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Introduction: Collagenous gastritis (CG), a rare disorder of unknown etiology, has been postulated to have immune-mediated mechanisms. We investigated (i) the incidence and prevalence of CG in a pediatric population; (ii) the clinical, endoscopic, and histologic characteristics of childhood-onset CG; and (iii) the evidence for autoimmunity and/or inflammatory activity in these patients., Methods: Clinical, endoscopic, and histologic data were reviewed longitudinally in a population-based Swedish cohort of 15 patients with childhood-onset CG diagnosed in the period 2008-2019. A set of 11 autoantibodies, 4 blood inflammatory biomarkers, and the human leukocyte antigen DQ2/DQ8 genotype was analyzed cross-sectionally., Results: The incidence rate of childhood-onset CG was 0.25/100,000 person-years, with an incidence rate ratio of girls to boys of 4.2 (95% confidence interval, 1.2-15). The prevalence of CG was 2.1/100,000 in children aged younger than 18 years. The endoscopic and histologic findings remained pathologic in all the examined patients during a median follow-up of 4.4 years. Many patients had heredity for autoimmune disorders (47%) and/or tested positive for autoantibodies (40%) or human leukocyte antigen DQ2/DQ8 (53%). No associated autoimmune comorbidities were observed. The serum levels of calprotectin and amyloid A were increased in 10/15 (67%) and 5/15 (33%) of the patients, respectively, whereas plasma C-reactive protein levels were normal in all, but 1 patient., Discussion: The results indicate that childhood-onset CG is rare and has a chronic disease course. Although signs of autoimmune predisposition are frequent, early development of autoimmune comorbidities seems seldom. Serum calprotectin and amyloid A represent novel candidate biomarkers of inflammatory activity in CG (see Visual Abstract, Supplementary Digital Content 4, http://links.lww.com/CTG/A349).

Objective: There is strong evidence accumulating that chronic infection with Helicobacter pylori (H. pylori) interferes with inhibitory pathways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cell to gastrin commonly observed in patients suffering from duodenal ulcer disease (DU), however, remains largely unexplained. Insufficient evidence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer disease (PUD) and how they are related to H. pylori-induced gastritis. The aim of this study was to compare basal gastric acid secretion (BAO), MAO, and the sensitivity of the parietal cell to gastrin in H. pylori-positive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin release and the degree of gastric antral and corpus gastritis., Methods: H. pylori status was assessed by CLO test and histology (two biopsies each from the antrum and the corpus) in 14 H. pylori-positive and 16 H. pylori-negative nonulcer patients of comparable age, weight and gender. Gastritis score was assessed by a pathologist, who was unaware of the acid secretory data. Following determination of BAO, the relation of pentagastrin and gastric acid secretion was established with a cumulative pentagastrin dose response curve for the dose range 0.03-6.0 microg/kg(-1) h(-1) and MAO (Vmax) and pentagastrin sensitivity (ED50) were determined. Basal and postprandial gastrin release was measured by radioimmunoassay., Results: There was a significant higher gastritis score in the H. pylori-positive compared with the H. pylori-negative subjects. The dose response curves of the pentagastrin stimulated gastric acid secretion were not different between H. pylori-positive and H. pylori-negative groups. No correlation was seen between the gastritis score, basal acid output (BAO) peak acid output (PAO), maximum acid output (MAO), ED50 values and the plasma gastrin values. There was, however, a considerable larger variation of the PAO and MAO data of the H. pylori-infected subjects and >50% of the respective data was above or below the relatively low range of the respective values of the noninfected subjects., Conclusions: H. pylori-induced gastritis does not regularly enhance maximum acid output in nonulcer patients, nor does it modify the sensitivity of the parietal cell to gastrin. H. pylori infection is thus unlikely to be directly responsible for an increase of these parameters in DU disease. Our data support, however, the concept that chronic H. pylori infection can either enhance or attenuate maximum acid secretory capacity in certain subgroups of patients.

Objective: The aim of this study was to clarify the mechanism of inappropriate hypergastrinemia in Helicobacter pylori (H. pylori)-infected subjects., Methods: We measured fasting serum gastrin (SG) concentrations, and investigated immunohistochemically G and D cell numbers in 47 subjects with normal mucosa, 24 subjects with chronic gastritis, and 24 subjects with duodenal ulcer (DU). The degree of inflammation and atrophy were classified into four categories based on criteria established in the Sydney System: none, mild, moderate, and severe. Avidin-biotin complex methods were used to identify G and D cells, which were counted per unit square (0.25 mm2) in five random fields from each of two well-oriented antral and fundic biopsies. SG concentrations were measured by radioimmunoassay., Results: The G cell number was not significantly different between 24 subjects with H. pylori-associated gastritis and those with DU. However, the number of antral D cells was significantly lower and the G/D cell ratio was significantly higher in subjects with DU than in those with H. pylori-associated gastritis (p < 0.01), although the degree of inflammation and atrophy in the antrum and H. pylori status were similar between the two groups. The mean fasting SG concentration was higher in subjects with DU than in those with H. pylori-associated gastritis, but the difference was not statistically significant., Conclusions: Our results demonstrate that a marked decrease in antral D cell number with a high G/D cell ratio may contribute to hypergastrinemia and the pathogenesis of DU.

