Abstract

BackgroundDistributions of serum pepsinogen (PG) values were assessed in Helicobacter pylori-infected and non-infected junior high school students (aged 12–15 years) in Japan.MethodsAll junior high school students (1,225 in total) in Sasayama city, who were basically healthy, were asked to provide urine and serum samples, which were used to measure urine and serum H. pylori antibodies using ELISA kits and PG values. The subjects, whose urine and serum antibodies were both positive, were considered H. pylori infected.ResultsOf the 187 subjects who provided urine and blood samples, 8 were infected, 4 had discrepant results, 4 had negative serum antibody titers no less than 3.0 U/ml, and 171 were non-infected. In the H. pylori non-infected subjects, the median PG I and PG II values and PG I to PG II ratio (PG I/II) were 40.8 ng/mL, 9.5 ng/mL, and 4.4, respectively, whereas in the infected subjects, these values were 55.4 ng/mL, 17.0 ng/mL, and 3.3, respectively (each P < 0.01). In the non-infected subjects, PG I and PG II were significantly higher in males than in females (P < 0.01).ConclusionsThe PG I and PG II values were higher, and the PG I/II was lower in H. pylori infected students than in non-infected students. In H. pylori non-infected students, males showed higher PG I and PG II values than females. The distributions of PG values in junior high school students differed from those in adults.

Highlights

  • Pepsinogen is a precursor of pepsin, and human gastric mucosa cells produce two immunochemically distinct forms of PG.[1]

  • Inflammation upregulates production of both PG I and PG II in gastric mucosal cells and increases the amount discharged to serum, where elevation of PG II is usually larger so that the PG I=II ratio declines

  • PG values were used as a marker of gastric mucosal atrophy that is strongly related to gastric cancer risk.[7,8,9]

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Summary

Introduction

Pepsinogen is a precursor of pepsin, and human gastric mucosa cells produce two immunochemically distinct forms of PG.[1]. Inflammation upregulates production of both PG I and PG II in gastric mucosal cells and increases the amount discharged to serum, where elevation of PG II is usually larger so that the PG I=II ratio declines. As the decrease of cells producing PG I is more crucial, the PG I=II ratio declines with the progression of atrophy.[3,4,5,6] In adults, PG values were used as a marker of gastric mucosal atrophy that is strongly related to gastric cancer risk.[7,8,9] Recently, criteria of PG values to distinguish subjects with and without H. pylori infection have been proposed because PG values differ depending on the infection among adult subjects.[10] Adults with. Distributions of serum pepsinogen (PG) values were assessed in Helicobacter pylori-infected and non-infected junior high school students (aged 12–15 years) in Japan

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