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   <subfield code="a">10.1007/s10620-011-1758-z</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s10620-011-1758-z</subfield>
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   <subfield code="a">Gastric Juice Prostaglandins and Peptide Growth Factors as Potential Markers of Chronic Atrophic Gastritis, Intestinal Metaplasia and Gastric Cancer: Their Potential Clinical Implications Based on this Pilot Study</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Ajoy Dias, Cesar Garcia, Marek Majewski, Grzegorz Wallner, Richard McCallum, Cezary Poplawski, Jerzy Sarosiek]</subfield>
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   <subfield code="a">Background: Gastric secretion can provide valuable information especially when Helicobacter pylori (Hp) infection results in chronic atrophic gastritis (CAG) and intestinal metaplasia (IM) preceding adenocarcinoma (AdCa). Aims: Looking for a potential biomarker of malignant transformation in the setting of chronic inflammation we studied the levels of prostaglandin E2 (PGE2), as well as peptide growth factors [epidermal growth factor (EGF) and transforming growth factor α (TGFα)], harbingers of injury and repair, in gastric juice aspirated at endoscopy from patients with CAG, CAG/IM, AdCa, and controls. Methods: The PGE2, EGF and TGFα concentrations in the gastric juice were measured using radioimmunoassays (RIAs). Results: In patients with AdCa gastric juice PGE2 increased fivefold versus controls (P&lt;0.01) and almost threefold versus patients with CAG (P&lt;0.05). The EGF levels in patients with AdCa were fourfold higher versus controls (P&lt;0.001) and almost threefold higher versus CAG (P&lt;0.05). In patients with CAG/IM the EGF levels were also almost 3 times higher versus controls. The TGFα levels in patients with AdCa were half the value of controls and CAG (P&lt;0.05). In patients with CAG/IM the levels were as low as 1/5 of controls or CAG (P&lt;0.05). Conclusions: Testing the gastric juice for PGE2, EGF, and TGFα in patients with endoscopy and biopsy proven CAG, may be helpful in follow up of patients who may potentially progress to IM and ultimately AdCa. This could be considered as an adjunct to histologic assessment especially that even the best surveillance biopsy specimen regimens are inherited with sampling errors.</subfield>
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   <subfield code="a">The Author(s), 2011</subfield>
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   <subfield code="a">Gastritis</subfield>
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   <subfield code="a">Adenocarcinoma</subfield>
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   <subfield code="a">Helicobacter pylori</subfield>
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   <subfield code="a">Prostaglandins</subfield>
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   <subfield code="a">Dias</subfield>
   <subfield code="D">Ajoy</subfield>
   <subfield code="u">Department of Internal Medicine, TTUHSC Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, 4800 Alberta Avenue, 79905-2709, El Paso, TX, USA</subfield>
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   <subfield code="a">Garcia</subfield>
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   <subfield code="u">Department of Internal Medicine, TTUHSC Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, 4800 Alberta Avenue, 79905-2709, El Paso, TX, USA</subfield>
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   <subfield code="a">Majewski</subfield>
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   <subfield code="u">Medical University of Lublin, Lublin, Poland</subfield>
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   <subfield code="a">Wallner</subfield>
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   <subfield code="u">Medical University of Lublin, Lublin, Poland</subfield>
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   <subfield code="a">McCallum</subfield>
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   <subfield code="u">Department of Internal Medicine, TTUHSC Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, 4800 Alberta Avenue, 79905-2709, El Paso, TX, USA</subfield>
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