K. Sumii

Helicobacter pylori Infection Is a Major Risk Factor for Gastric Carcinoma in Young Patients

Background: Helicobacter pylori has been established as a risk factor for gastric carcinoma (GCa). Since before the discovery of H. pylori, atrophic gastritis and intestinal metaplasia have been linked to GCa, especially the intestinal-type tumor. The prevalence of H. pylori infection and atrophic gastritis increase with age. Thus, analysis of H. pylori infection in young patients with GCa could help clarify the role of this bacterium in the development of GCa. Accordingly, we investigated the relationship between H. pylori infection, GCa, and histologic gastritis in patients less than 30 years old. Methods: Fifty GCa patients less than 30 years (mean, 26.4 years) and 100 sex- and age-matched controls (mean, 26.8 years) were examined for the presence of H. pylori infection and histologic gastritis. Results: The prevalence of H. pylori infection was significantly higher in GCa patients than in controls (94% versus 40%, P < 0.01). Its prevalence was not associated with tumor location, tumor stage, or histologic type. Gastritis, atrophy, and intestinal metaplasia significantly increased the risk of GCa. By means of multiple logistic regression analysis, the odds ratio for the risk of GCa in H. pylori-positive subjects was found to be 23.5 (95% confidence interval, 6.84-80.7). Conclusions: We confirmed a strong association between H. pylori infection and GCa in young patients. Along with H. pylori infection, histologic gastritis might play an important role in the pathogenesis of GCa in these patients.BACKGROUND Helicobacter pylori has been established as a risk factor for gastric carcinoma (GCa). Since before the discovery of H. pylori, atrophic gastritis and intestinal metaplasia have been linked to GCa, especially the intestinal-type tumor. The prevalence of H. pylori infection and atrophic gastritis increase with age. Thus, analysis of H. pylori infection in young patients with GCa could help clarify the role of this bacterium in the development of GCa. Accordingly, we investigated the relationship between H. pylori infection, GCa, and histologic gastritis in patients less than 30 years old. METHODS Fifty GCa patients less than 30 years (mean, 26.4 years) and 100 sex- and age-matched controls (mean, 26.8 years) were examined for the presence of H. pylori infection and histologic gastritis. RESULTS The prevalence of H. pylori infection was significantly higher in GCa patients than in controls (94% versus 40%, P < 0.01). Its prevalence was not associated with tumor location, tumor stage, or histologic type. Gastritis, atrophy, and intestinal metaplasia significantly increased the risk of GCa. By means of multiple logistic regression analysis, the odds ratio for the risk of GCa in H. pylori-positive subjects was found to be 23.5 (95% confidence interval, 6.84-80.7). CONCLUSIONS We confirmed a strong association between H. pylori infection and GCa in young patients. Along with H. pylori infection, histologic gastritis might play an important role in the pathogenesis of GCa in these patients.

Ultrasonographic evaluation of the bowel wall in inflammatory bowel disease: Comparison of in vivo and in vitro studies

To assist in the evaluation of inflammatory changes of the affected bowel, we classified the transabdominal ultrasonographic findings into types A-C. We compared the in vivo and in vitro sonographic images to the histopathologic findings of resected specimens. A total of 22 bowel specimens (five normal, 12 with Crohns disease, five with ulcerative colitis) were examined sonographically with a 3.75-MHz curved and a 7.5-MHz linear array scanner; histologic examination of the same area of tissue was performed afterwards. These three examinations corresponded well to each other. Our classification scheme is useful in quantifying the severity of inflammatory changes in the affected bowel.

Quantitation of Duodenogastric Reflux and Antral Motility by Color Doppler Ultrasonography: Study in Healthy Volunteers and Patients with Gastric Ulcer

BACKGROUND Our objective was to develop a simple, noninvasive method for evaluating duodenogastric reflux, along with antral motility and gastric emptying of a liquid meal. METHODS Antral motility and gastric emptying were measured by ordinary ultrasonography after a meal of 400 ml consommé. Duodenogastric reflux was evaluated by means of color Doppler. In a preliminary in vitro study we demonstrated that the test meal (consommé) contained oil particles suitable as a marker for color Doppler. We then investigated duodenogastric reflux, antral motility, and gastric emptying of a liquid meal in 43 asymptomatic healthy volunteers and in 24 patients with gastric ulcer. RESULTS This approach was feasible in 65 (97.0%) of the 67 subjects studied. Duodenogastric reflux was demonstrated in 26 (61.9%) of the 42 healthy volunteers and in 20 (87.0%) of the 23 patients with gastric ulcer. The frequency of the duodenogastric reflux and the reflux index were significantly increased in patients with gastric ulcer as compared with asymptomatic healthy volunteers. Gastric emptying and the motility index of antral contractions were significantly decreased in patients with gastric ulcer as compared with asymptomatic healthy volunteers. CONCLUSIONS Ultrasonography with color Doppler is useful for evaluating abnormalities of gastroduodenal motility and can be used to understand the pathogenesis of such disorders.

