Helicobacter pylori infection and coronary heart disease in the North Glasgow MONICA population

AIM: Recent evidence suggests that Helicobacter pylori infection is associated with coronary heart disease. We investigated whether H. Pylori infection is related to prevalent coronary heart disease, in a random sample of 1428 men and women aged 25-74 years. METHODS AND RESULTS: Coronary heart disease was assessed by questionnaire and electrocardiography (ECG). Standard risk factors for coronary heart disease, fibrinogen concentration and serum concentrations of H. pylori-specific IgG antibody were measured. H. pylori seropositivity increased with age (P < or = 0.001) and was significantly more prevalent in men than women. H. pylori infection was associated with current smoking and a higher systolic blood pressure in men but not in women. There was no significant increase in the odds ratio in those seropositive for H. pylori with regard to any manifestation of coronary heart disease, after adjustment for age, standard cardiovascular risk factors and social class. Likewise, age-adjusted plasma fibrinogen was no higher in seropositives. CONCLUSION: Seropositivity to H. pylori is associated with a trend towards a greater prevalence of coronary heart disease. However, that association is likely to be spurious and can be adequately explained by the much stronger association of H. pylori infection with age and social class, both of which are linked with coronary heart disease.     

Cytotoxin genes of Helicobacter pylori in chronic gastritis, gastroduodenal ulcer and gastric cancer: an age and gender matched case-control study

Helicobacter pylori (H. pylori) infection is involved in many gastrointestinal diseases, such as chronic gastritis (CAG), peptic ulcer and gastric cancer (GCA). Both host factors and H. pylori strain differences may contribute to differences in the diseases. Thus, we conducted an age and gender matched case-control study of 35 patients each with CAG, gastric ulcer (GUL), duodenal ulcer (DUL) and gastric cancer (GCA) to examine the role of strain differences of the H. pylori cytotoxin genes cagA and vacA in these diseases. We employed polymerase chain reaction to examine the gastric juice for H. pylori DNA. The test was positive for 26 (74.3%) CAG, 29 (82.9%) GUL, 28 (80.0%) DUL and 27 (77.1%) GCA patients, showing no statistically significant difference among the diseases (P = 0.84). cagA and vacA genes (picked up by using a vacA1 + vacA2 primer pair which detected non-variable regions of the vacA gene) were detected by PCR in the H. pylori DNA-positive cases as follows: CAG, 92.3% and 76.9%; GUL, 100% and 86.2%; DUL, 89.3% and 89.3%; GCA, 92.6% and 85.2%, respectively. No statistically significant differences were found in the frequencies of these cytotoxin genes in H. pylori-positive cases among the various gastric diseases (P = 0.39 for cagA and P = 0.64 for vacA).     

Helicobacter pylori does not release cysteamine into gastric juice

AIM: To determine whether Helicobacter pylori releases cysteamine into gastric juice as cysteamine is known to be ulcerogenic. METHODS: Samples of fasting gastric juice were collected from 22 individuals (four women); 10 subjects were H pylori negative. The presence of infection was confirmed by examination and culture of gastric biopsies. Cysteamine in gastric juice was measured by reversed phase gradient high performance liquid chromatography with a detection limit of 10 mumol/l. RESULTS: Cysteamine was not detected in any of the gastric juice samples or in extracts of cultured H pylori. CONCLUSIONS: If H pylori produces cysteamine then the amounts produced are insignificant and are unlikely to explain the association between H pylori infection and the development of duodenal ulcer disease.     

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.     

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.     

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.     

Survival after accidental poisoning with a triple lethal dose of paraquat (Gramoxon)

Anti-Helicobacter pylori antibodies were determined in 157 institutionalised Cantonese children, mean age 9.5 +/- 3.9 (SD) years, with profound neurodevelopmental disabilities. Eighty-seven (55.4%) were H. pylori seropositive compared with four of 50 (8%, P > 0.0002) of an age-matched control group, mean age 7.2 +/- 4.3 (SD) years. Eight of 15 seropositive children with a recent history of upper gastrointestinal bleeding underwent endoscopy and in all cases gastric infection with H.pylori was confirmed. Anthropometric data from institutionalised children revealed marked malnutrition but showed no significant difference between seropositive and seronegative children. Disabled children receiving long-term residential care in Hong Kong are confirmed to be at increased risk of H.pylori infection.     

