Elemental Diet Improves Steroid-Dependent Eosinophilic Gastroenteritis and Reverses Growth Failure

Justinich, Christopher J.; Katz, Amos; Gurbindo, C.; Lepage, Guy; Chad, Zave; Bouthillier, L. P.; Seidman, Ernest G.

doi:10.1097/00005176-199607000-00014

Cited by 76 publications

(56 citation statements)

References 23 publications

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“…The presence of specific IgE on esophageal mast cells [4,5,6,7] would lead to the liberation of its mediators (IL-5, IL-8, RANTES) in the presence of the causal antigen, which could contribute to the eosinophilic infiltrate at this level.…”

Section: Discussionmentioning

confidence: 99%

Food Allergies and Eosinophilic Esophagitis – Two Case Studies

Martín-Muñoz¹,

Lucendo²,

Navarro³

et al. 2006

Digestion

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Eosinophilic esophagitis (EE) is a clinical-pathological disorder which is being increasingly diagnosed. It is etiologically associated with hypersensitivity to airborne allergens and/or dietary components. However, immediate hypersensitivity to foods has rarely been proven as the etiologic cause of the disorder. Two patients are presented with a history of rhinoconjunctivitis, allergic asthma, atopic dermatitis and food allergies which are currently under control and who show specific IgE to pulses and chicken respectively. These patients developed acute dysphagia and vomiting immediately after ingesting these foods and following appropriate examination were diagnosed as suffering from EE. The study also showed signs of blood hypereosinophilia while the esophageal manometry revealed a motor disorder characterized by aperistalsis and non-propulsive simultaneous waves affecting the lower two-thirds of the organ composed of smooth muscle. Topical treatment with fluticasone propionate was administered over a period of 3 months, in addition to a diet abstaining from the aforementioned foods and this led to remission of dysphagia and normalization of the endoscopic, histological and manometric studies of the esophagus. This situation remained stable for a considerable length of time after steroid treatment was discontinued, which showed that exposure to foods seemed to be the cause of the esophageal disorder. Similarly, allergies to inhalants and other digestive symptoms which appear upon immediate ingestion of the foods involved would not justify the sudden onset of dysphagia. We offer a pathophysiological explanation for the mechanisms of the disease based on the activation of eosinophils and mast cells by IgE and their ability to disturb the dynamic behavior of the neural and muscle components of the esophageal wall.

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Section: Discussionmentioning

confidence: 99%

Food Allergies and Eosinophilic Esophagitis – Two Case Studies

Martín-Muñoz¹,

Lucendo²,

Navarro³

et al. 2006

Digestion

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“…Therefore, it is important to eliminate any known provocative factors triggering the disorder. Eliminations diet improve steroid dependency and reverse growth failure in infants diagnosed with EG [Justinich et al 1996]. This suggests that such elimination diets might also benefit adults with EC, although treatment of EC in older individuals usually requires medical management because IgE-associated triggers are rarely identified.…”

Section: Dietmentioning

confidence: 99%

Eosinophilic colitis: epidemiology, clinical features, and current management

Alfadda

Storr

Shaffer

2010

Therap Adv Gastroenterol

126

137

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Primary eosinophilic gastrointestinal disorders (EGIDs) represent a spectrum of inflammatory gastrointestinal disorders in which eosinophils infiltrate the gut in the absence of known causes for such tissue eosinophilia. EGIDs can be subgrouped as eosinophilic esophagitis (EE), eosinophilic gastroenteritis (EG), and eosinophilic colitis (EC). The least frequent manifestation of EGIDs is EC. EC is a heterogeneous entity with a bimodal age distribution, presenting with either an acute self-limited bloody diarrhea in otherwise healthy infants or as a more chronic relapsing colitis in young adults. The pathophysiology of primary EC appears related to altered hypersensitivity, principally as a food allergy in infants and T lymphocytemediated (i.e. non-IgE associated) in young adults. In adults, symptoms include diarrhea, abdominal pain, and weight loss. Endoscopic changes are generally modest, featuring edema and patchy granularity. Although standardized criteria are not yet established, the diagnosis of EC depends on histopathology that identifies an excess of eosinophils. Therapeutic approaches are based on case reports and small case series, as prospective randomized controlled trials are lacking. Eosinophilic colitis in infants is a rather benign, frequently food-related entity and dietary elimination of the aggressor often resolves the disorder within days. Adolescent or older patients require more aggressive medical management including: glucocorticoids, antihistamines, leukotriene receptors antagonists as well as novel approaches employing biologics that target interleukin-5 (IL-5) and IgE. This review article summarizes the current knowledge of EC, its epidemiology, clinical manifestations, diagnosis, and treatment.

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“…Eliminating the dietary intake of the foods implicated by skin prick testing (or RAST testing) has variable effects, but complete resolution is generally achieved with an amino acid-based elemental diet. [57] Once disease remission has been obtained by dietary modification, the specific food groups are slowly reintroduced (at ∼3 week intervals for each food group) and endoscopy is performed every 3 months, to identify sustained remission or disease flare-up. Drugs such as cromoglycate, montelukast, ketotifen, suplatast tosilate, mycophenolate mofetil (a inosine monophosphate dehydrogenase inhibitor), and "alternative Chinese medicines" have been advocated, [22,23] but are generally not successful in the author's experience.…”

Section: Treatment Of Egidmentioning

confidence: 99%