Helicobacter pylori infection in a randomly selected population, healthy volunteers, and patients with gastric ulcer and gastric adenocarcinoma. A seroprevalence study in Taiwan

To investigate the association of Helicobacter pylori and gastric ulcer and adenocarcinoma, IgG antibodies against H. pylori were examined in 823 randomly selected subjects, 92 healthy volunteers, 117 patients with gastric ulcer, and 148 with gastric adenocarcinomas in Taiwan, where the prevalence of gastric adenocarcinoma is high. The seropositivity of this population in Taiwan was 54.4%. Gastric ulcer patients had a higher seropositivity (83.8%) than healthy volunteers (62.0%) and gastric adenocarcinoma patients (62.2%) (P < 0.001). Gender difference, blood type, and habit of smoking were not associated with the seroprevalence in any study groups. Gastric ulcer coexistent with duodenal ulcer had a higher seropositivity (94.7%) (P < 0.05). The seropositivity of H. pylori in gastric adenocarcinoma patients was higher than in healthy volunteers only in younger age and was not associated with histologic type, invasion, and location of major tumors. The results reemphasize the association of H. pylori infection with gastric ulcer but not with gastric adenocarcinoma in Taiwan.     

Serum antibodies against Helicobacter pylori proteins VacA and CagA are associated with increased risk for gastric adenocarcinoma

Infection with Helicobacter pylori is associated with the development of gastric cancer. To study whether the infection with H. pylori strains expressing the vacuolating cytotoxin (VacA) and/or the cytotoxin-associated protein (CagA) is associated with an increased risk of developing gastric adenocarcinoma, sera of 90 patients with gastric cancer and 90 matched controls with cardiovascular diseases were investigated for the presence of antibodies to VacA and CagA by immunoblot. Although no significant difference in the overall H. pylori seropositivity was found between cancer patients and controls, antibodies against VacA or CagA were significantly more frequent in cancer patients than in control subjects. Seventy-five (97.4%) of 77 H. pylori-positive patients in the cancer group, but only 60 (84.5%) of 71 H pylori-positive control patients had antibodies against either VacA or CagA (chi 2 = 6.63; relative risk, 2.00; 95% confidence interval, 1.18-3.39; P = 0.01). The presence of antibodies against VacA or CagA alone was also associated with an increased cancer risk (92.2% vs 80.3%; chi 2 = 5.30; relative risk, 1.74; 95% confidence interval, 1.08-2.78; P = 0.021, for VacA; and 87.0% vs 74.6%; chi 2 = 4.90; relative risk, 1.61; 95% confidence interval, 1.06-2.45; P = 0.037, for CagA). The relative risk for gastric cancer was mainly elevated in patients under 65 years, but not in patients at or over 65 years. There is evidence that infection with VacA- or CagA-producing H. pylori strains increases the risk of developing gastric cancer, especially in younger patients.     

Helicobacter pylori infection and genetic polymorphisms for cancer-related genes in gastric carcinogenesis

The development of gastric cancer is a multistep process that is multi-factorial. An association with the Helicobacter pylori infections, gastric atrophy and gastric cancer has received recent attention. The objective of this study was to elucidate the risk factors for gastric cancer by using molecular epidemiological techniques for genetic susceptibility, gastric atrophy and serum markers including H pylori infection. We used an age- and gender-matched case-control study, where patients with benign gastric lesions were the controls. Low serum pepsinogen I levels (cut-off < 50 ng/mL) and low pepsinogen I/pepsinogen II ratios (cut-off < 3.0) were significantly associated with the risk of gastric cancer (odds ratio [OR] = 3.53: 95% confidence interval [CI] = 2.46-5.09 and OR = 4.73: 3.26-6.88, respectively). However, seropositivity of serum immunoglobulin G (IgG) antibody against H pylori (OR = 1.09: 0.74-1.61) was not associated with gastric cancer, even when analyzed by age greater than or less then 50 years. Specific genotypes of the cytochrome p450 2E1 (CYP2E1) RsaI polymorphism and glutathione-S-transferase (GST) M1 gene deletion were determined but were not associated with gastric cancer; however, a Lmyc genetic polymorphism was associated with gastric cancer (OR = 1.55: 1.03-2.34). Therefore, in this Japanese study, atrophic mucosal change, indicated by serum pepsinogen levels, is a possible risk factor for gastric cancer.     

