High prevalence of serum immunoglobulin G antibody to Helicobacter pylori and raised serum gastrin and pepsinogen levels in enlarged fold gastritis.

To clarify the prevalence of Helicobacter pylori infection in enlarged fold gastritis, serum immunoglobulin (Ig) G antibody to H pylori was determined in 19 patients with severely enlarged gastric body folds (the widest fold greater than 10 mm on the radiograph), 55 patients with moderately enlarged folds (6 to 10 mm) and 44 control subjects (5 mm or less). The prevalence of serum IgG antibody to H pylori in the severe (100%) and moderate groups (100%) was significantly higher than that in controls (34.1%) (P < 0.01). There were significant differences among the three groups in serum gastrin, pepsinogen I and pepsinogen II levels (severe had the highest levels, followed by moderate and then controls, P < 0.001). H pylori colonization in the gastric mucosa was confirmed by culture, urease test or both, and inflammation by hematoxylin and eosin stain in the 25 H pylori seropositive patients who underwent endoscopy and biopsy. Results suggest that H pylori infection is highly prevalent in enlarged fold gastritis. Further studies on enlarged fold gastritis and H pylori infection are needed.

Serum pepsinogen I levels and acid secretion in Helicobacter pylori associated enlarged fold gastritis.

It has been shown that serum pepsinogen I levels are correlated with maximal acid outputs and can be used as an indicator for parietal cell mass. In this study, the effect of Helicobacter pylori infection on the relationship between serum pepsinogen I levels and maximal acid outputs was investigated in 27 patients with Helicobacter pylori associated enlarged fold gastritis. Before treatment, serum pepsinogen I levels and maximal acid outputs were not significantly correlated. After eradication of Helicobacter pylori, a significant positive correlation was found between serum pepsinogen I levels and maximal acid outputs with a significant increase in pepsinogen I levels and a significant increase in maximal acid outputs. These results indicate that Helicobacter pylori infection distorts the relationship between serum pepsinogen I levels and maximal acid outputs by elevating the former and lowering the latter, and that serum pepsinogen I level after eradication of Helicobacter pylori may reflect parietal cell mass in patients with Helicobacter pylori associated enlarged fold gastritis.

Improved fold width and increased acid secretion after eradication of the organism in Helicobacter pylori associated enlarged fold gastritis.

This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.

Serum gastrin, pepsinogens, parietal cell and Helicobacter pylori antibodies in patients with gastric polyps.

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.

Serum gastrin, pepsinogens, parietal cell and Helicobacter pylori antibodies in patients with gastric polyps

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.

Serum gastrin, pepsinogens, parietal cell and Helicobacter pylori antibodies in patients with gastric polyps.

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.

Campylobacter pilórico, gastritis crónica, úlcera gástrica y úlcera duodenal / Pyloric campylobacter, chronic gastritis, gastric ulcer and duodenal ulcer

Diversos trabajos demuestram un elevado porcentaje de hallazgo del campylobacter pilórico en casos de gastritis crónica y úlcera péptica. Presentamos nuestra experiencia en 672 pacientes evaluados mediante esofagogastroduodenoscopía, por presentar síntomas del tracto gastrointestinal superior. Se utilizó el Panendoscopio Olympus GIF-k2 tomándose dos biopsias del antro gástrico. Los especimenes fueron sometidos a coloración con hematoxilinaeosina y con plata, métodos que nos han dado los mejores resultados diagnósticos. El diagnóstico de úlcera gástrica o duodenal se hizo sobre la base del hallazgo endoscópico y para el diagnóstico de gastritis crônica se consideró el criterio histológico. La gastritis se ha dividido en activa e inactica. Se ha cuantificado el daño mucinoso y el grado colonización bacteriana. Hemos encontrado a la bacteria en el 91.8% de pacientes con gastritis crónica activa, 72.7% con úlcera gástrica y 84.2% con úlcera duodenal. Nuestros resultados sosn concordantes con los de otros autores. Concluimos que el campylobacter pilórico no es un germen oportunista en el estómago, pues produce cuadro inflamatorio y daño celular mucinoso. Su presencia puede jugar algún rol en la etiopatogenia de la úlcera péptica y gastritis