Helicobacter pylori seropositivity in subjects with acute myocardial infarction.

OBJECTIVE: To determine whether Helicobacter pylori infection increases the risk of myocardial infarction. DESIGN: Case-control study. SETTING: University teaching hospital. METHODS: Serological evidence of H pylori infection was determined in 342 consecutive patients with acute myocardial infarction admitted into the coronary care unit and in 236 population-based controls recruited from visitors to patients on medical and surgical wards. RESULTS: 206/342 (60.2%) of cases were H pylori positive compared with 132/236 (55.9%) of controls (P = 0.30). Age and sex stratified odds ratio for myocardial infarction associated with H pylori seropositivity was 1.05 (95% CI 0.7 to 1.53, P = 0.87) and this remained non-significant (P = 0.46) when other risk factors for ischaemic heart disease were taken into account using logistic regression analysis. H pylori seropositivity was not associated with several coronary risk factors in either cases or controls. CONCLUSION: No increase was found in H pylori seropositivity in subjects with acute myocardial infarction. This suggests that previous H pylori infection is not a major risk factor for acute myocardial infarction.     

Association between chronic Helicobacter pylori infection and acute ischemic stroke: Fukuoka Harasanshin Atherosclerosis Trial (FHAT)

Helicobacter pylori (H. pylori) have been associated both epidemiologically and pathogenetically with coronary atherosclerosis, but data on the relationship between chronic H. pylori infection and stroke are lacking. Therefore, we investigated the relationship between H. pylori infection and acute ischemic stroke in 62 patients with their first stroke and 143 controls. The stroke patients were all admitted to Harasanshin General Hospital (Fukuoka, Japan) and the controls were asymptomatic age-matched outpatients with hyperlipidemia who did not have cardiac disease or infections. All patients underwent cranial CT scanning and/or brain magnetic resonance imaging, duplex ultrasonography of the extracranial carotid arteries, and transthoracic echocardiography. H. pylori infection was diagnosed by detection of anti-H. pylori IgG antibodies, the 13C-urea breath test, and histology. Conditional logistic regression analysis was performed to analyze the data. The 62 stroke patients and 143 controls were aged from 41 to 92 years. Chronic H. pylori infection was associated with a higher risk of stroke due to small artery occlusion (odds ratio: 9.68; 95% CI: 3.56-33.08, P <0.001) and a lower risk of cardioembolic stroke (odds ratio: 0.27; 95% CI: 0.03-1.53). Chronic H. pylori infection still showed an overall association with ischemic stroke (odds ratio for all subtypes combined: 2.57; 95% CI: 1.09-6.08) after adjusting for major cardiovascular risk factors. These results suggest that chronic H. pylori infection may be a triggering factor that increases the risk of acute ischemic stroke.     

The relationship between chronic H. pylori infection, CagA seropositivity and stroke: meta-analysis

AIMS: There is contrasting evidence on the relevance of chronic infection by Helicobacter pylori (H. pylori) as a risk factor for stroke. We performed a meta-analysis of case-control studies to assess association of H. pylori infection and more virulent H. pylori strains, bearing the cytotoxin-associated gene-A (CagA) antigen, with different types of stroke. METHODS: Outcome measures were: H. pylori and CagA seroprevalence in (1) patients with stroke versus controls, and (2) patients with stroke due to large vessel stroke versus patients with other types of stroke and controls. RESULTS: Seven cross-sectional, case-control studies were included. Odds ratio for individual case-control studies and pooled OR for the association between H. pylori seropositivity and stroke was 1.49 (95% CI 1.24-1.81), for the association between stroke and anti-CagA positivity was 2.23 (95% CI 1.49-3.36). Patients with large vessel stroke had higher odds for H. pylori infection than patients with other types of stroke (odds ratio 1.65; 95% CI 1.12-2.45), and than controls (odds ratio 1.61; 95% CI 1.13-2.32). CONCLUSIONS: Association between H. pylori positivity, anti-CagA positivity and stroke is modest and seems higher with stroke due to large vessel disease. This meta-analysis suggests that the role of CagA positive H. pylori strains in different stroke etiologic subclasses should be the target of future prospective investigation.     

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.     