Objectives: Blood group antigens traditionally have been associated with a risk of developing peptic ulcer and gastric cancer. Helicobacter pylori is a bacterium associated with chronic active gastritis and ulcer disease, and its attachment to gastric mucosa was recently shown in vitro to be mediated by blood group Lewisb and H antigens. This study was designed to test the clinical relevance of this laboratory observation in patients undergoing endoscopy and gastric biopsy., Methods: Blood group phenotypes and gastric biopsies for H. pylori and histology were determined and correlated in 384 patients undergoing upper endoscopy. Blood from healthy blood donors was tested for the same blood group antigens and used as a control group., Results: The distribution of blood groups ABO, Lewis, Rhesus, and MN was similar among the patients undergoing endoscopy and a control group of 2369 healthy blood donors from the same geographic area. There was no correlation between H. pylori infection or the H. pylori-associated diseases, peptic ulcer or chronic active gastritis, with any blood group phenotype, including Lewisb, blood group O, or both., Conclusion: No in vivo correlation between H. pylori infection or disease and Lewisb or H antigen could be demonstrated. Moreover, patients with H. pylori infection and disease have a distribution of blood group antigens similar to a control population.

Objectives: Helicobacter pylori (Hp) infection is known to cause several gastroduodenal diseases. In patients with non-ulcer dyspepsia, we assessed the link between Hp infection and gastric mucosal inflammation, as well as the influence of Hp and inflammation on the serum levels of anti-Hp antibodies (IgG), pepsinogen A (PGA), pepsinogen C (PGC), and gastrin., Methods: Entering the study were 221 patients with non-ulcer dyspepsia, all of whom underwent upper gastrointestinal endoscopy., Results: Of the 221 patients investigated, 135 (61%) were Hp positive. The higher the bacterial load, the worse the associated gastritis, the gastric antrum and body being considered. All of the serological indices studied were found to be influenced by gastritis. Serum IgG satisfactorily discriminated between Hp-positive and Hp-negative subjects, with a sensitivity of 84% and a specificity of 86%. PGC, PGA, and gastrin were less accurate. Only PGC only found to be correlated with Hp load. The product of IgG and PGC improved the diagnostic accuracy of IgG alone., Conclusions: Hp infection, frequently found in patients with non-ulcer dyspepsia, is associated with gastric mucosal inflammation; of the indices studied, serum IgG and PGC most accurately indicated Hp infection, and their product may be proposed as an aid in diagnosing Hp infection in dyspeptic patients.

Objectives: To study the relationship between Helicobacter pylori infection, gastric inflammatory scores, and fasting gastrin and pepsinogen A and C concentrations, and to evaluate the effect of treatment on these parameters., Methods: Gastrin and pepsinogen A and C concentrations were measured in 36 patients with gastritis, 10 gastric ulcer patients, 12 duodenal ulcer patients, and in 15 subjects with normal gastric mucosa, by standard radioimmunoassay techniques. Fifteen patients with H. pylori infection underwent triple therapy (bismuth subsalicylate, amoxicillin, metronidazole) and were reassessed 1 month later., Results: Fasting gastrin and pepsinogen A and C concentrations were significantly higher in H. pylori-positive gastritis and peptic ulcer patients than in subjects with normal mucosa and in patients with H. pylori-negative gastritis. There was a significant correlation between inflammatory scores and serum gastrin (r = 0.45, p < 0.0001), and pepsinogen A (r = 0.33, p < 0.006) and pepsinogen C (r = 0.55, p < 0.0001) concentrations. Neither sex nor age affected basal gastrin and pepsinogen concentrations. Eradication of H. pylori infection was successful in 12 patients and resulted in a significant fall in serum gastrin and in pepsinogen A and C concentrations, and in a concomitant improvement of the inflammatory scores. Serum peptide levels and gastritis scores were unchanged in those patients in whom H. pylori infection persisted., Conclusions: These findings suggest that hypergastrinemia and hyperpepsinogenemia are secondary to H. pylori infection and are related to mucosal inflammation.

In patients with gastric cancer who were to undergo gastrectomy, the fasting serum gastrin concentration in the peripheral vein was estimated by radioimmunoassay. The blood samples were also collected from the gastric veins and artery during the time of operations. These gastrin values were compared with morphological findings in the resected stomach. No significant differences in serum gastrin concentration was found between the patients of gastric cancer and normal subjects. In the patients with mucosal atrophy in the oxyntic gland area but with no atrophy in the pyloric gland area, however, significant increase in serum gastrin concentration was observed. In cases where fundal atrophy was accompanied by atrophy in the pyloric gland area, the increase was not observed. The amount of gastrin content in cancer tissue was negligible. These results indicate that the increase in serum gastrin concentration in some patients with gastric cancer might be due to the accompanied atrophy of oxyntic glands in the stomach.

Fasting serum gastrin was determined in 35 Chinese patients with various types of chronic gastritis and in 23 Chinese control subjects. The mean (+/- S.D.) fasting serum gastrin levels for 13 patients with chronic atrophic gastritis, 16 patients with chronic gastritis and six patients with acute-on-chronic gastritis were 32.1 (+/- 38.9) pg./ml., 36.1 (+/- 23.2) pg./ml. and 33.7 (+/- 19.4) pg./ml., respectively. The mean (+/- S.D.) fasting serum gastrin levels for the whole gastritis group (35 patients) and the control group were 34.2 (+/- 28.8) pg./ml. and 24.6 (+/- 13.7) pg./ml., respectively. Statistical analysis showed that the mean basal serum gastrin levels of the three gastritis groups did not differ significantly from control subjects and with each other.