Possible role of Helicobacter pylori infection in early gastric cancer development

BACKGROUND: Gastric cancer is the most frequently diagnosed malignancy in Japan. The possible relationship between Helicobacter pylori infection and gastric cancer in Japan was evaluated. METHODS: H. pylori infection was identified by the presence of anti-H. pylori IgG. The frequency of H. pylori infection was compared in 213 patients with gastric cancer and the same number of asymptomatic control subjects matched for age and sex. RESULTS: The presence of IgG antibody to H. pylori was significantly more prevalent (P < 0.001) in those with gastric cancer compared with asymptomatic control subjects (88.2% versus 74.6%). H. pylori positive rates were significantly greater in patients with the intestinal type (90.4%, P < 0.001) and diffuse type (86.4%, P < 0.05) of gastric cancer than in control subjects. Ninety-three percent of the patients with early gastric cancer tested positive for H. pylori (P < 0.001 compared with control subjects), whereas no significant difference was observed between those with advanced gastric cancer and control subjects. The intestinal type of early gastric cancer showed only the significantly increased frequency of high titer (optical density > 1.50) of H. pylori IgG antibody (P < 0.001) compared with control subjects without cancer. CONCLUSIONS: These results suggest that H. pylori infection may be associated with the development of early gastric cancer in Japan.     

Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer

Although epidemiological studies strongly suggest an association between gastric cancer and Helicobacter pylori infection, there has been no clinical report indicating that cure of the infection prevents cancer. We conducted a nonrandomized H. pylori eradication trial in patients whose gastric cancer was removed by endoscopic resection (ER). We investigated the effect of treatment on the histopathology of the gastric mucosa, as well as on the incidence of metachronous gastric cancer during the long-term clinical and endoscopic follow-up. One hundred and thirty-two patients with early gastric cancer underwent ER and had H. pylori infection. Sixty-five (group A) were treated with omeprazole and antibiotics to eradicate the infection, and 67 (group B) were not. All patients were followed for 2 years post ER. After eradication treatment in group A, the disappearance of neutrophil infiltration in the antrum and body of the stomach was observed as was a decrease of the severity of intestinal metaplasia. Endoscopy after ER detected no new gastric cancers in these patients. After 3 years of follow-up, 6 (9%) of the 67 patients in group B had a new early-stage, intestinal-type gastric cancer endoscopically diagnosed. The above results suggest that H. pylori eradication may improve neutrophil infiltration and intestinal metaplasia in the gastric mucosa and inhibit the development of new carcinomas. This finding should be confirmed in a randomized, controlled trial.     

Variants of the 3' region of the cagA gene in Helicobacter pylori isolates from patients with different H. pylori-associated diseases

The CagA protein of Helicobacter pylori is an immunogenic antigen of variable size and unknown function that has been associated with increased virulence as well as two mutually exclusive diseases, duodenal ulcer and gastric carcinoma. The 3' region of the cagA gene contains repeated sequences. To determine whether there are structural changes in the 3' region of cagA that predict outcome of H. pylori infection, we examined 155 cagA gene-positive H. pylori isolates from Japanese patients including 50 patients with simple gastritis, 40 with gastric ulcer, 35 with duodenal ulcer, and 30 with gastric cancer. The 3' region of the cagA gene was amplified by PCR followed by sequencing. CagA proteins were detected by immunoblotting using a polyclonal antibody against recombinant CagA. One hundred forty-five strains yielded PCR products of 642 to 651 bp; 10 strains had products of 756 to 813 bp. The sequence of the 3' region of the cagA gene in Japan differs markedly from the primary sequence of cagA genes from Western isolates. Sequence analysis of the PCR products showed four types of primary gene structure (designated types A, B, C, and D) depending on the type and number of repeats. Six of the seven type C strains were found in patients with gastric cancer (P < 0.01 in comparison to noncancer patients). Comparison of type A and type C strains from patients with gastric cancer showed that type C was associated with higher levels of CagA antibody and more severe degrees of atrophy. Differences in cagA genotype may be useful for molecular epidemiology and may provide a marker for differences in virulence among cagA-positive H. pylori strains.     