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.     

Helicobacter pylori and gastroduodenal lesions in 547 symptomatic young adults

OBJECTIVES: Helicobacter pylori (H. pylori) is involved in the pathogenesis of gastric inflammatory disorders. Both antral chronic gastritis and H. pylori infection prevalence increase with age. The aim of the study was to assess the prevalence of H. pylori infection in young adults and to study the relationship between endoscopical and histological features and H. pylori infection. METHODS: The study concerned 547 young patients (age: 18-25 years), undergoing endoscopy for upper gastrointestinal symptoms. The severity and the activity of chronic gastritis was graded by histological examination of antral biopsies. The diagnosis of H. pylori infection was based on histology and culture or urease test. RESULTS: Fifty-three percent of the patients had a normal endoscopy; 44 ulcers were found: 34 duodenal ulcers and 10 gastric ulcers. H. pylori infection was detected in 34% of cases. The prevalence of H. pylori infection was 29.8% in non-ulcer patients, 50% in gastric ulcers and 91% in duodenal ulcers (P < 0.01). Duodenal ulcer, aspect of antral mosaic mucosa and nodular gastritis, were closely related to the presence of H. pylori. There was a significant relationship between H. pylori infection and both the severity (P < 0.01) and the activity (P < 0.01) of the antral chronic gastritis. The prevalence of follicular gastritis was 22% : it was present in 60% of H. pylori positive patients and 2.4% of H. pylori negative patients. H. pylori infection was more frequent in patients from Africa than in Europeans (P < 0.01). There was no significant association between H. pylori infection and different types of diets, settlements (rural vs urban) or symptoms. CONCLUSION: These results show that in the young population studied, duodenal ulcer, nodular gastritis, antral mosaic mucosa, active chronic gastric and follicular gastritis are closely related to H. pylori infection. They suggest that in the subgroup of non ulcer symptomatic patients, H. pylori prevalence is higher than in the general population.     

Subcorneal pustular dermatosis in a patient with hyperthyroidism

OBJECTIVES: Gastric carcinoma is the world's second most common cancer. Recent studies suggest an association between Helicobacter pylori and gastric carcinoma. The aim of this study was to address the effects of H. pylori infection on gastric antrum mucosal cell proliferation. METHODS: Forty patients undergoing upper endoscopy for standard indications were included in the study. A rapid urease test was used to determine the presence of H. pylori. Epithelial cell proliferation was determined by immunohistochemical techniques utilizing monoclonal antibody to bromodeoxyuridine. RESULTS: There were no significant differences in the number of labeled cells and in the proliferation fraction (p > 0.1) when patients with H. pylori were compared with those without, and when those over the age of 50 were compared to those under 50. The presence of ulcers similarly had no effect (p > 0.1). CONCLUSION: Helicobacter pylori infection does not increase gastric antrum mucosal cell proliferation.     

The role of Helicobacter pylori in the pathophysiology of duodenal ulcer disease and gastric cancer

Helicobacter pylori infection is now recognized to be an important acquired factor in the pathogenesis of duodenal ulcer disease. There is also an association between H pylori and the subsequent development of gastric cancer. The mechanism of the association between the infection and those disorders is incompletely understood but there is increasing evidence that H pylori-induced disturbances of gastric function play a pivotal role. In this article we review the role of H pylori infection in the pathophysiology of these important upper gastrointestinal diseases.     

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.     

Early gastric cancer and Helicobacter pylori: 34 years of experience at Charity Hospital in New Orleans

