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Eosinophilic Gastroenteritis

  • Author: MyNgoc T Nguyen, MD; Chief Editor: Julian Katz, MD  more...
 
Updated: Dec 29, 2015
 

Background

Eosinophilic gastroenteritis (EGE) is an uncommon gastrointestinal disease affecting both children and adults. Eosinophilic gastroenteritis is characterized by the following:

  • The presence of abnormal gastrointestinal (GI) symptoms, most often abdominal pain
  • Eosinophilic infiltration in one or more areas of the GI tract, defined as 20 or more eosinophils per high-power field
  • The absence of an identified cause of eosinophilia
  • The exclusion of eosinophilic involvement in organs other than the GI tract

A history of atopy or food allergies is often present.

Clinical symptoms are determined by the anatomical locations of eosinophilic infiltrates and the depth of GI involvement.[1] Kaijser was probably the first to report a patient with eosinophilic gastroenteritis in 1937; since then, the number of case reports has increased. Treatments are often unsatisfactory, and long-term outcomes are uncertain.

For patient education resources, see  Digestive Disorders Center, as well as, Gastroenteritis.

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Pathophysiology

The underlying molecular mechanism predisposing to the clinical manifestation of eosinophilic gastroenteritis is unknown. Eosinophilic gastritis, enteritis, and gastroenteritis are diseases characterized by the selective infiltration of eosinophils in the stomach, small intestine, or both.[2] The disorders are classified into primary and secondary subtypes. The primary subtypes, which have also been called idiopathic or allergic gastroenteritis, include the atopic, nonatopic, and familial subtypes.

In patients, manifestations of their diseases are based on histologic involvement: mucosal, muscularis, or serosal forms.[1] Any layer of the GI tract can be involved. The secondary subtypes may be divided into 2 groups: systemic eosinophilic disorders (ie, hypereosinophilic disorders) and noneosinophilic disorders (eg, celiac disease, inflammatory bowel disease, vasculitis).

Although these diseases are idiopathic, recent investigations support the role of eosinophils, T helper 2 (Th2) cytokines (interleukin [IL]-3, IL-4, IL-5, and IL-13), and eotaxin as the critical factors in the pathogenesis of eosinophilic gastroenteritis. Eosinophils function as antigen presenting cells as they express major histocompatibility complex (MHC) class II molecules.

In addition, eosinophils can mediate proinflammatory effects, including the up-regulation of adhesion systems, modulation of cell trafficking, and cellular activation states by releasing cytokines (IL-2, IL-4, IL-5, IL-10, IL-12, IL-13, IL-16, IL-18, and transforming growth factor [TGF]-alpha/beta), chemokines (RANTES and eotaxin), and lipid mediators (platelet activating factor [PAF] and leukotriene C4).

Finally, eosinophils can serve as major effector cells, inducing tissue damage and dysfunction by releasing toxic granule proteins (major basic protein [MBP], eosinophilic cationic protein [ECP], eosinophil peroxidase [EPO], and eosinophil-derived neurotoxin [EDN]) and lipid mediators, which are cytotoxic.

Atopy is present in a subset of patients, as these patients demonstrate increased total immunoglobulin E (IgE) on food-specific IgE radioallergosorbent assay test (RAST) or skin tests. Furthermore, lamina propria T cells from the duodenum of these patients proliferated in response to milk proteins and secreted Th2 cytokines (IL-13). However, other studies suggest a non–IgE-mediated mechanism.

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Epidemiology

United States data

The disease is rare, and the incidence is difficult to estimate. However, since the description of eosinophilic gastroenteritis by Kaijser in 1937, more than 280 cases have been reported in the medical literature.

International data

Although cases have been reported worldwide, the exact incidence of eosinophilic gastroenteritis is unclear. A confounding factor is lack of diagnostic precision.