Rapid recurrence of Helicobacter pylori infection in Peruvian patients after successful eradication. Gastrointestinal Physiology Working Group of the Universidad Peruana Cayetano Heredia and The Johns Hopkins University

Helicobacter pylori is associated with gastritis, peptic ulcer disease, and gastric cancer. Since gastric cancer is common in Peru, eradication of H. pylori may help to reduce the occurrence of gastric cancer. This study involved three randomized trials to determine the efficacy of four different triple-drug therapy regimens. The most successful regimen was furazolidone combined with bismuth subsalicylate and amoxicillin, which eradicated infection in 82% of patients. Patients successfully treated were followed every 2-3 months to determine the recurrence rate of H. pylori infection. Of 105 patients with H. pylori eradication documented by pathology and culture, 52% (55) returned for follow-up endoscopy, and in 73% (40) of these 55 the infection recurred during the 8-month follow-up period. Thirty-five patients from whom H. pylori was eradicated and who were tested for antibodies to H. pylori remained consistently seropositive. Rapid recurrence of H. pylori infection after successful eradication suggests that measures other than antimicrobial therapy are needed to fight H. pylori in developing countries.     

Helicobacter pylori CagA antigen antibodies

BACKGROUND: CagA antigen of Helicobacter pylori is highly immunogenic in humans. There is an increasing evidence that infection with CagA-positive strains is related to the development of peptic ulcer disease, atrophic gastritis, or gastric cancer. The aim of our study was to assess seropositivity to CagA in a group of 95 clinically symptomatic adults who underwent gastroduodenoscopy and to correlate results to their disease characteristics. METHODS AND RESULTS: Serum immunoglobulin G antibodies to CagA detected by ELISA kit (Helicobacter p120, Viva Diagnostika, Germany) were compared to standard IgG specific antibodies against a pool of H. pylori antigens Synelisa Pin plate, ELIAS, Germany). Immunoglobulin G antibodies to CagA were present in 5/31 (16%) serum samples from H. pylori negative persons and 10/28 (36%) serum samples from H. pylori positive patients without peptic ulcer disease compared with 8/11 (73%) H. pylori positive patients with peptic ulcer disease in the past, 11/13 (85%) H. pylori positive patients with duodenal ulcers or duodenitis and 4/5 (80%) H. pylori positive (1/7, 14% H. pylori negative) serum samples from patients with gastric resection for peptic ulcers in the past. Serum levels of antibodies to CagA in the groups of patients with peptic ulcer disease in the past, with present duodenal ulcers of duodenitis and in H. pylori infected patients with gastric resection were significantly higher then those of H. pylori infected patients without peptic ulcer disease (P < 0.05). On the other hand, there was no significant difference in the presence of the specific antibodies against at pool of H. pylori antigens between these four groups. CONCLUSIONS: These data suggest that serologic response to the CagA antigen is more prevalent in H. pylori positive persons with present or past peptic ulceration than among infected persons without peptic ulcer disease. The presence of antibodies to CagA in H. pylori positive persons may be useful for the identification of patients with higher risk or more severe disease.     

