The pathophysiology of eosinophilic esophagitis (EoE) is largely unknown. We hypothesize that in EoE an impaired epithelial barrier due to acidic reflux could result in a deep penetration of food antigens into the epithelium and subsequent…
ID
Bron
Aandoening
Eosinophilic esophagitis, pathophysiology, etiology, epithelial barrier integrity, permeability.
Eosinofiele oesofagitis, pathofysiologie, etiologie, epitheliale barrierefunctie, permeabiliteit.
Ondersteuning
Onderzoeksproduct en/of interventie
Uitkomstmaten
Primaire uitkomstmaten
1. Size of esophageal epithelial intercellular spaces in EoE patients and healthy controls;<br>
2. Permeability of esophageal mucosa to small molecules in EoE patients and healthy controls;<br>
3. Tissue impedance of esophageal epithelium (in vivo) in EoE patients and healthy controls;<br>
4. Numbers of esophageal intraepithelial mast cells and eosinophils in EoE patients and healthy controls.
Achtergrond van het onderzoek
The pathophysiology of EoE is largely unknown. We hypothesize that in EoE an impaired epithelial barrier due to acidic reflux could result in a deep penetration of food antigens into the epithelium and subsequent processing and activation of antigen presenting cells followed by activation of an inflammatory Th2 response.
Therefore, epithelial barrier function in EoE patients will be measured using several modalities and compared to epithelial barrier function of healthy controls. Furthermore, the effect of 8 weeks of proton pump inhibition on the epithelial barrier function will be determined in EoE patients.
Doel van het onderzoek
The pathophysiology of eosinophilic esophagitis (EoE) is largely unknown. We hypothesize that in EoE an impaired epithelial barrier due to acidic reflux could result in a deep penetration of food antigens into the epithelium and subsequent processing and activation of antigen presenting cells followed by activation of an inflammatory Th2 response. Evidence for an acid-induced impaired epithelial barrier in EoE will significantly contribute to our understanding of the pathophysiology of this disorder and therefore will be helpful for the development of an acceptable therapy.
Onderzoeksopzet
All parameters are measured at baseline in EoE patients and healthy controls.
Measurements are repeated in EoE patients after 8 weeks of treatment with esomeprazole.
Onderzoeksproduct en/of interventie
Eosinophilic esophagitis patients are treated with esomeprazole 40 mg bd for 8 weeks.
The controls will receive no treatment.
Publiek
Academic Medical Center<br>
PO Box 22660
B.D. Rhijn, van
Amsterdam 1100 DD
The Netherlands
+31 (0)20 5665584
b.d.vanrhijn@amc.uva.nl
Wetenschappelijk
Academic Medical Center<br>
PO Box 22660
B.D. Rhijn, van
Amsterdam 1100 DD
The Netherlands
+31 (0)20 5665584
b.d.vanrhijn@amc.uva.nl
Belangrijkste voorwaarden om deel te mogen nemen (Inclusiecriteria)
Eosinophilic esophagitis group:
1. Previous diagnosis of EoE confirmed by histopathology e.g. presence of >15 eosinophilic granulocytes per high power field (hpf) in mid-esophageal biopsies before the start of any therapy;
2. Written informed consent;
3. Age 18 – 75 years.
Healthy control group:
1. Written informed consent;
2. Age 18 – 75 years.
Belangrijkste redenen om niet deel te kunnen nemen (Exclusiecriteria)
Eosinophilic esophagitis group:
1. Inability to stop topical corticosteroids;
2. Inability to stop PPI, H2-receptor antagonist or prokinetic drug for 8 weeks;
3. Use of systemic corticosteroids, leukotriene inhibitors, or monoclonal antibodies, in the two month period preceding the study;
4. Use of anticoagulants;
5. Use of NSAIDs;
6. History of peptic ulcer disease;
7. History of Barrett’s esophagus;
8. History of GI cancer;
9. History of GI tract surgery (except appendectomy);
10. ASA class IV or V.
Healthy control group:
1. Use of systemic corticosteroids, leukotriene inhibitors, or monoclonal antibodies;
2. Use of anticoagulants;
3. Use of NSAIDs;
4. Personal history of atopic, skin or systemic diseases;
5. Symptoms suggestive of esophageal disease;
6. History of GI cancer;
7. History of GI tract surgery (except appendectomy);
8. History of PPI, H2-receptor antagonist, or prokinetic drug use;
9. ASA class IV or V.
Opzet
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