Esophageal remodeling in pediatric eosinophilic esophagitis

Aceves, Seema S.; Newbury, Robert; Dohil, Ranjan; Bastian, John F.; Broide, David H.

doi:10.1016/j.jaci.2006.10.016

Cited by 407 publications

(382 citation statements)

References 41 publications

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“…with fibrosis and stricture formation. [18,19] After these initial findings and the work that followed, it became evident that EoE should be treated. [8,9,18,19] Due to the rareness of purely observational studies, our understanding of the natural history of EoE remains limited.…”

Section: Discussionmentioning

confidence: 99%

Delay in Diagnosis of Eosinophilic Esophagitis Increases Risk for Stricture Formation in a Time-Dependent Manner

Schoepfer

Safroneeva

Bussmann³

et al. 2013

Gastroenterology

632

517

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Section: Discussionmentioning

confidence: 99%

Delay in Diagnosis of Eosinophilic Esophagitis Increases Risk for Stricture Formation in a Time-Dependent Manner

Schoepfer

Safroneeva

Bussmann³

et al. 2013

Gastroenterology

632

517

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“…2,3 Similarly, chronic inflammatory diseases involve extensive changes in tissue architecture, such as goblet cell metaplasia, airway wall thickening and increased airflow resistance in asthma, 4 and tissue fibrosis in diseases such as eosinophilic esophagitis (EE). 5,6 Eosinophilic esophagitis is an emerging worldwide disease, as documented by recent case series from Switzerland, Australia, Israel, Italy, Spain, Japan, England, and the United States. 7 EE clinically mimics gastroesophageal reflux disease and can lead to esophageal fibrosis, narrowing, and stricture 8 likely due to tissue remodeling that leads to impaired functional responses (e.g., motility).…”

Section: Introductionmentioning

confidence: 99%

Periostin facilitates eosinophil tissue infiltration in allergic lung and esophageal responses

et al. 2008

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Periostin is an extracellular matrix protein that has been primarily studied in the context of the heart, where it has been shown to promote cardiac repair and remodeling. In this study, we focused on the role of periostin in an allergic eosinophilic inflammatory disease (eosinophilic esophagitis (EE)) known to involve extensive tissue remodeling. Periostin was indeed markedly overexpressed (35-fold) in the esophagus of EE patients, particularly in the papillae, compared with control individuals. Periostin expression was downstream from transforming growth factor-β and interleukin-13, as these cytokines were elevated in EE esophageal samples and markedly induced periostin production by primary esophageal fibroblasts (107-and 295-fold, respectively, at 10 ng ml −1 ). A functional role for periostin in eliciting esophageal eosinophilia was demonstrated, as periostin-null mice had a specific defect in allergen-induced eosinophil recruitment to the lungs and esophagus (66 and 72% decrease, respectively). Mechanistic analyses revealed that periostin increased (5.8-fold) eosinophil adhesion to fibronectin. As such, these findings extend the involvement of periostin to esophagitis and uncover a novel role for periostin in directly regulating leukocyte (eosinophil) accumulation in T helper type 2-associated mucosal inflammation in both mice and humans.

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“…Indeed, esophageal tissue remodeling with resultant fibrosis, angiogenesis, and smooth muscle hypertrophy appears to underlie the major EoE complications of food impactions and stricture as well as the predominant EoE symptom of dysphagia [55][56][57]. Underscoring the importance of tissue remodeling, pivotal adult studies have demonstrated that long-standing, untreated EoE progresses almost uniformly to esophageal stricture [58 • , 59 • ].…”

Section: Update On a New Diagnostic Modalities And Natural Historymentioning

confidence: 99%

Non-IgE Medicated Food Allergy: Eosinophilic Esophagitis Update on the Pathogenesis, Clinical Features, and Management of Eosinophilic Esophagitis in Children

Greenhawt

Aceves

2014

Curr Pediatr Rep

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Eosinophilic esophagitis (EoE) is a chronic allergic disorder of increasing worldwide prevalence. Diagnosis and management require upper gastrointestinal endoscopy with biopsy. Therapeutic strategies in children and adults include empiric and testing-based elimination diets as well as topical esophageal corticosteroids. The last 12 months have provided a number of insights including updated diagnostic/management guidelines, the role of PPI therapy, and an understanding that EoE disease mechanisms rely on basophils and mast cells in addition to eosinophils. Novel diagnostic techniques have been described and include the esophageal string test and a molecular gene array panel. In addition, new techniques for assessing esophageal rigidity have been reported. In this review, we summarize the most impactful findings in EoE over the last 12-15 months.

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Esophageal remodeling in pediatric eosinophilic esophagitis

Cited by 407 publications

References 41 publications

Delay in Diagnosis of Eosinophilic Esophagitis Increases Risk for Stricture Formation in a Time-Dependent Manner

Delay in Diagnosis of Eosinophilic Esophagitis Increases Risk for Stricture Formation in a Time-Dependent Manner

Periostin facilitates eosinophil tissue infiltration in allergic lung and esophageal responses

Non-IgE Medicated Food Allergy: Eosinophilic Esophagitis Update on the Pathogenesis, Clinical Features, and Management of Eosinophilic Esophagitis in Children

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