Trends in state laws and regulations affecting nurse-midwives: 1995-1997

Increased epithelial cell proliferation is associated with an increased risk of gastric carcinoma. Helicobacter pylori infection is an established risk factor for gastric cancer and the organism has recently been classified as a group I carcinogen by an IARC working group. In this study, we describe differences in gastric epithelial cell proliferation between a H. pylori eradicated group (n = 21) and a not eradicated group (n = 8) after anti-H. pylori eradication therapy to show that increased cell proliferation is associated with H. pylori infection. H. pylori infection was determined by rapid urease test and immunohistochemical method with anti-H. pylori polyclonal antibody. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Ki-67 positive cells in H. pylori associated chronic active gastritis were observed in the glandular neck and the upper portion of foveolar epithelium. Patients who cleared their H. pylori infections showed a significant decrease of Ki-67 labeling index after therapy (0.73 +/- 0.10 vs. 0.48 +/- 0.08, p < 0.01). By contrast, Ki-67 labeling index before and after treatment in patients who remained positive for H. pylori showed no significant difference (0.78 +/- 0.08 vs 0.74 +/- 0.10, p > 0.05). These results indicate that H. pylori infection increases the proliferation of gastric foveolar epithelium, which is reduced by the eradication therapy. We suggest that anti-H. pylori eradication therapy can prevent mucosal cell proliferation to be closely associated with gastric carcinogenesis.     

DNA repair capacity and cisplatin sensitivity of human testis tumour cells

To identify characteristics of gastric cancer associated with hereditary non-polyposis colorectal cancer (HNPCC), we gathered clinical data and tumor samples relating to patients recorded in the Finnish HNPCC registry. Our series included 51 families with a characterized mutation and/or that met the Amsterdam criteria. Of 570 members affected by malignancy, gastric cancer occurred in 62. Adequate clinical data were obtained for 45 patients. Tumor samples from 24 patients were re-examined. The mean age of diagnosis of gastric cancer was 56 years. The average percentage of all cancers within a family was 11 (range 0-40). Nineteen were of the intestinal type. Only 3 were of the diffuse type. Helicobacter pylori infection was demonstrated in 3 of 15 cases. Replication error (RER) phenotype was present clearly in 7 cases and at least fairly clearly in 11. The overall 5-year survival rate was 15%. The 5-year survival rate was 48% in cases in whom radical surgery had been undertaken. Our results support the view that gastric cancer belongs to the tumor spectrum of HNPCC. The intestinal type of histology is characteristic, as is the RER+ phenotype, but H. pylori infection was rare.     

Development of Helicobacter pylori-induced gastric carcinoma in Mongolian gerbils

Helicobacter pylori is classified by IARC/WHO as a definite human gastric carcinogen, despite "inadequate experimental evidence." To obtain direct evidence concerning this relationship, we investigated the histopathological findings of gastric mucosa using a model of H. pylori infection in Mongolian gerbils. The animals were challenged p.o. with H. pylori ATCC-43504 and sacrificed at 6, 12, and 18 months after inoculation for histological examination. All inoculated animals were infected with H. pylori. Severe infiltration of the lamina propria by polymorphonuclear and mononuclear cells appeared in the lesser curvature of the antrum, with an increase in epithelial cell proliferation, and the infiltration extended to the body. Atrophic gastritis and focal intestinal metaplasia also appeared in the lesser curvature of the antral mucosa at 6 months after inoculation. Intestinal metaplasia became severe, with dysplasia, after that. At 18 months after H. pylori inoculation, two of five infected animals showed three well-differentiated gastric cancers. The uninfected control animals showed no abnormal findings throughout the entire observation period. Here, it was confirmed that H. pylori infection alone causes gastric cancer in an animal model.     

