The Validity of a Biomarker Method for Indirect Detection of Gastric Mucosal Atrophy Versus Standard Histopathology
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Atrophy of the stomach mucosa is considered to be premalignant lesion for gastric cancer development; easy identification of this condition from a blood-sample would allow identifying the group of individuals at increased risk for cancer development.
The objective of the current study was to validate a biomarker method (pepsinogen I/II ratio and gastrin-17) for indirect detection of atrophy of the stomach mucosa versus standard histopathology in Caucasian and Asian populations.
Altogether, 241 patients aged 55 and above referred for upper endoscopy due to dyspeptic symptoms (125 from Latvia, 76 from Lithuania, and 40 from Taiwan) were enrolled.
Pepsinogen I, pepsinogen II, gastrin-17 (the latter after stimulation with protein-rich meal) and IgG/IgA antibodies to Helicobacter pylori infection were determined by ELISA method; standard histopathology according to the updated Sydney classification read by two independent expert pathologists was used for the comparison.
Pepsinogen I/II ratio below 3 was well related to atrophy (moderate to severe) in the corpus part of the stomach (P < 0.0001) with 83.3% sensitivity and 87.1% specificity. Gastrin-17 below 5 pmol/L was related to atrophy in the antral part (P = 0.007) with 36.8% sensitivity and 86.5% specificity.
Decreased pepsinogen I/II ratio is a reliable marker for atrophy in the corpus, and may be recommended for identification of individuals with this type of atrophy. The utility of gastrin-17 for the detection of atrophy in the antral part of the stomach still requires further evaluation due to the low sensitivity.
KeywordsAtrophic gastritis H. pylori Pepsinogen Gastrin-17 Biomarkers
The study was partially co-founded by Taiwan National Research council, Ministries of Education and Research in Latvia and Lithuania as well as State Research Program in Health in Latvia. The authors acknowledge Prof. Pentti Sipponen for his involvement in the pathology investigations as well as Biohit, Plc. for the support in performing the ELISA tests. We also acknowledge Abbott Pharmaceuticals, AstraZeneca Pharmaceuticals, Innothera Baltics, and KingMark Scientific Corp. for their support for the study by free supplying of eradication medication. We also acknowledge Prof. Uldis Teibe for the advisory assistance in the statistical analysis. We acknowledge the work performed by the other members of the Baltic-Taiwan atrophic gastritis study group, in particular: in Latvia: Viesturs Boka, Galina Cui, Ilva Daugule, Viesturs Krumins, Aija Line, Viesturs Putnins, Armands Sivins, Dans Stirna, Ivars Tolmanis, Aigars Vanags, Uldis Vikmanis; in Taiwan: Ming-Shiang Wu, Yi-Chia Lee.
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