Infection with virulent strains of Helicobacter pylori is not associated with ischaemic heart disease: evidence from a population-based case-control study of myocardial infarction

BACKGROUND: Although the majority of evidence does not support association between Helicobacter pylori infection and ischaemic heart disease, the nature of this relationship may differ when virulence of the infecting strains are examined. METHODS AND RESULTS: The prevalence of IgG antibody evidence of infection with CagA positive stains of H. pylori was investigated in stored plasma samples from 259 cases of myocardial infarction (aged 25-70 years, 74 males) and 259 population based controls from the same area in Northern Ireland. Two-hundred and seventy (52.1%) subjects were seropositive for anti-CagA IgG. CagA seropositivity was more common in cases than in controls: 56.4 vs 47.9%, odds ratio for seropositivity in cases (95% CI) 1.41 (1.00, 1.99). Substantial attenuation of this relationship occurred on adjustment for age, sex, number of siblings, smoking and measures of socio-economic status: odds ratio (95% CI) 1.16 (0.79, 1.70). A similar pattern was seen for seropositivity for all H. pylori strains. CONCLUSION: Infection with the more virulent strains of H. pylori, as with all strains, is not associated with myocardial infarction.     

Clinical significance of cytotoxin-associated gene A status of Helicobacter pylori among non-steroidal anti-inflammatory drug users with peptic ulcer bleeding: a multicenter case-control study

BACKGROUND: The role of Helicobacter pylori infection and especially of the cytotoxin-associated gene A (CagA) product strain in peptic ulcer bleeding among non-steroidal anti-inflammatory drugs (NSAIDs) users remains controversial. METHODS: A case-control study was carried out including 191 consecutive chronic NSAIDs users admitted to hospital because of peptic ulcer bleeding. Peptic ulcer was verified by endoscopy. Controls comprised 196 chronic NSAIDs users without signs of bleeding of similar age and gender to cases. Multivariate regression analysis was performed for further evaluation of the relationship between H. pylori, CagA status and other risk factors. RESULTS: H. pylori infection was present in 121 (63.4%) cases compared with 119 (60.7%) controls (odds ratio (OR) = 1.14, 95% CI, 0.76-1.72). CagA-positive strains were found to be significantly more frequent in cases than in controls (65/106 versus 41/99 P = 0.008). Current smoking (OR = 2.65; 95% CI, 1.14-6.15; P= 0.02), CagA status (OR = 2.28; 95% CI, 1.24-4.19; P = 0.008), dyspepsia (OR = 6.89; 95% CI, 1.84-25.76; P = 0.004) and past history of peptic ulcer disease (OR=3.15; 95% CI, 1.43-6.92; P=0.004) were associated significantly with increased risk of bleeding peptic ulcer. CONCLUSIONS: The results suggest that CagA-positive H. pylori infection is associated with a more than 2-fold increased risk of bleeding peptic ulcer among chronic NSAIDs users.     

Helicobacter pylori and CagA seropositivity and its association with gastric and oesophageal carcinoma

OBJECTIVE: Helicobacter pylori infection is an established risk factor for non-cardia gastric adenocarcinoma. Infection with H. pylori strains harbouring the cagA pathology island may augment this association. H. pylori infection may at the same time reduce the risk for oesophageal carcinoma. However, prospective data on the association between CagA seropositivity and gastric or oesophageal carcinomas are limited. The purpose of this study was to investigate whether CagA seropositivity among H. pylori seropositive subjects is associated with gastric or oesophageal carcinomas. MATERIAL AND METHODS: A nested case-control study was performed in the Malm? Preventive Medicine cohort consisting of 32,906 middle-aged subjects. Tumour cases were identified by the Swedish National Cancer Registry. The Western blot method Helicoblot 2.1 was used to detect H. pylori and CagA seropositivity. RESULTS: Non-cardia gastric adenocarcinoma was associated with H. pylori seropositivity, odds ratio 17.8 (95% CI: 4.2-74.8; 67 cases). The odds ratio for CagA seropositivity among H. pylori seropositive subjects was 9.7 (95% CI: 1.5-infinity). No significant associations were found between cardia gastric adenocarcinoma and H. pylori or CagA seropositivity among H. pylori seropositive subjects; odds ratios were 1.5 (95% CI: 0.51-4.8) and 2.7 (95% CI: 0.38-infinity), respectively (24 cases). Oesophageal adenocarcinoma and oesophageal squamous cell carcinoma were not significantly associated with H. pylori seropositivity or with CagA seropositivity among H. pylori seropositive subjects; the odds ratios associated with oesophageal adenocarcinoma were 0.46 (95% CI: 0.07-2.6) and 0.38 (95% CI: 0.02-24), respectively. Corresponding odds ratios for oesophageal squamous cell carcinoma were 0.44 (95% CI: 0.15-1.2; 37 cases) and 2.0 (95% CI: 0.24-infinity), respectively. CONCLUSIONS: CagA seropositivity among H. pylori seropositive subjects is a risk factor for non-cardia gastric adenocarcinoma.     