Adenocarcinoma in the middle third of the stomach--an evaluation for the prognostic significance of clinicopathological features

BACKGROUND/AIMS: The prognosis of patients with gastric adenocarcinoma varies with the location of the tumor. Adenocarcinoma in the middle third of the stomach has been claimed to have a better outcome than those in other locations. However, there is still very limited information specifically regarding the prognostic factors which influence the survival time of patients with adenocarcinoma in the middle third of the stomach. This retrospective study was designed with the aim to evaluate and uncover the possible significant clinicopathological parameters for adenocarcinoma in the middle third of the stomach. METHODOLOGY: Between 1986 and 1992, 363 patients underwent gastric resection for primary gastric adenocarcinoma at this hospital. Fifty-two (14.3%) of these patients were included in this study and they all met the following criteria: 1) tumor primarily located in the middle third of the stomach without distant metastases or peritoneal seeding, 2) undergoing curative resection and 3) undergoing R2 nodal dissection, at least. The clinicopathological findings were obtained by detailed review of the medical records and the histologic slides. All surviving patients were also contacted and their current conditions were recorded. RESULTS: The overall 5-year survival rate (Kaplan-Meier method) was 42.5%. In univariate survival analysis by Kaplan-Meier method and long-rank test, serosal invasion (p < 0.01), lymph node metastasis (p < 0.01) and lymphatic involvement (p < 0.01) had an individual prognostic significance. When a multivariate analysis using Cox proportional hazards regression was performed, serosal invasion (P < 0.01) and lymphatic involvement (p < 0.05) appeared as the only two independent prognostic factors regarding long-term survival. When these 52 patients were categorized into patients with early gastric cancer (n = 10) and patients with advanced gastric cancer (n = 42), there was a significant difference (p < 0.01) between the survival rates (90.0% vs. 29.1%). When these tumors were further categorized into early gastric cancer (n = 10), early simulating advanced gastric cancer (n = 14) and Borrmann type advanced gastric cancer (n = 28), there were significant differences (P < 0.01 and P < 0.01, respectively) in 5-year overall survival rates between early gastric cancer (90.0%) and Borrmann type advanced gastric cancer (18.9%), also between early simulating advanced gastric cancer (52.5%) and Borrmann type advanced gastric cancer (18.9%). UICC stage also had significant influence (P < 0.01) on the survival rates. CONCLUSIONS: Serosal invasion and lymphatic involvement are the significant, independent prognostic factors in predicting the survival rate of patients with adenocarcinoma in the middle third of the stomach. Since more advanced stage tumors usually carry a poorer prognosis, early detection is of extreme importance for improving the survival rate.     

Surgical treatment of metastatic lung tumors

To evaluate an association between Helicobacter pylori (H. pylori) infection and chronic atrophic gastritis (CAG), an established precursor of gastric cancer, we performed a cross-sectional study using IgG antibody against H. pylori and pepsinogens of blood donors in four prefectures in Japan. Although a geographic correlation between the age-adjusted prevalence rates for H. pylori infection and those for CAG was not seen, the age-adjusted odds ratios (OR) of H. pylori infection for CAG were high in each area (around five for men and from four to 12.6 for women). The association between them weakened with advancing age; the ORs in the youngest age group (16-29 yrs) and in the oldest age group (50-64 yrs) were 12.5 and 2.8 for men, and 11.5 and 5.2 for women, respectively. These findings suggest that H. pylori infection is strongly associated with CAG, while there are some other factors interacting in the development of CAG. A prospective cohort study in which CAG and H. pylori infection are taken into account will be necessary to assess the risks of gastric cancer.     

Cloning, genomic structure, and expression of mouse ring finger protein gene Znf179

