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Summary: Background: Gastric cancer ranks fourth in terms of global cancer‐related deaths. Timely identification of high‐risk populations is crucial to reduce mortality. Although a family history of gastric cancer increases risk, European and British guidelines report weak recommendations and low‐quality evidence about the management of these patients. Aim: To quantify the association in case–control studies of patients with gastric cancer with first‐degree relatives with gastric cancer compared to those who do not. Methods: We conducted a systematic review and meta‐analysis of case–control studies up to November 2023. Data extraction was performed independently by two reviewers. The heterogeneity of effects across studies was quantified by I2. We calculated odds ratios (OR) with 95% confidence intervals (CI) using random effects models. Results: We included 30 studies in the systematic review. In all studies, a first‐degree family history of gastric cancer represented a risk factor for gastric cancer. We included 21 studies on the risk of gastric cancer. There was a significantly increased association between gastric cancer and having first‐degree relative(s) with gastric cancer, but with significant heterogeneity among studies (OR = 2.92; 95% CI 2.402–3.552; p < 0.001; I2 = 81.85%; p < 0.001). Conclusion: This meta‐analysis highlights the relevance of patients' family history of gastric cancer and the importance of this risk factor for the early detection of neoplastic conditions. [ABSTRACT FROM AUTHOR]

Background: The burden of gastric precancerous conditions and factors associated with their detection have not been fully investigated in community-based settings. Little is known about adherence to Sydney system for histopathology of gastric biopsies. Objective: We aimed to investigate what really happens in clinical practice with regard to the detection of gastric atrophy and intestinal metaplasia in dyspeptic patients. Methods: We performed a nationwide survey of 979 consecutive patients (50-65 years old) with dyspeptic symptoms, examined at 24 gastrointestinal endoscopy units throughout Italy. Clinical information was collected from questionnaires; a standard bioptic mapping was performed in each unit, biopsies from each patient were analyzed by histopathology performed according to daily clinical practice in each local histopathology center. Results: Separate descriptions of antral and corporal biopsies were included in 679 pathology reports (69%), whereas Sydney system was applied in 324 reports (33%). Gastric atrophy without intestinal metaplasia (GA) and gastric atrophy with intestinal metaplasia (GIM) were detected in 322 (33%) patients. The full adherence to Sydney system significantly increased the probability of detecting GIM (OR 9.6, 95% CI 5.5-16.7), GA (OR 1.92, 95% CI 1.07-3.44), and either of the conditions (OR 6.67, 95% CI 4.36-10.19). Conclusions: This nationwide survey showed that in one-third of dyspeptic patients, gastric precancerous conditions are detected. In daily routine practice, only 1/3 of histology reports were worked out adhering to Sydney system showing that international guidelines are poorly observed in clinical practice. This may represent a critical element for surveillance strategies for gastric cancer. [ABSTRACT FROM AUTHOR]

Background: Many micronutrients depend on a healthy stomach for absorption. Helicobacter pylori chronic gastritis may alter gastric physiology affecting homeostasis of vitamins and minerals. Objectives: Systematic review to assess whether H. pylori infection is associated with reduced micronutrient levels (other than iron) in the plasma or gastric juice and whether low micronutrient levels are modified by eradication treatment. Method: Medline was searched for relevant publications from inception to June 2010. Studies describing micronutrient levels in H. pylori-infected and not-infected adults and/or the effect of eradication treatment on micronutrient levels were included. Findings: Fifty-two publications were selected: 46 investigated the association between H. pylori infection and reduced micronutrient levels and 14 the effect of eradication treatment on micronutrient levels. Sixty-four studies investigated vitamins (23 ascorbic acid, four ß-carotene, 21 cobalamin, 11 folate, and five α-tocopherol) and 10 addressed minerals (one calcium, one copper, one magnesium, one phosphorus, three selenium, and three zinc). Pooled standardized mean differences in micronutrient levels showed positive associations with H. pylori infection for ascorbic acid (gastric juice, −1.087) and cobalamin (−0.744), and a positive effect of eradication treatment, which increased ascorbic acid in the gastric juice (−1.408) and serum cobalamin (−1.910). No significant association between infection and low folate levels was observed. Meta-analyses for other micronutrients were not performed owing to insufficient data. Conclusions: Meta-analyses indicate that H. pylori infection is associated with reduced levels of ascorbic acid and cobalamin, supported by the positive effect of eradication treatment. For other micronutrients, further studies are needed. [ABSTRACT FROM AUTHOR]