Greater than normal prevalence of seropositivity for Helicobacter pylori among patients who have suffered myocardial infarction

BACKGROUND: There is evidence to suggest that inflammation plays a role in the development of atherosclerosis. Chronic infections may activate an inflammatory response in the walls of blood vessels. OBJECTIVE: To investigate the possibility of there being an association between infection with Helicobacter pylori (H. pylori) and coronary heart disease. METHODS: We examined 100 consecutive patients documented to have recently suffered acute myocardial infarction and 100 control subjects from the same geographical area for whom there was no evidence of coronary heart disease, carefully matched both for age and sex. Blood samples were tested for the presence of immunoglobulin G antibodies against H. pylori with a serological test. RESULTS: In comparison with controls, patients were more commonly smokers (26 versus 12%/0, P < 0.05) and had more commonly been treated for hypertension (37 versus 20%, P< 0.01). There was a significant association between seropositivity for H. pylori and having previously suffered acute myocardial infarction (68 versus 53%, odds ratio 1.36 with 95% confidence interval 1.02-1.82, P=0.034). These findings remained valid in a multivariate analysis including possible confounding factors (age, sex, smoking and hypertension; odds ratio 1.35 with 95% confidence interval 1.01-1.83, P=0.046). CONCLUSIONS: The positive association between seropositivity for H. pylori and having previously suffered acute myocardial infarction found in this study provides further support for the hypothesis that there is a causal association between chronic infection with H. pylori and the development of coronary heart disease.     

Prevalence of Helicobacter pylori infection and its link to coronary risk factors in Japanese patients with acute myocardial infarction.

The association between Helicobacter pylori (H. pylori) infection and coronary artery disease, as well as the association between H. pylori infection and classic coronary risk factors, is controversial in patients from Western countries. The high prevalence of H. pylori infection in Japanese subjects enables an examination of these associations in a large population, especially in young patients, because coronary risk factors may be more strongly associated with younger individuals than with older individuals. The IgG seropositivity to H. pylori was assessed in 618 cases with acute myocardial infarction (AMI) and in 967 controls. The prevalence of seropositivity to H. pylori was similar between cases and controls, but in subjects younger than 55 years, the rate was significantly higher in cases than in controls (58.7% vs 43.3%, p = 0.009). After adjustment for age, gender, diabetes mellitus, hypertension, smoking, body mass index, total cholesterol, and high density lipoprotein cholesterol, the odds ratio for acute myocardial infarction was 2.97 (95% confidence interval, 1.37-6.41; p = 0.006). Worsening of classic coronary risk factors was not associated with H. pylori infection in subjects younger than 55 years. These results suggest that in younger individuals in Japan, H. pylori infection is significantly associated with AMI independent of the classic coronary risk factors.     

Could Helicobacter pylori infection increase the risk of coronary heart disease by modifying serum lipid concentrations?

OBJECTIVE: To investigate the relation between Helicobacter pylori infection and coronary heart disease (CHD). DESIGN: A case-control study. SETTING: Northern Finland (about 650,000 inhabitants). PATIENTS: 116 patients with angiographically documented CHD and 116 controls matched for age and gender randomly recruited from the register of the Finnish Social Insurance Institute. MAIN OUTCOME MEASURES: The odds ratio (OR) estimates for the association of H pylori infection with CHD. RESULTS: 64% of the CHD patients and 53% of the controls were seropositive for H pylori; the OR adjusted for age and gender was 1.5 (95% confidence interval (CI) 0.9 to 2.5). An additional adjustment for the common risk factors of CHD, including lipid concentrations, in a logistic regression analysis produced an OR estimate of 1.1 (95% CI 0.6 to 2.1). Among the controls, those who were H pylori positive had significantly (P = 0.03) higher concentrations of serum triglycerides than those who were H pylori negative: the trend among the cases was similar, but non-significant. The concentrations of HDL cholesterol tended to be lower in those who were H pylori positive than in those who were H pylori negative, among both the cases and the controls. CONCLUSIONS: The impact of H pylori infection as an independent risk factor for CHD seems to be minor. On the other hand the results are consistent with the hypothesis that H pylori infection might modify the serum lipid concentrations in a way that could increase the risk of CHD.     