OBJECTIVE: H. pylori causes chronic gastritis, which may progress to peptic ulcer, gastric atrophy, or gastric cancer. However, little is known about the role of H. pylori infection in reflux esophagitis and the relationship between reflux esophagitis and atrophic gastritis needs to be clarified. We sought to identify the possible interrelationships among Helicobacter pylori infection, reflux esophagitis, and atrophic gastritis, to signal areas in which researchers should consider focusing their attention. METHODS: A broad-based Medline search was performed to identify all related publications addressing H. pylori infection, atrophic gastritis, gastroesophageal reflux disease (GERD), secretion of gastric acid, and gastric motility published between 1966 and July 1997. RESULTS: Whereas some studies have shown no significant association between H. pylori infection and reflux esophagitis, others have observed that the prevalence of H. pylori infection was lower in patients with GERD, implying a protective role. Eradication of H. pylori leads to occurrence of reflux esophagitis in some cases, but the mechanisms inducing posteradication reflux esophagitis are unknown. H. pylori infection may lead to atrophic gastritis (and hence hypochlorhydia) through both bacterial and host factors, although gastric atrophy and subsequent intestinal metaplasia are hostile to H. pylori because of hypochlorhydria. Although it has been reported that long-term proton pump inhibitor therapy for refractory reflux esophagitis may induce or enhance the development of gastric atrophy in H. pylori-infected patients, this relationship has been disputed. CONCLUSIONS: H. pylori infection may be negatively associated with reflux esophagitis, but this requires confirmation. Research then needs to focus on whether this is explained through motility- or acid-related mechanisms. The potential costs of maintenance antireflux therapy may need to be taken into account when evaluating the cost effectiveness of anti-H. pylori therapy.     

Regional anaesthesia--children are different

Is Helicobacter pylori a true carcinogen? Most carcinogens are physical, chemical or viral agents which give rise to the development of neoplasia by inducing alterations in cellular DNA. Evidence for the carcinogenic potency of such agents is usually based on dose-response curves and animal models and there is often a direct association with (epi-) genetic events. Despite the absence of such data, H. pylori has been designated as a definite cause of human cancer. This designation is largely based on epidemiological evidence. H. pylori is a carcinogen in the sense that infection with this organism induces a persistently inflamed gastric mucosa which is associated with an increased proliferative state and an increased gastric cancer risk. As such, 1-2% of the infected subjects are estimated to develop cancer, with an incidence probably close to nine times higher than that among non-infected subjects. There is a need for additional mechanistic knowledge on this association between chronic epithelial inflammation and carcinogenesis. An additional important question is whether H. pylori eradication may contribute to gastric cancer prevention. As progressive mucosal abnormalities such as atrophy and metaplasia do not regress after such intervention, the major benefit in terms of cancer prevention is likely to be to infected subjects who have not yet developed permanent gastric mucosal damage. This is in agreement with data suggesting that the role of H. pylori may be confined to the initial stages of carcinogenesis.     

Successful eradication of H. pylori in an elderly patient with gastric cancer after effective UFT-E therapy

The patient was a 83-year-old female with 2' T2-type gastric cancer associated with positive H. pylori in the lesser curvature of the stomach. The patient was treated with oral UFT-E alone in a daily dose of 400 mg. The tumor exhibited an O' IIa + IIc-like appearance 4 weeks after the start of administration and became scarred 8 weeks later, revealing marked tumor reduction in a short period of time. At 8 weeks, biopsy showed marked polymorphonuclear cells infiltration of gastric mucosa with no evidence of malignancy. In an attempt to eradicate H. pylori, 30 mg of lansoprazole, 400 mg of clarithromycin, and 2.0 g of ecabet-Na (3.0 g of Gastrom) were administered for 2 weeks. H. pylori was found to have been successfully eradicated, and the inflammatory lesions were no longer visible histologically. UFT-E was highly effective in this patient, and the eradication of H. pylori may contribute to the prevention of cancer recurrence.     

Prognostic role of cisteine and serin proteases in gastriC cancer

Cysteine proteases (cathepsin B and L), the serine protease urokinase-type plasminogen activator and its inhibitor type-1 play an important part in cancer invasion and metastasis. The authors determined the protease concentrations in gastric cancer tissues, using the ELISA method, in patients with gastric cancer. They evaluated the prognostic role of proteases and the relationship that these proteases may have with other histomorphological prognostic parameters such as tumor staging, grading, histotype, Borrmann classification. The Cox survival analysis showed that cathepsin B (p = 0.002), urokinase-type plasminogen activator (p = 0.0001) and the inhibitor type-1 (p = 0.0004) significantly correlated with poor prognosis. The tumor staging, grading, Borrmann classification correlated also significantly with survival time. Urokinase-type plasminogen activator was selected as the single independent variable in the Cox model (p = 0.0001).     

