Effect of Age on the Relationship between Gastric Cancer and Helicobacter pylori

Helicobacter pylori is thought to be involved in the pathogenesis of gastric cancer, but the time point at which it produces its effects (critical time) is unknown. We measured the serum level of H. pylori antibody in 787 gastric cancer patients and 1007 controls aged 20 to 69. Odds ratios for different gastric cancer types and stages were determined for each 10-year age class. The overall odds ratio for gastric cancer decreased with age, being 7.0 for those aged 20–29, 14.5 for those aged 30–39, 9.1 for those aged 40–49, 3.5 for those aged 50–59, and 1.5 for those aged 60–69 (trend in odds ratios: P < 0.01). However, there was no such age-dependent trend for early diffuse-type cancer; the odds ratios were 12.6, 4.0, 7.2, 6.5, and 18.5 respectively ( P =0.29). Early cancer tended to show higher seroprevalence than advanced cancer, especially in older subjects. No significant difference in seroprevalence was observed between diffuse and intestinal cancers within each age-class. Seroreversion must have occurred in the time interval between the critical time and the diagnosis of the cancer, especially in older patients. The age-dependent relationship between H. pylori and gastric cancer may be due to seroreversion, which itself may be independent of age. This age-independence indicates that prolonged exposure to H. pylori does not increase the magnitude of its influence on gastric carcinogenesis. Possible mechanisms through which H. pylori exerts pathogenic effects are continuous inflammation in adulthood and/or irreversible damage to gastric mucosa in childhood or the teenage years.     

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 (≥l/week vs. ≥3/month, OR=2.82; 95%CI, 1.06–7.48) and lettuce (≥ I/week vs. ≤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.     

Salty Food Intake and Risk of Helicobacter pylori Infection

To clarify the risk factors for Helicobacter pylori infection, which is considered to play an etiologic role in atrophic gastritis, duodenal ulcer and gastric cancer, various parameters including diet and socioeconomic characteristics were compared between H. pylori -infected and non-infected men. In a cross-sectional study of 634 men aged 40 to 49 years selected randomly from five areas with different rates of gastric cancer mortality, 474 of 628 men evaluated were positive for IgG antibody against H. pylori . After logistic regression analysis adjusted for area, the results showed a significant association between frequent intake of pickled vegetables and prevalence of H. pylori antibody (odds ratios against men who consume < 1 day/week were 1.19 for 1–2 days/week, 1.92 for 3–4 days/week, 1.90 for 5–7 days/week; P for trend = 0.02). Daily consumption of miso soup was also associated with an increased risk (odds ratio against non-daily consumer = 1.60, 95% confidence interval = 1.03–2.49). Occupation, number of siblings, education, smoking and alcohol drinking, and other dietary habits were not significantly associated with the prevalence of infection in this population. Although there are limitations in a cross-sectional study such as this, consumption of salty foods appears to increase the risk of H. pylori infection, which could be a marker of salty food intake or an intermediate risk factor in the etiologic sequence between salty food intake and gastric cancer.     

Clinical and Socio- Demographic Risk Factors for Acquisition of Helicobacter pylori Infection in Nigeria

Background: The aim of the study was to assess clinical and socio-demographic characteristics as well as priordrug usage as risk factors for Helicobacter pylori (H. pylori) infection in Nigeria. Methods: A total of 347 respondentswere surveyed by assessing their clinical and socio-demographic characteristics in comparison with the non-invasivegold standard for H. pylori diagnosis, the urea breath test (UBT). Chi-square test and odds ratio analyses wereconducted in order to assess if variables such as socio-demographic factors, drug intake, and history of ulcer/gastritis/gastric cancer within the family significantly predicted test results. Results: A total of 130 (37.5%) respondents werepositive for H. pylori by the UBT. Living with more than three people in an apartment and a history of ulcer/gastritiswithin the family were significantly associated with H. pylori (p ≤0.05), as well as current antibiotic intake (p ≤0.05).Nationality, stay outside Nigeria, level of education, main occupation, smoking and drinking habits, sources of drinkingwater, number of children and history of gastric cancer had no significant association with H. pylori infection (p ≥ 0.05).Conclusion: The results of the questionnaire revealed that most socio-demographic characteristics of the respondentshad no significant association with H. pylori. Overcrowding, having siblings/parents with history of ulcer/gastritis aswell as prior antibiotic usage had a significant association.     