Relationship between Helicobacter pylori CagA status and colorectal cancer

OBJECTIVES: Infection with Helicobacter pylori, particularly with strains positive for CagA protein, increases the risk of gastric adenocarcinoma. Few studies have explored the possible association between H. pylori infection and colorectal cancer. This study evaluated whether the seroprevalence of CagA in H. pylori-infected patients affected risk for colorectal cancer independently of H. pylori status. METHODS: In this study, we tested serum IgG antibodies against H. pylori (ELISA) and CagA protein (Western blot assay) in 67 patients with colorectal adenocarcinoma, 36 with gastric adenocarcinoma, 47 with other malignancies (cancer controls), and 45 hospitalized for transesophageal echocardiography (TEE controls). Colonic cancer and gastric cancer patients with H. pylori infection were compared to each control group and to the pooled controls using simple and adjusted analyses. RESULTS: H. pylori infection was noted in 50 colon cancer patients, 31 gastric cancer patients, 31 cancer controls, and 32 TEE controls. In all, 41 (82%), 29 (94%), 11 (35%), and 13 (41%), respectively, of these H. pylori-positive sera expressed CagA reactivity (p < 0.001 for all pairwise comparisons between cases and controls). In the adjusted analysis, infection with H. pylori CagA+ compared to H. pylori CagA- was associated with increased risk for colorectal adenocarcinoma (odds ratio = 10.6; 95% CI = 2.7-41.3; p = 0.001) and gastric adenocarcinoma (odds ratio = 88.1; 95% CI = 6.3-1229.2; p = 0.001). CONCLUSIONS: Among patients infected with H. pylori, CagA+ seropositivity is associated with increased risk for both gastric and colonic cancer. This finding should stimulate additional research into the role of cagA+ H. pylori infection in the development of colorectal cancer.     

Helicobacter pylori antigens in the faeces of asymptomatic children in the Buea and Limbe health districts of Cameroon: a pilot study

OBJECTIVE: To determine the prevalence and identify intra-familial risk factors associated with Helicobacter pylori infection in a paediatric population. METHODS: Cross-sectional study in the Buea and Limbe health districts, South West Cameroon. Stool samples were collected from 176 randomly selected apparently healthy children from two communities with different socioeconomic status. They comprised 86 males and 90 females aged 0-10 years with a mean age of 4.29. Helicobacter pylori status was determined using an enzyme-linked immunosorbent assay, the H. pylori stool antigen (HpSA) test. The test uses polyclonal anti-H. pylori capture antibody to detect H. pylori antigens in human stool. Epidemiological data were analysed using the Fisher test and odds ratio (OR) at 95% confidence intervals (CI). RESULTS: The overall prevalence of H. pylori was 52.27% (92 of 176). Univariate analysis showed that H. pylori prevalence was significantly higher in children of the low socioeconomic class, 62.50% (55 of 88) than in those of the high socioeconomic class, 42.05% (37 of 88) (P < 0.05; OR = 2.41, 95% CI: 1.26-4.64). Helicobacter pylori prevalence increased with age from 37.50% (12 of 32) for children aged <3 years, 50.00% (53 of 106) aged 3-6 years and 71.05% (27 of 38) aged 7-10 years (P > 0.05; OR = 0.81, 95% CI: 0.34-1.91). The frequency of infection was significantly higher in males, 64.00% (55 of 86) than in females, 41.11% (37 of 90), (P < 0.05; OR = 2.67, 95% CI: 1.39-5.17). CONCLUSIONS: This study highlights the continuing importance of age, sex and socioeconomic status in the acquisition of H. pylori infection.     