A systematic review that evaluated the racial differences in eosinophilic gastrointestinal disorders between white and Asian populations found that eosinophilic gastroenteritis affects more commonly affects Asian patients (72%), whereas eosinophilic esophagitis is more common in white patients (94%).[3] Asian patients with eosinophilic esophagitis exhibited significantly fewer symptoms of heartburn and dysphagia but more vomiting and abdominal pain compared to white patients. In addition, Asian patients with eosinophilic gastroenteritis were significantly more likely to have eosinophil infiltration of the colon but the stomach was less likely to be affected.[3]

Kim et al reported 31 new cases of eosinophilic gastroenteritis in Seoul, Korea, between January 1970 and July 2003.[4]

Chen et al reported on 15 patients, including 2 children, with eosinophilic gastroenteritis who were evaluated over an 18-year period at a hospital in China in 2003.[5]

Venkataraman et al reported 7 new diagnoses of eosinophilic gastroenteritis over a 10-year period in India.[6]

Race-, sex-, and age-related demographics

Cases of eosinophilic gastroenteritis are reported mostly in white individuals, with some cases occurring in Asians.

A slight male preponderance has been reported.

Patients present clinically in the third to fifth decades of life, but the disease can affect any age group, from infancy through the seventh decade.

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Prognosis

The natural history of eosinophilic gastroenteritis (EGE) has not been well documented. Eosinophilic gastroenteritis is a chronic, waxing and waning condition. Mild and sporadic symptoms can be managed with reassurance and observation, whereas disabling gastrointestinal (GI) symptom flare-ups can often be controlled with oral corticosteroids. When the disease manifests in infancy and specific food sensitization can be identified, the likelihood of disease remission by late childhood is high.

Morbidity includes malnutrition and intestinal obstruction and perforation​. Fatal outcomes are rare, GI obstruction is the most common complication, and the risk of cancer is not increased. 

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Etiology

The cause or mechanism of eosinophilic infiltration is not known.

Patients with eosinophilic gastroenteritis have elevated IgE and eosinophilia of tissue and blood. An imbalance in the T-cell paradigm causing an increase in the production of IL-13, IL-4, and IL-5 and cytokines has been postulated as the cause of IgE synthesis and eosinophilia.

In one study, immunohistochemistry detected IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 in the granule matrix of eosinophils, the release of which is thought to be involved in the perpetuation of intestinal eosinophil infiltration and inflammation.

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Contributor Information and Disclosures
Author

MyNgoc T Nguyen, MD Clinical Associate Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine

MyNgoc T Nguyen, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology

Disclosure: Nothing to disclose.

Coauthor(s)

Jean-Luc Szpakowski, MD 

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors

Ronnie Fass, MD, FACP, FACG Chief of Gastroenterology, Head of Neuroenteric Clinical Research Group, Southern Arizona Veterans Affairs Health Care System; Professor of Medicine, Division of Gastroenterology, University of Arizona School of Medicine

Ronnie Fass, MD, FACP, FACG is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Neurogastroenterology and Motility Society, American Society for Gastrointestinal Endoscopy, Israeli Medical Association

Disclosure: Received grant/research funds from Takeda Pharmaceuticals for conducting research; Received consulting fee from Takeda Pharmaceuticals for consulting; Received honoraria from Takeda Pharmaceuticals for speaking and teaching; Received consulting fee from Vecta for consulting; Received consulting fee from XenoPort for consulting; Received honoraria from Eisai for speaking and teaching; Received grant/research funds from Wyeth Pharmaceuticals for conducting research; Received grant/research funds f.

Acknowledgements

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

References
  1. Uppal V, Kreiger P, Kutsch E. Eosinophilic gastroenteritis and colitis: a comprehensive review. Clin Rev Allergy Immunol. 2015 Jun 9. [Medline].

  2. Mehta P, Furuta GT. Eosinophils in gastrointestinal disorders: eosinophilic gastrointestinal diseases, celiac disease, inflammatory bowel diseases, and parasitic infections. Immunol Allergy Clin North Am. 2015 Aug. 35 (3):413-37. [Medline].