Gastric Acid Secretion, Serum Pepsinogen I, and Serum Gastrin in Japanese with Gastric Hyperplastic Polyps or Polypoid-Type Early Gastric Carcinoma

We determined the maximum secretion of gastric acid and the fasting serum levels of pepsinogen I and gastrin in Japanese patients with gastric hyperplastic polyps or polypoid-type early gastric carcinoma, comparing those findings with observations in control subjects. Both the maximum acid secretion and fasting levels of serum pepsinogen I were significantly lower in the patients with gastric hyperplastic polyps or polypoid-type early gastric carcinoma than in the controls. Fasting serum gastrin levels were significantly higher in the patients with gastric hyperplastic polyps than in the other two groups of subjects. These data demonstrated that the combination of hypochlorhydria, a low level of pepsinogen I, and hypergastrinemia (type-A gastritis) was common in the patients with gastric hyperplastic polyps, whereas hypochlorhydria and a low pepsinogen I without hypergastrinemia (type-B gastritis) were common in those with polypoid-type early gastric carcinoma.

Gastric corpus IL‐8 concentration and neutrophil infiltration in duodenal ulcer patients

Background: The purpose of the present study was to examine the association between interleukin‐8 (IL‐8) in the gastric body due to Helicobacter pylori infection and histological gastritis, as well as elucidating the effect of acid secretion inhibitors on H. pylori associated body gastritis in duodenal ulcer patients.

Effects of octreotide, a somatostatin analogue, on gastric function evaluated by real‐time ultrasonography

Background: Somatostatin exerts inhibitory effects on physiological functions in the gastrointestinal tract. The actions differ, however, depending on the test meal, dose, and other factors.

Cetraxate, a mucosal protective agent, combined with omeprazole, amoxycillin, and clarithromycin increases the eradication rate of Helicobacter pylori in smokers

Our previous study demonstrated that Helicobacter pylori eradication was less effective in smokers than in non‐smokers. Cetraxate is an anti‐ulcer drug that increases gastric mucosal blood flow.

Helicobacter pylori Infection Is Associated with Low Antral Somatostatin Content in Young Adults Implications for the Pathogenesis of Hypergastrinemia

BACKGROUND Recent studies on the role of Helicobacter pylori in the pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections cause exaggerated gastrin release. METHODS We determined meal-stimulated serum gastrin concentrations and antral somatostatin content in 24 asymptomatic volunteers (6 H. pylori-infected, 18 H. pylori-uninfected). Somatostatin content was determined by radioimmunoassay in biopsy specimens obtained from the antrum. RESULTS Fasting and integrated 2-h gastrin concentrations were significantly higher in H. pylori-positive volunteers than in H. pylori-negative volunteers (fasting, 111 +/- 16.3 pmol/l versus 53.4 +/- 3.5 pmol/l; p < 0.05; integrated 2-h, 267 +/- 41.2 pmol/l versus 70.1 +/- 2.1 pmol/l; p < 0.01). Antral somatostatin content was 0.764 +/- 0.173 ng/mg and 2.931 +/- 0.414 ng/mg in H. pylori-positive and -negative volunteers, respectively (p < 0.01). CONCLUSIONS Low antral somatostatin content may cause hypergastrinemia in asymptomatic healthy volunteers, and H. pylori may contribute to the pathogenesis of duodenal ulcer, through this mechanism.

Increased serum pepsinogen I and recurrence of duodenal ulcer

To determine whether the serum pepsinogen I (PG I) level would be a suitable marker for selecting patients at risk for duodenal ulcer recurrence and, thus, would benefit from maintenance therapy, we treated duodenal ulcer patients with H2-receptor antagonists. After healing 140 ulcer patients we assessed the recurrence rate at 1 year with and without maintenance therapy. The annual recurrence rates in duodenal ulcer patients with hyper-PGI (95 ng/ml or more), with 66 ng/ml less than or equal to PGI less than 95 ng/ml, and with PGI less than 66 ng/ml were 87.0%, 27.3%, and 17.9%, respectively, when they did not receive maintenance therapy. In patients with hyper-PGI the recurrence rate was significantly lower in patients receiving maintenance therapy than in patients not receiving maintenance therapy, whereas in patients with PGI less than 66 ng/ml the recurrence rate was as low as 20% regardless of maintenance therapy. These results indicate that maintenance therapy with half the dose of H2-receptor antagonist is not required by patients with PGI less than 66 ng/ml, whereas those with hyper-PGI may be good candidates for long-term maintenance therapy.

Characteristics of Teen-age Patients with Juvenile Duodenal Ulcer Relation between Inherited Hyperpepsinogenemia I and Duodenal Ulcer

We analyzed environmental factors, family history of peptic ulcer, gastric acid secretion, and serum levels of pepsinogen I (PG I) and gastrin in 56 juvenile patients with duodenal ulcer and 39 normal teenage subjects. Basal acid output and maximal acid output were significantly higher in our duodenal ulcer patients than in controls without ulcer (both, p < 0.01), and patients with duodenal ulcer showed significantly higher serum levels of PG I and gastrin than the controls (both, p < 0.001). There were no significant differences in any environmental factor between the patients and controls. Fifteen of the 17 patients who had one or both parents with hyperpepsinogenemia I had high serum PG I levels. Over half of the duodenal ulcer patients had high serum gastrin levels, irrespective of family history of hypergastrinemia. Our findings suggest that hyperpepsinogenemia I and hypergastrinemia are important characteristics and that genetic background, particularly the inheritance of a gastric mucosal trait expressed as hyperpepsinogenemia I, is frequently involved in the pathogenesis of juvenile duodenal ulcer.