Helicobacter pylori risk associated with childhood home environment

Helicobacter pylori (H. pylori) is considered to be a cause of gastric ulcer, gastric cancer and other diseases. The relationship between infection and the hygiene or housing circumstances of such patients in their childhood was explored. The study subjects were those who applied for a H. pylori antibody test, and were asked to fill out a questionnaire enclosed with a test kit, inquiring as to their hygiene and housing conditions when they were 10 years old. Of 5971 applicants, 5854 agreed to participate in the study. Associations between the six factors in the questionnaire and infection were calculated, and adjusted for sex, age and district. Drinking water, type of toilet, residential area, number of people in the house, and birth order showed significant correlations with H. pylori infection. The odds ratios (95% confidence intervals) were 0.73 (0.55–0.96) for tap water, 0.72 (0.63–0.84) for flush toilets, 0.74 (0.66–0.83) for urban location, 1.34 (1.09–1.64) for 7 or more people in the household, 1.19 (1.00–1.41) for 4th or 5th in birth order, and 1.47 (1.17–1.85) for 6th or more in birth order. No significant association with breast feeding was observed. These results suggest that infection with H. pylori may be associated with water-related sanitary factors in childhood, and that the bacillus may be transmitted within a family.     

Individual and joint contribution of family history and Helicobacter pylori infection to the risk of gastric carcinoma

BACKGROUND: Helicobacter pylori infection and a positive family history of gastric carcinoma have been identified as risk factors for the disease. It is unclear, however, to what degree their impact on the risk of gastric carcinoma is independent, because H. pylori also clusters within families. METHODS: The authors carried out a population-based, statewide case-control study in Saarland, Germany, to assess the individual and joint contributions of family history and H. pylori infection to the risk of gastric carcinoma. Cases included 68 patients with histologically verified gastric carcinoma. Controls included 239 patients with colorectal carcinoma who were matched to the cases by age and gender. Information on family history (defined as gastric carcinoma in at least one first-degree relative) and potential confounders was collected by standardized interviews. Immunoglobulin G antibodies against H. pylori were measured by enzyme-linked immunosorbent assay. In addition, antibodies against the CagA antigen were determined by Western blot analysis. RESULTS: H. pylori infection and family history were positively related, and both risk factors were more common among cases than among controls. Although the association between family history and gastric carcinoma was somewhat reduced by control for H. pylori infection, both risk factors still showed strong independent relations with gastric carcinoma after control for each other. Compared with uninfected subjects who had no family history, subjects with both a positive family history and infection with a CagA positive H. pylori strain had a more than 8-fold total risk of gastric carcinoma (adjusted odds ratio [OR], 8.2; 95% confidence interval [CI], 2.2-30.4) and a 16-fold risk of noncardia gastric carcinoma (OR, 16.0; 95% CI, 3.9-66.4). CONCLUSIONS: Infection with CagA positive H. pylori strains and a positive family history appear to be strong independent risk factors for gastric carcinoma. They may be useful markers for identifying subjects at high risk for the disease and for targeting efforts of prevention and early detection.     

Assessment of gastric carcinoma risk associated with Helicobacter pylori may vary depending on the antigen used: CagA specific enzyme-linked immunoadsorbent assay (ELISA) versus commercially available H. pylori ELISAs

BACKGROUND: Previous epidemiologic studies produced inconsistent results when examining the relation between Helicobacter pylori infection and the risk of gastric carcinoma by measuring various anti-H. pylori antibodies. This study investigated the increased risk of cancer by examining different antibodies, including the specific anti-CagA antibody and antibodies from two commercially available kits. METHODS: An ELISA for the detection of serum anti-CagA was established using a recombinant CagA protein that the authors previously reported. Serum anti-CagA titer was determined for 80 patients with gastric carcinoma and 80 gender- and age-matched controls. Two anti-H. pylori antibodies from the commercially available kits HEL-p (Amrad, Kew Vic, Australia) and HM-CAP (Enteric Product Inc., Westbury, NY) were also evaluated. RESULTS: Anti-CagA seropositivity differed significantly between gastric carcinoma patients and controls (92.5% vs. 55.0%; P = 0. 0001), showing an odds ratio of 10.4 (95% confidence interval [CI]: 4.23-29.74). The difference was less prominent for the seropositivity of HEL-p (77.5% vs. 58.8%; P = 0.0139; odds ratio: 2. 38; 95% CI: 1.20-4.82) and insignificant for that of HM-CAP (65.0% vs. 57.5%; P = 0.4325; odds ratio: 1.30; 95% CI: 0.68-2.49). CONCLUSIONS: The current study revealed that the antibody assay system used could be one important factor in the assessment of gastric carcinoma risk for patients with H. pylori.     