  3. Ito J, Fujiwara T, Kojima R, Nomura I. Racial differences in eosinophilic gastrointestinal disorders among Caucasian and Asian. Allergol Int. 2015 Jul. 64 (3):253-9. [Medline].

  4. Kim NI, Jo YJ, Song MH, et al. Clinical features of eosinophilic gastroenteritis [in Korean]. Korean J Gastroenterol. 2004 Oct. 44(4):217-23. [Medline].

  5. Chen MJ, Chu CH, Lin SC, et al. Eosinophilic gastroenteritis: clinical experience with 15 patients. World J Gastroenterol. 2003 Dec. 9(12):2813-6. [Medline].

  6. Venkataraman S, Ramakrishna BS, Mathan M, et al. Eosinophilic gastroenteritis--an Indian experience. Indian J Gastroenterol. 1998 Oct-Dec. 17(4):148-9. [Medline].

  7. Tien FM, Wu JF, Jeng YM, Hsu HY, Ni YH, Chang MH, et al. Clinical features and treatment responses of children with eosinophilic gastroenteritis. Pediatr Neonatol. 2011 Oct. 52(5):272-8. [Medline].

  8. Zhang L, Duan L, Ding S, Lu J, Jin Z, Cui R, et al. Eosinophilic gastroenteritis: clinical manifestations and morphological characteristics, a retrospective study of 42 patients. Scand J Gastroenterol. 2011 Sep. 46(9):1074-80. [Medline].

  9. Lecouffe-Desprets M, Groh M, Bour B, Le Jeunne C, Puechal X. Eosinophilic gastrointestinal disorders associated with autoimmune connective tissue disease. Joint Bone Spine. 2015 Dec 18. [Medline].

  10. Cianferoni A, Spergel JM. Eosinophilic esophagitis and gastroenteritis. Curr Allergy Asthma Rep. 2015 Sep. 15 (9):58. [Medline].

  11. Savino A, Salvatore R, Cafarotti A, Cecamore C, De Sanctis S, Angelucci D, et al. Role Of Ultrasonography in the Diagnosis and Follow-Up of Pediatric Eosinophilic Gastroenteritis: a Case Report and Review of the Literature. Ultraschall Med. 2011 Dec 9. [Medline].

  12. [Guideline] Liacouras CA, Furuta GT, Hirano I, Atkins D, Attwood SE, Bonis PA, et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011 Jul. 128(1):3-20.e6; quiz 21-2. [Medline].

  13. [Guideline] Sharaf RN, Shergill AK, Odze RD, Krinsky ML, Fukami N, Jain R, et al. Endoscopic mucosal tissue sampling. Gastrointest Endosc. 2013 Aug. 78(2):216-24. [Medline]. [Full Text].

  14. Lucendo AJ, Serrano-Montalban B, Arias A, Redondo O, Tenias JM. Efficacy of dietary treatment for inducing disease remission in eosinophilic gastroenteritis. J Pediatr Gastroenterol Nutr. 2015 Jul. 61 (1):56-64. [Medline].

  15. Prussin C. Eosinophilic gastroenteritis and related eosinophilic disorders. Gastroenterol Clin North Am. 2014 Jun. 43 (2):317-27. [Medline].

  16. Elliott JA, McCormack O, Tchrakian N, et al. Eosinophilic ascites with marked peripheral eosinophilia: a diagnostic challenge. Eur J Gastroenterol Hepatol. 2014 Apr. 26 (4):478-84. [Medline].

  17. Gupta N, Aggarwal A, Gupta R, Sule S, Wolf DC. The management of eosinophilic gastroenteritis. Scand J Gastroenterol. 2015. 50 (11):1309-14. [Medline].

 
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Biopsy specimen of eosinophilic gastroenteritis.
Biopsy specimen of eosinophilic gastroenteritis.
Biopsy specimen of eosinophilic gastroenteritis.
 
 
 
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