Good survival rates have been reported for resected early gastric adenocarcinoma (EGC) in patients found via screening procedures. However, the prevalence of Helicobacter pylori in EGC in unscreened populations is unclear. The major purpose of this investigation was to analyze the clinical experience and incidence of H. pylori in unscreened patients presenting with EGC at Charity Hospital over a 34-year period. From 1963 through 1997, the tumor registry at Charity Hospital compiled data on 2497 patients evaluated for gastric carcinoma. Of these patients, 26 (1%) had lesions that were confined to the mucosa or submucosa, i.e., T1N0M0 (American Joint Commission on Cancer classification). Pathology specimens and medical records were retrieved for confirmation of diagnosis and retrospective analysis for H. pylori. H. pylori was analyzed by Steiner staining and immunohistochemistry using a polyclonal antibody. EGC was detected in 12 men and 14 women with a mean age of 62 years. Upper gastrointestinal X-ray studies were performed on 19 of the 26 patients and failed to conclusively demonstrate a lesion in any case. Endoscopy was performed on 22 patients, and preoperative biopsies were positive in 95 per cent of these. Operative procedures included 2 local excisions and 22 subtotal and 2 total gastrectomies. No extended nodal dissections were performed. Microscopic evaluation revealed lesions limited to the mucosa in 63 per cent of cases and involving the submucosa in 37 per cent of the cases. Of the 14 patients evaluable of H. pylori, 79 per cent were positive for the bacterium. The status of 2 patients is unknown, and only 1 patient died of the original gastric cancer, for a disease-free survival of 96 per cent. The 5-year and 10-year overall survival rates were calculated to be 50 per cent and 21 per cent, respectively, when all causes of death were taken into consideration. Median follow-up of the survivors was 64 months. Resection of early gastric carcinoma in unscreened patients without extended lymphadenectomy yielded excellent results. H. pylori was present in 79 per cent of cases. These data suggest an association between H. pylori and EGC. Whether H. pylori infection is an etiologic factor in gastric cancer remains an area of active research.     

Helicobacter pylori infection: relation with cardiovascular risk factors, ischaemic heart disease, and social class

OBJECTIVE: To determine whether Helicobacter pylori infection is associated with the development of ischaemic heart disease and whether such infection can explain the social class inequality in ischaemic heart disease. DESIGN: Cardiovascular risk factor levels, prevalence of ischaemic heart disease (Rose questionnaire angina, and/or a history of myocardial infarction), and serum antibodies to H pylori (enzyme linked immunosorbent assay) were assessed in a cross sectional population based survey. SETTING: Belfast and surrounding districts, Northern Ireland. PARTICIPANTS: 1182 men and 1198 women aged 25-64 years randomly selected from the Central Services Agency's general practitioner lists. MAIN OUTCOME MEASURES: The relation of H pylori infection with cardiovascular risk factors and ischaemic heart disease. The association of social class with ischaemic heart disease. RESULTS: Systolic and diastolic blood pressure, plasma viscosity, and total cholesterol were not associated with H pylori infection. A weak negative association existed between H pylori infection and fibrinogen (mean (SE) difference in fibrinogen between infected and uninfected individuals -0.09 (0.04) g/l, P = 0.02) and between infection in women and high density lipoprotein (HDL) cholesterol (mean (SE) difference in HDL cholesterol between infected and uninfected individuals -0.06 (0.02) mmol/l, P = 0.006). A potentially important association was demonstrated between H pylori infection and ischaemic heart disease but this did not reach statistical significance (odds ratio (95% confidence interval (CI) 1.51 (0.93 to 2.45), P = 0.1). Social class was associated with ischaemic heart disease independently of cardiovascular risk factors and H pylori infection (odds ratio, manual v non-manual (95% CI) 1.82 (1.14 to 2.91), P = 0.01). CONCLUSION: H pylori may be independently associated with the development of ischaemic heart disease but if this is so the mechanism by which this effect is exerted is not through increased concentration of plasma fibrinogen. H pylori infection does not explain the social class inequality in ischaemic heart disease which exists independently of known cardiovascular risk factors.     

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.     

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.     