Role of Helicobacter pylori infection among offspring or siblings of gastric cancer patients

A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. There was no specific relationship between CagA and VacA, and H. pylori infection. Atrophic gastritis and/or intestinal metaplasia were more frequently found in H. pylori-infected relatives of cancer patients (26.1%) than in H. pylori-infected controls (12.9%). These results strongly support a role for H. pylori infection in familial aggregation of gastric cancer. The prophylactic eradication of H. pylori infection in the offspring or siblings of gastric cancer patients may be clinically beneficial.     

Helicobacter pylori seropositivity and subsite-specific gastric cancer risks in Linxian, China

BACKGROUND: Helicobacter pylori carriage (i.e., persistent exposure to the organism without gastric epithelial cell invasion) is an established risk factor for noncardia gastric cancer. However, its association with the risk of cancer of the gastric cardia is controversial. Consequently, we designed this prospective, nested case-control study to further explore the subsite-specific gastric cancer risks associated with H. pylori seropositivity (a surrogate marker for persistent exposure). METHODS: A total of 99 patients with gastric cardia cancer, 82 patients with noncardia gastric cancer, and 192 cancer-free subjects were selected from among the participants (n = 29 584) of a nutrition intervention trial previously conducted in Linxian, China. H. pylori seropositivity was determined by assaying for the presence of H. pylori whole cell and CagA antibodies in baseline serum samples from all subjects. Seropositivity was defined as one or both serum assays being positive. Odds ratios (ORs) for subsite-specific gastric cancer were estimated by multivariate logistic regression analyses. All statistical comparisons were two-sided (alpha =.05). RESULTS: H. pylori seropositivity rates for subjects with gastric cardia cancer, noncardia gastric cancer, and gastric cardia and noncardia cancers combined were 70% (P =.02), 72% (P: =.01), and 71% (P =.003) compared with 56% for cancer-free control subjects. OR estimates for H. pylori seropositivity were 1.87 (95% confidence interval [CI] = 1.10 to 3.17) for gastric cardia cancer, 2.29 (95% CI = 1.26 to 4.14) for noncardia gastric cancer, and 2.04 (95% CI = 1.31 to 3.18) for gastric cardia and noncardia cancers combined. CONCLUSIONS: H. pylori seropositivity was associated with increased risks for both gastric cardia cancer and noncardia gastric cancer in this well-characterized cohort. Thus, H. pylori carriage may increase the risk of cancer throughout the stomach.     

Effect of age on the relationship between gastric cancer and Helicobacter pylori. Tokyo Research Group of Prevention for Gastric Cancer.

Helicobacter pylori is thought to be involved in the pathogenesis of gastric cancer, but the time point at which it produces its effects (critical time) is unknown. We measured the serum level of H. pylori antibody in 787 gastric cancer patients and 1007 controls aged 20 to 69. Odds ratios for different gastric cancer types and stages were determined for each 10-year age class. The overall odds ratio for gastric cancer decreased with age, being 7.0 for those aged 20 - 29, 14.5 for those aged 30 - 39, 9.1 for those aged 40 - 49, 3.5 for those aged 50 - 59, and 1.5 for those aged 60 - 69 (trend in odds ratios: P < 0.01). However, there was no such age-dependent trend for early diffuse-type cancer; the odds ratios were 12.6, 4.0, 7.2, 6.5, and 18.5 respectively (P = 0.29). Early cancer tended to show higher seroprevalence than advanced cancer, especially in older subjects. No significant difference in seroprevalence was observed between diffuse and intestinal cancers within each age-class. Seroreversion must have occurred in the time interval between the critical time and the diagnosis of the cancer, especially in older patients. The age-dependent relationship between H. pylori and gastric cancer may be due to seroreversion, which itself may be independent of age. This age-independence indicates that prolonged exposure to H. pylori does not increase the magnitude of its influence on gastric carcinogenesis. Possible mechanisms through which H. pylori exerts pathogenic effects are continuous inflammation in adulthood and / or irreversible damage to gastric mucosa in childhood or the teenage years.