The diagnosis of paraneoplastic GI motor dysfunction requires a high index of clinical suspicion. A panel of serological tests for paraneoplastic autoantibodies, scintigraphic gastric emptying, and esophageal manometry are useful as first-line screening tests. Seropositivity for ANNA-1, PCA-1, or N-type calcium channel-binding antibodies should prompt further evaluation for an underlying malignancy even when routine imaging studies are negative.

Background:Irritable bowel syndrome is one of the most commonly encountered gastrointestinal disorders, for which there are no established diagnostic criteria. Thus, a diagnosis of IBS is made by exclusion of any organic diseases. Recently, important attempts for the positive diagnosis of irritable bowel syndrome by questionnaire surveys of physical symptoms have been made. We performed a questionnaire survey to evaluate the diagnostic value of the Manning criteria and to observe the major symptoms in irritable bowel syndrome.Methods:A symptom questionnaire which consisted of 22 items, including 6 cardinal symptoms of the Manning criteria, were answered by 172 outpatients who had gastrointestinal complaints. According to a final diagnosis based on independent clinical evaluation, all patients were categorized in three groups: irritable bowel syndrome group, nonulcer dyspepsia group and organic gastrointestinal disease group. The results of the questionnaire were analyzed for each group.Results:The sensitivity and specificity of the Manning criteria for the diagnosis of irritable bowel syndrome were 67% and 70% if three or more items were regarded as positive. The mean score and overall frequency of the Manning criteria were significantly higher in irritable bowel syndrome group than in nonulcer dyspepsia (p<0.01) or organic gastointestinal disease group (p<0.05) Among subgroups of the irritable bowel syndrome group, the pain-predominant subgroup showed a significantly higher score and overall frequency than the painless subgroup(p<0.05).Conclusions:The Manning criteria would be useful as a simple and reliable backup tool for the diagnosis of irritable bowel syndrome and seem to be more useful in pain-predominant subgroup. More detailed history-taking should prevent unnecessary extensive investigations for the diagnosis of irritable bowel syndrome.

ObjectivesHelicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells.MethodsThe numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted.ResultsFasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3±23.5 vs 47.6±14.1 pg/ml, p<0.001). The number of G-cells per gastric gland was similar in infected and uninfected patients (7.1±3.1 vs 7.3±3.9, respectively, p>0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3±0.4 vs 2.5±1.6, respectively, p<0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7±2.7 vs 3.5±1.9, respectively, p<0.001).ConclusionsThese results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.

Background:Helicobacter pylori is known to be a cause of active chronic gastritis and has been proposed as an etiologic factor in the development of peptic ulcer disease, but controversy continues regarding the pathogenic importance and mechanism. We examined the prevalence of H. pylori infection in patients with peptic ulcers and non-ulcer dyspepsia.Method:749 patients (373 with duodenal ulcer, 303 with gastric ulcer, 73 with non-ulcer dyspepsia) were included. Endoscopic mucosal biopsies were done at antrum, duodenum, and, if present, ulcer margin. The specimens were tested by Gram staining, Giemsa staining, culture, urease testing for identification of H. pylori. Antibody to H. pylori was examined in 83 patient of these patients by ELISA, and the result was compared with the results of bacteriologic studies.Result:Prevalence of H. pylori in antral mucosa was higher in patients with duodenal ulcers (81.5%) than in patients with gastric ulcer and non-ulcer dyspepsia (56% and 52.8%) (P<0.05). Also in the duodenal mucosa of non-ulcer sites, and the ulcer margin of patients with duodenal ulcers, the detection rates (12% and 40.7%) were higher than those in the duodenal mucosa of patients with gastric ulcer and non-ulcer dyspepsia (7% and 8%)(p<0.005). Antibody to H. pylori was detected in all patients with duodenal and gastric ulcers and non-ulcer dyspepsia who were tested for antibody. In contrast, the detection rates of antibody in adult control and child control were 33.3% and 27%. Among patients with antibody to H. pylori, H. pylori was detected in 85.7% of patients with duodenal ulcer, 62.5% of patients with gastric ulcers and 22.2% of patients with non-ulcer dyspepsia(p<0.05).Conclusion:These data suggest that H. pylori is a possible pathogen for duodenal ulcer by duodenal colonization probably via gastric metaplasia. Also the past or present infection of H. pylori in antral mucosa may play a role at least partially in generation of upper gastrointestinal symptoms.

Background:A randomized prospective study on the response of fasting serum gastrin concentrations in peptic ulcer patients was performed in order to test the hypothesis that H. pylori infection in the gastric antrum increases gastrin release, and to examine whether the high fasting serum gastrin concentrations respond to treatment that eradicates H. pylori.Methods:One hundred and twenty-seven patients with gastric or duodenal ulcer were included in this study. Patients were divided into three groups on the basis of antral H. pylori status and therapeutic modalities. The first group, 58 patients infected by H. pylori, was treated with metronidazole and tripotassium dicitrato bismuthate combined with ranitidine and mylanta. The second group, 40 patients also infected by H. Pylori, was treated with ranitidine and mylanta. The third group, 29 patients, free of H. pylori infection, was designed to evaluate the influence of H2-receptor antagonist on the change of gastrin. When ulcers were completely healed, changes of gastrin concentrations and H. pylori status were re-examined.Results:H. pylori was eradicated in all patients who have received antibacterial therapy in 4 weeks, and serum gastrin concentrations were significantly decreased after eradication of the organism both in gastric and in duodenal ulcer diseases. (Gastric ulcer: 129.3±47.0 pg/ml before and 63.7±21.6 pg/ml after treatment. Duodenal ulcer: 108.3±35.0 pg/ml and 66.5±21.9 pg/ml, respectively. Total: 112.7±38.2 pg/ml vs 66.0±21.6 pg/ml) (p<0.01). In contrast, H. pylori-positive patients who have not received antibacterial therapy were still infected at the completion of the study, and serum gastrin concentrations increased even though the difference was not significant. (Gastric ulcer: 118.4±51.2 pg/ml vs 124.0±56.5 pg/ml. Duodenal ulcer: 85.4±35.1 pg/ml vs 104.6±43.5. Total: 99.5±45.3 vs 112.9±48.7 pg/ml.) (p>0.05) None of the patients who were initially H. pylori-negative has been reinfected during the period of the study, and their serum gastrin concentrations were not changed. (Gastric ulcer: 69.8±38.0 pg/ml. Total: 63.2±31.1 pg/ml. Duodenal ulcer: 55.1±17.6 pg/ml vs 55.8±13.8 pg/ml. Total: 63.2±31.1 pg/ml vs 63.4±30.0 pg/ml) Four- to six-week therapy of H2-receptor antagonist and antacid had no influence on serum gastrin concentrations.Conclusions:On the basis of the above results, we confirmed that the chronic infection of H. pylori of gastric antrum in peptic ulcer patients causes increased release of serum gastrin, and eradication of the organism results in a significant fall in serum gastrin concentrations