Functional dyspepsia, gastric emptying of solids, and Helicobacter pylori infection

The origin of functional dyspepsia (FD) is unknown, however, abnormal gastric emptying and infection by H. pylori have been suggested as possible causes. OBJECTIVE: The aim of this study was to test the hypothesis that infection by H. pylori could be related to alterations in gastric emptying of solids and play a role in the pathophysiology of dyspepsia. METHODS: Studies were performed on 12 controls: 6 males, 6 females, age 40 +/- 13, and on 45 FD patients: 15 males and 30 females, age 43.5 +/- 12. Clinical criteria for FD diagnosis were post-prandial epigastric pain, nausea, vomiting or epigastric bloating, with normal blood test, upper endoscopy and abdominal ultrasound. Diagnosis of H. pylori infection was either by growth positive on culture of antral biopsy or by all of the following: on Gram stain, urease test positive and visualization of microorganisms in the antral biopsy. Gastric emptying of solids was studied with a radio-nuclide technique. Patients were prospectively classified in 4 groups according to the main symptom: reflux-like, ulcer-like, dysmotility, and non-specific. RESULTS: H. pylori infection was observed in 21/32 (66%) FD patients. No significant differences in the gastric emptying of solids between the control group and patients with FD (tl/2 80 +/- 17 minutes vs 75 +/- 16 min). The presence of H. pylori infection did not influence gastric emptying rates (78 +/- 16 minutes in infected patients vs 73 +/- 15 min in non infected patients). Gastric emptying times were similar among the four subgroups of FD patients. CONCLUSIONS: No significant differences in gastric emptying of solids were found in H. pylori infected persons as compared with the controls. These findings suggest that H. pylori infection and/or changes in gastric emptying of solids do not play a role in the pathophysiology of FD.     

Eradication of Helicobacter pylori in patients with end-stage renal disease undergoing dialysis treatment

The aim of the present study was to examine the efficacy and safety of combination therapy with amoxicillin (AMPC), lansoprazole, and plaunotol for the eradication of H. pylori in dialysis patients. The subjects consisted of 15 dialysis patients (10 men and 5 women, mean age of 56 +/- 2.4 years) in whom H. pylori was found in the stomach. H. pylori status was evaluated by histology, culture and rapid urease test with biopsy specimens of the gastric mucosa. The patients were treated with AMPC 500 mg once a day for 3 weeks, lansoprazole 30 mg once a day for 8 weeks and plaunotol 80 mg three times a day for 24 weeks. In addition, the concentrations of serum gastrin and gastric juice ammonia were measured. Fourteen patients completed the treatment schedule, while one discontinued treatment because of nausea and diarrhea. Among the 14 patients, H. pylori was eradicated in 11 without any side effects (eradication rate 78.6%). Concentrations of gastric juice ammonia and serum gastrin were reduced significantly in patients who became H. pylori-negative. The present study indicates that combination therapy with AMPC, lansoprazole and plaunotol is safe and efficient for the eradication of H. pylori in dialysis patients. The results also suggested that elevated concentrations of gastric juice ammonia and serum gastrin in dialysis patients can be attributed, at least in part, to H. pylori infection.     

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.     

Lifestyle and anti-Helicobacter pylori immunoglobulin G antibody among outpatients

Since eradication of Helicobacter pylori (H. pylori) is thought to be a preventive measure against stomach cancer, several studies have examined factors associated with the infection. This paper reports the association of the infection with lifestyle factors observed in a hospital-based case-control study. Cases were 140 anti-H. pylori IgG antibody-positive outpatients (75 males and 65 females). Controls were 52 antibody-negative outpatients (22 males and 30 females). Both groups had undergone gastroscopy at Aichi Cancer Center Hospital between February 1995 and February 1997, and lifestyle data collected on the first visit were linked to calculate odds ratios. A strong association was observed with smoking among males; age-adjusted odds ratio (OR) = 7.85, 95% confidence interval (CI), 2.03-30.4. Rice breakfast (OR = 3.74; 95% CI, 1.30-10.8) and soybean paste soup (every day vs. occasionally, OR = 5.24; 95% CI, 1.80-15.2) were also associated with antibody positivity in males, but not in females. In females, pickled Chinese cabbage (> or = 1/week vs. < or = 3/month, OR = 2.82; 95% CI, 1.06-7.48) and lettuce (> or = 1/week vs. < or = 3/month, OR = 2.90; 95% CI, 1.09-7.76) were significantly associated with positivity. Multivariate analysis gave similar estimates for the above factors. Although the association between smoking and H. pylori infection has not been detected in past studies of a general population, except one recent one, this study on outpatients suggested a possible association. Smoking may work as a cofactor disturbing incidental eradication of H. pylori by antibacterial agents administered for other reasons.