A case-control study of association of Helicobacter pylori infection with morbid obesity in Taiwan

BACKGROUND: Obesity is an increasing health problem in developed countries, where the prevalence of Helicobacter pylori infection is decreasing. Recent studies suggested colonization of the stomach by H pylori might affect gastric expression of appetite- and satiety-related hormone and patients cured of H pylori infection gained weight. It was hypothesized that H pylori could be a contributing pathogenic factor in childhood and adult obesity. METHODS: To determine whether H pylori infection is linked to obesity, a case-control study composed of 414 patients with morbid obesity (a body mass index [calculated as weight in kilograms divided by the square of height in meters] of > or = 35 with serious comorbidity or a body mass index of > or = 40) and 683 control subjects (a body mass index of <25) with a comparable socioeconomic status was conducted. Immunoglobulin G antibodies against H pylori were measured from frozen serum samples by an enzyme-linked immunosorbent assay. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (CI). RESULTS: The overall seropositivity was significantly lower in obese patients (181 [43.7%] of 414) than controls (410 [60.0%] of 683) (OR, 0.50; 95% CI, 0.39-0.65; P<.001). Differences in the estimated risk of the presence of H pylori were more pronounced in younger age groups, with ORs of 0.32 (95% CI, 0.10-1.00; P = .05) in those aged 10 to 19 years, 0.55 (95% CI, 0.34-0.89; P = .01) in those aged 20 to 29 years, 0.49 (95% CI, 0.30-0.80; P = .007) in those aged 30 to 39 years, and 0.58 (95% CI, 0.33-1.00; P = .05) in those aged 40 years or older. CONCLUSIONS: Our data indicated an inverse relationship between morbid obesity and H pylori seropositivity. These findings raise the hypothesis that a lack of H pylori infection, especially during childhood, might enhance the risk of the development of morbid obesity.     

Association of Helicobacter pylori infection with atrophic gastritis and intestinal metaplasia

AIMS: To evaluate the effect of Helicobacter pylori infection and aging on atrophy and intestinal metaplasia of the gastric mucosa. METHODS: One hundred and sixty-three patients were divided into three age groups and underwent an upper gastrointestinal endoscopy where no esophagitis, peptic ulcers, or malignancies were detected. Two biopsy specimens were obtained from the anterior and posterior walls of the antrum and of the fundus. These were used to evaluate the grade of gastritis, bacterial culture and histologic evidence of H. pylori infection. RESULTS: Helicobacter pylori infection was found to be directly associated with an increased risk of gastritis grade (odds ratio (OR) = 90 (95% CI; 30-270)). An age of 60 years and older along with H. pylori infection was also strongly associated with an increased risk of atrophy (OR = 6.6, (95% CI; 2.9-15.2)); OR = 9.8, (95% CI; 2.7-35.4)), as was intestinal metaplasia of the gastric mucosa (OR = 5.5, (95% CI; 1.7-17.6)); OR = 7.9, (95% CI; 2.8-46.1)). The prevalence of atrophic gastritis increased with advancing age in H. pylori-infected patients, but no such phenomenon was observed in H. pylori-uninfected patients. The prevalence of intestinal metaplasia significantly increased with advancing age, irrespective of the presence of H. pylori infection. In addition, H. pylori uninfected female patients had a decreased risk of intestinal metaplasia. CONCLUSIONS: These results suggest that atrophic gastritis is not a normal aging process, but instead is likely to be the result of H. pylori infection, while intestinal metaplasia is caused by both the aging process and H. pylori infection. A decreased risk of intestinal metaplasia found in uninfected female subjects may partly explain the lower prevalence of gastric cancer in females than in males.     

A prospective, controlled study of Helicobacter pylori seroprevalence in coronary artery disease

Objective: Recent studies have suggested that chronic infections may be a risk factor for coronary artery disease. The aim of this study was to determine whether Helicobacter pylori ( H. pylori ) infection was an independent risk factor for coronary artery disease.
Methods: A total of 179 patients undergoing coronary angiography for suspected coronary artery disease were prospectively studied. Angiograms were read by experienced invasive cardiologists blinded to the results of H. pylori serology, which was determined by a validated multiwell ELISA assay.
Results: A total of 121 patients (68%) had evidence of coronary artery disease, whereas 58 patients (32%) had normal coronary angiograms. Of the 121 patients with coronary artery disease, 29 had single vessel disease, 39 had double vessel disease, and 53 had triple vessel disease, respectively. There was no significant difference in seroprevalence of H. pylori infection in patients with and without coronary artery disease (   p = 0.63  ). The odds ratio (after adjustment for other known risk factors) for coronary artery disease in H. pylori -infected subjects was 0.45 (95% CI = 0.15, 1.37;   p = 0.107  ). In patients with coronary artery disease, H. pylori infection did not increase the likelihood of severe disease (odds ratio for triple vessel disease = 0.53; 95% CI 0.18, 1.60;   p = 0.201  ).
Conclusions: H. pylori infection rates are similar in patients with normal and abnormal coronary arteries, and infection with H. pylori is not an independent risk factor for coronary artery disease. In patients who have coronary artery disease, H. pylori infection is not a risk factor for more severe disease. These data argue against a causal role for H. pylori in the pathogenesis of coronary artery disease.     

