ABSTRACT
OBJECTIVES: To determine serum concentration of gastrin and pepsinogens (PGs) as markers for the gastric mucosal status and to elucidate the prevalence of serum Helicobacter pylori (H pylori) IgG antibodies and parietal cell autoantibodies (PCAs) in patients with gastric polyps. METHODS: The subjects in this study were composed of 36 patients with fundic glandular polyps (FGP), 25 patients with foveolar hyperplastic polyps (FHP), and 27 asymptomatic healthy volunteers (controls). Serum concentrations of gastrin and PGs were determined by radioinmmunoassay. H. pylori IgG antibodies were measured through an enzyme-linked immunosorbent assay. PCAs were detected by an indirect immunofluorescence technique using cryostat sections of rat gastric mucosa. RESULTS: There were no significant differences between FGP patients and controls in serum concentrations of gastrin, PG I and PG II. FHP patients showed significantly higher serum gastrin, lower PG I, higher PG II levels and, as a consequence, far lower PG I/PG II ratio compared with controls. The prevalence of H pylori infection was much higher in FHP patients (84.0%), whereas lower in FGP patients (19.44%) than that in controls (40.7%) was positive in 24.0% of FHP patients, 2.78% of FGP patients and 4% of controls. CONCLUSIONS: These results suggest that FHP often develops in a gastric mucosa associated with H pylori infection, while FGP does not appear to be related to H pylori infection.
Subject(s)
Antibodies, Bacterial/blood , Autoantibodies/blood , Gastrins/blood , Helicobacter Infections/immunology , Helicobacter pylori/immunology , Immunoglobulin G/blood , Parietal Cells, Gastric/immunology , Pepsinogens/blood , Polyps/immunology , Stomach Neoplasms/immunology , Biomarkers/blood , Female , Humans , Male , Middle Aged , Polyps/blood , Stomach Neoplasms/bloodABSTRACT
OBJECTIVES: To determine serum concentration of gastrin and pepsinogens (PGs) as markers for the gastric mucosal status and to elucidate the prevalence of serum Helicobacter pylori (H pylori) IgG antibodies and parietal cell autoantibodies (PCAs) in patients with gastric polyps. METHODS: The subjects in this study were composed of 36 patients with fundic glandular polyps (FGP), 25 patients with foveolar hyperplastic polyps (FHP), and 27 asymptomatic healthy volunteers (controls). Serum concentrations of gastrin and PGs were determined by radioinmmunoassay. H. pylori IgG antibodies were measured through an enzyme-linked immunosorbent assay. PCAs were detected by an indirect immunofluorescence technique using cryostat sections of rat gastric mucosa. RESULTS: There were no significant differences between FGP patients and controls in serum concentrations of gastrin, PG I and PG II. FHP patients showed significantly higher serum gastrin, lower PG I, higher PG II levels and, as a consequence, far lower PG I/PG II ratio compared with controls. The prevalence of H pylori infection was much higher in FHP patients (84.0
), whereas lower in FGP patients (19.44
) than that in controls (40.7
) was positive in 24.0
of FGP patients and 4
of controls. CONCLUSIONS: These results suggest that FHP often develops in a gastric mucosa associated with H pylori infection, while FGP does not appear to be related to H pylori infection.
ABSTRACT
OBJECTIVES: To determine serum concentration of gastrin and pepsinogens (PGs) as markers for the gastric mucosal status and to elucidate the prevalence of serum Helicobacter pylori (H pylori) IgG antibodies and parietal cell autoantibodies (PCAs) in patients with gastric polyps. METHODS: The subjects in this study were composed of 36 patients with fundic glandular polyps (FGP), 25 patients with foveolar hyperplastic polyps (FHP), and 27 asymptomatic healthy volunteers (controls). Serum concentrations of gastrin and PGs were determined by radioinmmunoassay. H. pylori IgG antibodies were measured through an enzyme-linked immunosorbent assay. PCAs were detected by an indirect immunofluorescence technique using cryostat sections of rat gastric mucosa. RESULTS: There were no significant differences between FGP patients and controls in serum concentrations of gastrin, PG I and PG II. FHP patients showed significantly higher serum gastrin, lower PG I, higher PG II levels and, as a consequence, far lower PG I/PG II ratio compared with controls. The prevalence of H pylori infection was much higher in FHP patients (84.0
), whereas lower in FGP patients (19.44
) than that in controls (40.7
) was positive in 24.0
of FHP patients, 2.78
of FGP patients and 4
of controls. CONCLUSIONS: These results suggest that FHP often develops in a gastric mucosa associated with H pylori infection, while FGP does not appear to be related to H pylori infection.