Background: Patients with intestinal metaplasia (IM) are at increased risk for gastric cancer. Endoscopic surveillance has been shown to anticipate cancer diagnosis in an earlier stage. Cost-effectiveness of endoscopic surveillance in IM patients is unknown. To assess the efficacy and cost-effectiveness of an yearly endoscopic surveillance in patients with IM. Methods: A decision analysis model was constructed in order to compare a strategy of performing an EGD every year for a 10-year period (surveillance strategy) following a new diagnosis of IM to a policy of nonsurveillance in a simulated cohort of 10,000 American patients. A 1.8% 10-year cumulative incidence of gastric cancer in IM patients was estimated from the literature. Endoscopic surveillance was simulated to downstage the detected cancers by 58–84%. Costs of EGD and cancer care were estimated from Medicare reimbursement data. The main outcome measurement was the incremental cost-effectiveness ratio. Results: The number of EGDs required to detect one cancer and to prevent one gastric cancer-related death in the surveillance arm were 556 and 3738, respectively. The incremental cost-effectiveness ratio of endoscopic surveillance as compared to a nonsurveillance policy was $72,519 per life-year gained (5–95% percentiles Monte Carlo analysis: $54,843–$98,853). At sensitivity analysis, cancer incidence and the rate of downstaging were the most important variables. Conclusions: According to our simulation, the relatively high risk of cancer in patients with IM and the substantial efficacy of endoscopic surveillance in reducing cancer-related mortality would support the cost-effectiveness of an endoscopic surveillance program in patients with IM. Further research is needed before implementing it in the clinical practice. [ABSTRACT FROM AUTHOR]

Background and Aim: Atrophic body gastritis (ABG) may be induced by H. pylori infection. It is difficult to diagnose H. pylori infection in this condition, since during progression of body atrophy the bacterium disappears. In 30% of patients with ABG no sign of H. pylori infection is detectable. We aimed to investigate whether patients with ABG, classified as H. pylori-negative by conventional methods (ELISA serology and Giemsa stain histology), have been previously exposed to the infection. Methods: Case series consisted of 138 outpatients with ABG, of whom 31 are H. pylori negative (histology and ELISA serology), and 107 are H. pylori related (histology and ELISA serology positive: active infection, n = 29; only serology positive: past infection, n = 78). Thirty control subjects who were H. pylori negative at histology and ELISA serology were investigated. Immunoblotting of sera against H. pylori whole-cell protein lysate was performed. Results: None of the control sera recognized CagA, VacA, heat-shock protein B, and urease B, yielding a specificity of 100%. All H. pylori-negative patients with ABG showed immunoblotting seroreactivity, including in each case either CagA or VacA. The concomitant seroreactivity against CagA and VacA was highly prevalent in the H. pylori-negative patients with ABG, comparable to those with active infection (77.4% vs. 86.2%) and with past infection (vs. 61.5%). Conclusions: Immunoblotting against CagA and VacA is able to prove past exposure to H. pylori infection in all patients with ABG defined as H. pylori-negative by conventional methods, suggesting a hidden role of H. pylori infection in gastric atrophy also in these patients. [ABSTRACT FROM AUTHOR]