Risk for gastric cancer in people with CagA positive or CagA negative Helicobacter pylori infection.

BACKGROUND AND AIMS: It is not known why some people with Helicobacter pylori infection develop gastric cancer whereas others do not. Whether the CagA phenotype of H pylori infection affected risk for cancer independently of other posited risk factors was evaluated. SUBJECTS: 242 persons who participated in a previous nested case-control study of gastric cancer. 179 (90 cases and 89 controls) were infected with H pylori as determined by enzyme linked immunosorbent assay (ELISA) in serum and 63 (13 cases and 50 controls) were uninfected. METHODS: Serum samples from cases and controls, obtained a mean of 14.2 years before diagnosis of cancer in the cases, were tested by ELISA for IgG antibodies against the CagA gene product of H pylori. They had previously been tested for pepsinogen I. Using logistic regression analysis, risk for cancer was compared among infected persons with CagA antibodies, infected persons without CagA antibodies, and uninfected persons. RESULTS: Subjects infected with H pylori who had CagA antibodies were 5.8-fold more likely than uninfected subjects to develop gastric cancer (95% confidence interval (95% CI) = 2.6-13.0). This was true for both intestinal (odds ratio (OR) 5.1, 95% CI = 2.1-12.2) and diffuse type (OR 10.1, 95% CI = 2.2-47.4) cancers. By contrast, H pylori infected subjects without CagA antibodies were only slightly, and not significantly, at increased risk for cancer (OR 2.2, 95% CI = 0.9-5.4) and any possible association was restricted to diffuse type carcinoma (OR 9.0, 95% CI = 1.2-65.8). Pepsinogen 1 < 50 ng/ml significantly increased risk for both cancer types in H pylori infected persons and lessened the magnitude of association between CagA and cancer. Educational attainment, cigarette smoking, and ABO blood group were not associated with malignancy. CONCLUSIONS: When compared with uninfected subjects, persons infected with CagA positive H pylori are at considerably increased risk of gastric cancer. CagA negative H pylori are less strongly linked to malignancy and may only be associated with diffuse type disease.     

Helicobacter pylori infection concomitant with metabolic syndrome further increase risk of colorectal adenomas

AIM: To investigate the association of colorectal adenomas with both Helicobacter pylori (H. pylori) infection and metabolic syndrome. METHODS: Using a cross-sectional hospital-based study, we analyzed physical examination data from 9311 healthy subjects with overnight physical examinations performed between January 2004 and December 2006. Examined data included gender, age, life style, anthropometric measurements, blood pressure, biochemical and hematological studies, H. pylori infection detected by esophagogastroduodenoscopy and biopsy urease tests, and colorectal adenomas detected with a complete total colonoscopy. RESULTS: The prevalence values for H. pylori infection, metabolic syndrome, and colorectal adenoma were39.2%, 18.7%, and 20.7%, respectively. Colorectal adenoma risk factors included male gender [odd ratio (OR): 2.005, 95% conf idence interval (CI): 1.740-2.310, P < 0.001], advanced age (OR: 1.046, 95% CI: 1.040-1.052, P < 0.001), smoking (OR: 1.377, 95% CI: 1.146-1.654, P = 0.001), increased body fat (OR: 1.016, 95% CI: 1.007-1.026, P = 0.001), higher white blood cell count (OR: 1.038, 95% CI: 1.005-1.073, P = 0.025), H. pylori infection (OR: 1.366, 95% CI: 1.230-1.517, P < 0.001), and metabolic syndrome (OR: 1.408, 95% CI: 1.231-1.610, P < 0.001). In addition, concomitant H. pylori infection with metabolic syndrome further increased the probability of colorectal adenomas. CONCLUSION: Our study revealed H. pylori infection with concomitant metabolic syndrome might further increase the risk of colorectal adenomas.     