Helicobacter pylori infection and gastric cancer. A nested case-control study in a rural area of Japan

We conducted a seroepidemiological nested case-control study to determine the association of gastric cancer with Helicobacter pylori infection and atrophic gastritis. A cohort of 2858 participants in an annual multiphasic health check-up were followed for eight years. Data for 45 gastric cancer cases and 225 sex-, age-, and address-matched control subjects were analyzed. Helicobacter pylori infection was determined by IgG antibodies, and atrophic gastritis was diagnosed by both serum pepsinogen I level (< or = 70 ng/ml) and the pepsinogen I/II ratio (< or = 3.0). Univariate analysis showed that Helicobacter pylori and atrophic gastritis were significantly associated with gastric cancer. In a multivariate analysis, atrophic gastritis was associated with significantly increased risk of cancer (odds ratio, 3.38; 95% confidence interval, 1.54-7.42); however, Helicobacter pylori was not associated with cancer (odds ratio, 1.84; 95% confidence interval, 0.59-5.72). These results suggest that Helicobacter pylori infection alone is not directly associated with gastric carcinogenesis but has an indirect relation to gastric cancer through the development of atrophic gastritis.     

Helicobacter pylori infection and gastric emptying of indigestible solids in patients with dysmotility-like dyspepsia

BACKGROUND: The role of Helicobacter pylori and gastric motility in dysmotility-like dyspepsia is unclear. The aim of this study was to determine whether delayed gastric emptying of indigestible solids and H. pylori infection are associated with dysmotility-like dyspepsia. METHODS: Thirty-two healthy volunteers and 72 patients fulfilling the criteria of dysmotility-like dyspepsia received a gastric emptying test using radiopaque markers, and the H. pylori status was determined by histology. RESULTS: Twenty-seven percent of volunteers were H. pylori-positive, compared with 32% in the dyspeptic groups (P = NS). Gastric emptying was significantly slower in dyspeptic patients than controls and in H. pylori-positive patients than H. pylori-negative patients. Subjects with gastroparesis have a higher chance of developing dysmotility-like dyspepsia (odds ratio (OR), 2.5) than subjects with normal gastric emptying. Subjects with H. pylori and gastroparesis have an increased likelihood of developing dysmotility-like dyspepsia (OR, 4.3) than if either factor were present alone. CONCLUSION: Our data suggest that gastroparesis alone and gastroparesis and H. pylori infection are associated with dysmotility-like dyspepsia.     

Duodenal ulcer, Helicobacter pylori, and gastric secretion

Patients with chronic dyspepsia were categorised by macroscopic appearance at oesophagogastroduodenoscopy as having duodenal ulceration (DU), other diagnosed lesions such as reflux oesophagitis, carcinoma of stomach, etc, or no organic lesion (non-ulcer dyspepsia, NUD). Material was collected to identify gastric infection with Helicobacter pylori (H pylori) by CP urease test, culture, and histological examination and to make the microscopic diagnosis of active chronic gastritis. Each patient in the DU and NUD categories was then invited to volunteer for a gastric secretion study in which maximal gastric secretion in response to histamine was measured. Sixty two gastric secretion tests were performed (31 DU, 31 NUD). The presence of H pylori was associated with active chronic gastritis (100%). DU patients secreted more acid than the NUD patients. H pylori positivity was associated with decreased maximal gastric secretion in both groups. There was a positive correlation between smoking and maximal acid output shown only in H pylori negative but not in H pylori positive patients. These findings were clear cut when all corrections of maximal gastric secretion were made for pyloric loss, duodenogastric reflux, and stature. This study failed to show any aetiological link between H pylori and DU by increased maximal gastric secretion.