Detection ofHelicobacter pyloriinfection in atrophic body gastritis (ABG) is difficult, as during progression of body atrophy,H. pyloridisappears.To increase the diagnostic yield of detection of activeH. pyloriinfection in atrophic body gastritis patients by using noninvasive tests such as13C-Urea Breath Test (13C-UBT) andH. pyloristool antigen test (HpSA) would be useful.27 consecutive patients with newly-diagnosed atrophic body gastritis (19F/7M, age 27–73 years).Gastroscopy with biopsies (antrum n = 3, body n = 3) and histology according to updated Sydney system,H. pyloriIgG serology,13C-UBT, and HpSA.All tests used in the diagnosis ofH. pyloriinfection were in agreement in 9/27 atrophic body gastritis patients (33.3%), being all positive in four (14.8%) and all negative in five patients (18.5%). Ten of the 27 (37%) patients were Giemsa stain-positive and serology-positive (group I). Seventeen of the 27 (63%) patients were Giemsa stain-negative: 5/17 with positive serology (group II) and 12/17 with negative serology (group III). In group I,5/10 (50%) were13C-UBT positive and 4/10 (40%) HpSA positive. In group II, two patients were13C-UBT positive, but all were HpSA negative. Also in group III, all patients were HpSA negative, but one had a positive13C-UBT.In atrophic body gastritis patients, neither13C-UBT nor HpSA per se add useful information regarding activeH. pyloriinfection, but these noninvasive tests may be important in combination with histology and serology to define theH. pyloristatus in some atrophic body gastritis patients. [ABSTRACT FROM AUTHOR]

ABSTRACT Background. Helicobacter pylori is involved in the induction of atrophic body gastritis (ABG). During the progression of atrophic gastritis the disappearance of H. pylori has been documented and in time serology is the only sign that indicates a previous infection. It has been shown that a positive serology, in ABG patients without histological evidence of infection, indicates an active H. pylori infection. Aim. To investigate in a population of patients with ABG the prevalence of H. pylori infection on the basis of histology and serology. Patients. A total of 150 consecutive outpatients with atrophic body gastritis were diagnosed on the basis of a screening system. Methods. All patients had a detailed assessment including measurement of specific anti-H. pylori antibodies, parietal cell antibodies, and fasting gastrin, gastroscopy with biopsies from gastric antrum and body. Results. 24.6% of patients were histologically and serologically negative (Group A). 52.7% H. pylori was not detected on histology but IgG to H. pylori were in all these patients elevated (Group B). 22.6% of patients were found to be positive at histology in the corpus mucosa; all but one of these patients had elevated circulating IgG to H. pylori (Group C). Mean corporal atrophy score in Group B patients was statistically lower than in Group A patients (2.43 ± 0.08 vs. 2.75 ± 0.09; p < .05), but was statistically higher than in Group C patients (1.79 ± 0.11; p < .001). Thus, in corporal mucosa a gradient of atrophy was shown: Group C < Group B < Group A. A similar gradient was observed for the presence of pernicious anemia being lowest in Group C 11.8% increasing to 45.6% in Group B and being highest in Group C 75.6%. A statistical correlation was obtained (r = .04791, p < .05) between the histological score of corporal atrophy and the titer of antibodies to parietal cells and an inverse correlation was obtained (r = - .2322, p < .0001) between the histological score... [ABSTRACT FROM AUTHOR]

Background: Detection of Helicobacter pylori infection in atrophic body gastritis (ABG) is difficult, as during progression of body atrophy, H. pylori disappears., Aim: To increase the diagnostic yield of detection of active H. pylori infection in atrophic body gastritis patients by using noninvasive tests such as (13)C-Urea Breath Test ((13)C-UBT) and H. pylori stool antigen test (HpSA) would be useful., Patients: 27 consecutive patients with newly-diagnosed atrophic body gastritis (19F/7M, age 27-73 years)., Methods: Gastroscopy with biopsies (antrum n = 3, body n = 3) and histology according to updated Sydney system, H. pylori IgG serology, (13)C-UBT, and HpSA., Results: All tests used in the diagnosis of H. pylori infection were in agreement in 9/27 atrophic body gastritis patients (33.3%), being all positive in four (14.8%) and all negative in five patients (18.5%). Ten of the 27 (37%) patients were Giemsa stain-positive and serology-positive (group I). Seventeen of the 27 (63%) patients were Giemsa stain-negative: 5/17 with positive serology (group II) and 12/17 with negative serology (group III). In group I, 5/10 (50%) were (13)C-UBT positive and 4/10 (40%) HpSA positive. In group II, two patients were (13)C-UBT positive, but all were HpSA negative. Also in group III, all patients were HpSA negative, but one had a positive (13)C-UBT., Conclusions: In atrophic body gastritis patients, neither (13)C-UBT nor HpSA per se add useful information regarding active H. pylori infection, but these noninvasive tests may be important in combination with histology and serology to define the H. pylori status in some atrophic body gastritis patients.