Prevalence of Helicobacter pylori infection in children from an urban community in north-east Brazil and risk factors for infection

OBJECTIVES: To investigate the prevalence of Helicobacter pylori infection in a randomly selected population of children from a low income community in Brazil and the risk factors for infection. DESIGN: A cross-sectional, randomised study of prevalence and risk factors. SUBJECTS: Children living in an urban community in north-east Brazil. METHODS: H. pylori infection was determined using the C-urea breath test. Risk factors were assessed using a structured interview schedule. RESULTS: The overall prevalence of H. pylori was 56% (197/353). The infection was most common for those aged 12-14 years. In this group 75.4% (49/65) (95% CI, 63.1-85) of all children were positive for H. pylori, while in children less than 2 years of age 35.1% (13/37) (95% CI, 20.2-52.5) were positive. The prevalence of H. pylori increased significantly with age (P < 0.0001). In the bivariate analysis, a significant difference was found in the prevalence of H. pylori infection and age, number of persons per room, the number of children per household, cup sharing, and type of drinking water (P < 0.05). However, after logistic regression modelling only age (odds ratio (OR) = 1.3; 95% confidence interval (CI), 1.07-1.65), and number of persons per room (OR = 2.58; 95% CI, 1.4-4.6) were risk factors for H. pylori infection. CONCLUSIONS: H. pylori is highly prevalent among children in a north-eastern Brazilian community characterised by poor living conditions, and this infection is largely acquired during early childhood. The infection increased with age, and domestic overcrowding. Further longitudinal studies must examine in depth the possible modes of transmission of the organism in young children.     

Helicobacter pylori infection in children: relation with current household living conditions.

BACKGROUND: Studies demonstrating that deprived household living conditions during childhood are risk factors for acquisition of Helicobacter pylori infection have been performed mainly in adults, who probably acquired the infection several decades ago. This study investigates whether deprived household living conditions remain important risk factors for infection in subjects (children) with recently acquired infection. AIMS: To examine the relation between current household living conditions and acquisition of H pylori infection in childhood. SUBJECTS/SETTING: Opportunistically recruited group of 367 children, aged 3 to 15 years, undergoing routine non-gastrointestinal day surgery. METHODS: Anti-H pylori IgG antibodies measured by a commercial enzyme linked immunosorbent assay validated for use in children. Postal questionnaire collecting sociodemographic data and data on household living conditions. RESULTS: Infection was associated with social class and overcrowding in the household. After adjustment for age, social class, and household density, a positive association remained between infection with H pylori and bed-sharing between children and parents on one or two nights per week, odds ratio for infection (95% CI), 2.29 (1.21, 4.32) or more frequently, odds ratio for infection (95% CI), 2.95 (1.35, 6.45). CONCLUSIONS: The continuing importance of household living conditions in the acquisition of H pylori infection is confirmed and household crowding and sharing a bed with a parent are identified as risk factors for infection.     

Macrophage migration inhibitory factor and the risk of myocardial infarction or death due to coronary artery disease in adults without prior myocardial infarction or stroke: the EPIC-Norfolk Prospective Population study

PURPOSE: To determine whether plasma levels of macrophage migration inhibitory factor, a proinflammatory cytokine involved in atherogenesis, are predictive of myocardial infarction or death from coronary artery disease. METHODS: We performed a prospective case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort. We selected men and women who did not report a history of myocardial infarction or stroke at baseline. Baseline concentrations of macrophage migration inhibitory factor were measured among 777 patients who had a myocardial infarction or died of coronary artery disease during follow-up, and 1554 matched controls who remained free of coronary artery disease. RESULTS: Baseline macrophage migration inhibitory factor concentrations were higher in cases than controls (median, 107.4 microg/L vs. 90.7 microg/L, P = 0.001). The risk of myocardial infarction or death from coronary artery disease increased with increasing quartiles of macrophage migration inhibitory factor (P for linearity <0.0001). Patients in the highest quartile had the greatest likelihood of myocardial infarction or death due to coronary artery disease (unadjusted odds ratio [OR] = 1.6; 95% confidence interval [CI]: 1.2 to 2.0). After adjustment for traditional risk factors and C-reactive protein level, the odds ratio decreased slightly (OR = 1.3; 95% CI: 1.0 to 1.7). Upon additional adjustment for white cell count, this association was no longer statistically significant. CONCLUSION: Prospective data suggest that the relation between macrophage migration inhibitory factor and the risk of myocardial infarction or death due to coronary artery disease in adults without a history of myocardial infarction or stroke is not very strong. However, the data support a regulatory role for macrophage migration inhibitory factor in the process of atherosclerosis.