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   <subfield code="a">10.1007/s10620-010-1458-0</subfield>
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   <subfield code="a">Intercellular Space Volume Is Mainly Increased in the Basal Layer of Esophageal Squamous Epithelium in Patients with GERD</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Helmut Neumann, Klaus Mönkemüller, Lucía Fry, Frank Dombrowski, Doerthe Kuester, Mike Beyer, Peter Malfertheiner]</subfield>
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   <subfield code="a">Background/Aims: At present, the dilation of esophageal intercellular spaces (ICS) is considered an early morphologic marker of acid damage in patients with GERD. Nevertheless, previous electron microscopic (EM) studies had focused only on the suprabasal layer of squamous epithelium or did not nearly specify which layer of squamous epithelium was studied. Therefore, we aimed to assess the volumetric amount of the ICS in all layers of SE in patients with GERD. Methods: In this study, 48 patients were prospectively included (NERD=18, ERD=17; Barrett′s esophagus=5, controls=8). All patients with ERD and NERD had typical reflux symptoms, as assessed by a valid GERD questionnaire. ICS volume was assessed by electron microscopy in the superficial, prickle cell, and basal layers of esophageal squamous epithelium using the method of Weibel. Results: ERD was associated with increased ICS volume in the basal layer (LA-A, p=0.038; LA-B, p=0.005) and prickle cell layer (LA-A, p=0.006; LA-B, p=0.007) as compared to controls. Comparisons between NERD and ERD patients revealed more dilated ICS in the basal layer (LA-B, p=0.007), prickle cell layer (LA-A, p=0.008; LA-B, p=0.001) and superficial layer (LA-B, p=0.018) in patients with ERD. Conclusions: Not only the diameter but also the volume of the ICS is increased in patients with GERD. Furthermore, the dilation of ICS is present in all three layers of the SE, being more pronounced in the basal layer. These findings support the concept that the impairment of the esophagus begins in the deeper parts of the esophageal epithelium.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2010</subfield>
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   <subfield code="a">Gastroesophageal reflux disease (GERD)</subfield>
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   <subfield code="a">Barrett′s esophagus</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Intestinal metaplasia</subfield>
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   <subfield code="a">Intercellular spaces</subfield>
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   <subfield code="a">Neumann</subfield>
   <subfield code="D">Helmut</subfield>
   <subfield code="u">Department of Medicine I, University of Erlangen-Nuremberg, Ulmenweg 18, 91054, Erlangen, Germany</subfield>
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   <subfield code="a">Mönkemüller</subfield>
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   <subfield code="u">Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University of Magdeburg, Magdeburg, Germany</subfield>
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   <subfield code="a">Fry</subfield>
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   <subfield code="u">Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University of Magdeburg, Magdeburg, Germany</subfield>
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   <subfield code="u">Institute of Pathology, Otto-von-Guericke University of Magdeburg, Magdeburg, Germany</subfield>
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   <subfield code="u">Institute of Pathology, Otto-von-Guericke University of Magdeburg, Magdeburg, Germany</subfield>
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