clinically, EE can only be diagnosed if gastroesophageal reflux is not responsive to a 6 week trial of twice-a-day high-dose proton-pump inhibitors (PPIs) or if a negative ambulatory pH study rules out gastroesophageal reflux disease (GERD).[3][7]

Histology. On esophagogastroduodenoscopic biopsy, numerous eosinophils can be seen in the superficial epithelium. A minimum of 15 eosinophils per high-power field are required to make the diagnosis. Eosinophilic inflammation is limited to the oesophagus alone, and does not extend into the stomach or duodenum. Profoundly degranulated eosinophils may also be present, as may microabcesses and an expansion of the basal layer.[1][8]

Endoscopy. Endoscopically, ridges, furrows, or rings may be seen in the oesophageal wall. Sometimes, multiple rings may occur in the esophagus, leading to the term "corrugated esophagus" or "feline esophagus" due to similarity of the rings to the cat esophagus. Presence of white exudates in esophagus is also suggestive of the diagnosis.[9]

Radiology. Radiologically, the term "ringed esophagus" has been used for the appearance of eosinophilic esophagitis on barium esophagrams to contrast with the appearance of transient transverse folds sometimes seen with esophageal reflux (termed "feline esophagus").[10]

Treatment[edit]

Treatment strategies include dietary modification to exclude food allergens, medical therapy, and mechanical dilatation of the esophagus.

The initial approach to the disorder is often allergy evaluation in an attempt to identify the allergens in the diet or environment that may be triggering the condition. If the offending agent is found, the diet is modified so that these allergens are eliminated. There are cases, especially in children, where there are multiple food allergies involved. Some patients require an elemental diet through the use of a specialty formula. Sticking to this diet and drinking the required amount of formula can be difficult. The use of feeding tubes in these situations is often required.[citation needed]

First-line therapy is with swallowed liquid corticosteroids and other anti-inflammatories, including fluticasone, a topical viscous budesonide oral suspension. .[citation needed] Patients with severe symptoms despite these interventions may require oral corticosteroids such as methylprednisolone.[citation needed] Other anti-inflammatory agents have also been trialled, including leukotriene antagonists such as montelukast, anti-interleukins such as the anti-IL-5 monoclonal antibody mepolizumab, and antihistamines such as loratadine. Unfortunately, these have shown little clinical benefit.[citation needed]

Mechanical dilatation may be considered in severe cases of EE that have progressed to esophageal stricture or severe stenosis. Dilatation is accomplished by passing dilators through the mouth and down the esophagus to gently expand its diameter. As the esophagus of patients with EE is rather thin and delicate, care is taken not to perforate the esophagus by overzealous dilatation.[citation needed]

PPI use. Despite EE being historically thought of as refractory to PPI treatment, there is some recent evidence to suggest a significant proportion of patients suffering from EE achieving remission following PPI therapy.[11]

See also[edit]

References[edit]

  1. ^ a b c d e f g Nurko, Samuel; Furuta, G T (2006). "Eosinophilic esophagitis". GI Motility online. doi:10.1038/gimo49. 
  2. ^ Blanchard C, Rothenberg ME (January 2008). "Basic pathogenesis of eosinophilic esophagitis". Gastrointest. Endosc. Clin. N. Am. 18 (1): 133–43; x. doi:10.1016/j.giec.2007.09.016. PMC 2194642. PMID 18061107. 
  3. ^ a b Noel, Richard J.; Putnam, Philip E.; Rothenberg, Marc E. (26 August 2004). "Eosinophilic Esophagitis". New England Journal of Medicine 351 (9): 940–941. doi:10.1056/NEJM200408263510924. 
  4. ^ Blanchard C, Wang N, Stringer KF, Mishra A, Fulkerson PC, Abonia JP, Jameson SC, Kirby C, Konikoff MR, Collins MH, Cohen MB, Akers R, Hogan SP, Assa'ad AH, Putnam PE, Aronow BJ, Rothenberg ME (February 2006). "Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis". J. Clin. Invest. 116 (2): 536–47. doi:10.1172/JCI26679. PMC 1359059. PMID 16453027. 
  5. ^ Molecular diagnosis of eosinophilic esophagitis by gene expression profiling. Wen T, Stucke EM, Grotjan TM, Kemme KA, Abonia JP, Putnam PE, Franciosi JP, Garza JM, Kaul A, King EC, Collins MH, Kushner JP, Rothenberg ME. Gastroenterology. 2013 Dec;145(6):1289-99. doi: 10.1053/j.gastro.2013.08.046. Epub 2013 Aug 23. PMID: 23978633 [PubMed - in process]
  6. ^ Stewart, Michael J; Shaffer, Eldon; Urbanski, Stephan J; Beck, Paul L; Storr, Martin A (1 January 2013). "The association between celiac disease and eosinophilic esophagitis in children and adults". BMC Gastroenterology 13 (1): 96. doi:10.1186/1471-230X-13-96. 
  7. ^ Furuta GT, Liacouras CA, Collins MH, Gupta SK, Justinich C, Putnam PE, Bonis P, Hassall E, Straumann A, Rothenberg ME; First International Gastrointestinal Eosinophil Research Symposium (FIGERS) Subcommittees. (Oct 2007). "Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment.". Gastroenterology. 133 (4): 1342–63. PMID 17919504. 
  8. ^ Furuta GT, Liacouras CA, Collins MH, Gupta SK, Justinich C, Putnam PE, Bonis P, Hassall E, Straumann A, Rothenberg ME; First International Gastrointestinal Eosinophil Research Symposium (FIGERS) Subcommittees. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007 Oct;133(4):1342-63.
  9. ^ Samadi F, Levine MS, Rubesin SE, Katzka DA, Laufer I (April 2010). "Feline esophagus and gastroesophageal reflux". AJR Am J Roentgenol 194 (4): 972–6. doi:10.2214/AJR.09.3352. PMID 20308499. 
  10. ^ Zimmerman SL, Levine MS, Rubesin SE, et al. (July 2005). "Idiopathic eosinophilic esophagitis in adults: the ringed esophagus". Radiology 236 (1): 159–65. doi:10.1148/radiol.2361041100. PMID 15983073. 
  11. ^ Molina-Infante, Javiar (2011). J Gastroenterology 46: 712–3. doi:10.1007/s00535-011-0388-8. 

External links[edit]