Odds Ratio Of Gastric Cancer Research Articles

Sensitivity of Ultrasonography for Gastric Cancer Diagnosis in Symptomatic Patients

Endoscopy with biopsy sampling is the gold standard used in gastric cancer diagnosis. However, the positive predictive value of signs and symptoms for the diagnosis of carcinomas is quite limited, and, therefore, many patients are subjected to non-diagnostic endoscopies, especially when symptoms are not so specific. This study shows that ultrasonography is sensitive enough for the diagnosis of gastric cancer, and, therefore, use of this technique would further ensure a better selection of patients for endoscopy. The study included 143 patients (86 men and 57 women, with an average age of 68.6 years) who were suspected of having gastric cancer. The diagnostic accuracy of ultrasonography was evaluated in a blind study. The conventional technique was used in all cases. Demographic parameters and a series of other clinical-analytical variables were studied to look for possible gastric cancer predictive factors, which when present would make ultrasonographic results irrelevant. Statistical analysis was done using SPSS 12.0, wherein a value of P < 0.05 was considered to be statistically significant. Of the 143 patients studied, 40 were diagnosed to have gastric cancer. Sonography was able to diagnose 37 cases correctly, while there were three false negative findings and eight false positive findings. This results in 92.5% sensitivity, 92.2% specificity, 82.2% positive predictive value, 96.9% negative predictive value, and a global accuracy of 92.3%. Univariate analysis showed that persistent vomiting (P = 0.021), hemoglobin level of less than 8 g/dl (P = 0.045) and a positive ultrasonography result (P < 0.0001) were associated with a higher frequency of gastric cancer. Multivariate analysis showed that persistent vomiting, with an odds ratio for gastric cancer of 3.68 (95% confidence interval 1.15-11.79; P = 0.039), and a positive ultrasonography result, with an odds ratio for gastric cancer of 117.78 (95% confidence interval 32.45-427.49; P < 0.0001), could be considered as independent predictive factors for gastric cancer. It was concluded that ultrasonography is a very sensitive and specific technique for diagnosing gastric cancer. Gastric cancer was found to be present in just 28% of the patients studied, and their condition was suspect because of the clinical manifestations. Only vomiting and a positive ultrasonography result can be considered as independent predictive factors of gastric cancer.

Helicobacter pyloriinfection and low serum pepsinogen I level as risk factors for gastric carcinoma

To study whether examination of CagA antibodies could increase the odds ratio for gastric cancer in a case-control study, and how often other serum markers of gastric cancer risk could be found in Helicobacter pylori -negative patients. H pylori CagA and parietal cell antibodies (PCAs), and serum pepsinogen I (SPGI) levels were compared between patients with gastric cancer and controls who received endoscopic examination due to reasons other than gastrointestinal malignancy. The odds ratio (OR) for gastric cancer was 2.9 (95% CI 1.4-5.8) in H pylori + patients, and 2.4 (95% CI 1.2-4.9) in CagA+ patients. When results of H pylori and CagA antibodies were combined, OR increased to 5.0 (95% CI 2.5-10.0). Furthermore, if cardia cancer patients were excluded, the OR increased to 6.8 (95% CI 3.1-14.8). Among patients with a low SPGI level, the OR was 12.0 (95% CI 4.1-35.3). However, the risk was significant only in the older age group. The number of patients with low SPGI was significantly higher in H pylori -/CagA+ patients as compared to other cancer patients. Examination of both H pylori and CagA antibodies increases the OR for gastric cancer in our case-control study. CagA antibodies are important in detecting previous H pylori infection in advanced atrophic gastritis or cancer when spontaneous decline of H pylori antibodies occurs. SPGI may be helpful in screening elderly gastric cancer patients.

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.

Evolution of precancerous lesions in a rural Chinese population at high risk of gastric cancer

The pathogenesis of gastric cancer (GC), particularly of the intestinal type, is thought to involve a multistep and multifactorial process. Our objective was to determine the rates of transition from early to advanced gastric lesions in a population in Linqu County, China, where the GC rates are among the highest in the world. An endoscopic screening survey was launched in 1989–1990 among 3,399 residents aged 34–64 years with precancerous lesions diagnosed from biopsies taken from 7 standard locations in the stomach and from any suspicious sites. The cohort was subsequently followed, with endoscopic and histopathologic examinations conducted in 1994. Logistic regression analysis was used to estimate odds ratios (ORs) of progression to advanced lesions of various levels of severity as a function of age, sex and baseline pathology. The rates of progression were higher among older subjects, among men and among subjects with more extensive gastric lesions. 34 incident GCs were identified during the follow-up period. The ORs of GC, adjusted for age and sex, varied from 17.1, for those with baseline diagnoses of superficial intestinal metaplasia (IM), to 29.3, for those with deep IM or mild dysplasia (DYS) or IM with glandular atrophy and neck hyperplasia, to 104.2, for those with moderate or severe DYS, as compared with subjects with superficial gastritis (SG) or chronic atrophic gastritis (CAG) at baseline. Our prospective study of a high-risk population revealed sharp increases in the risk of GC and advanced precursor lesions according to the severity of lesions diagnosed at the start of follow-up. Int. J. Cancer, 83:615-619, 1999. Published 1999 Wiley-Liss, Inc.

Evolution of precancerous lesions in a rural Chinese population at high risk of gastric cancer.

The pathogenesis of gastric cancer (GC), particularly of the intestinal type, is thought to involve a multistep and multifactorial process. Our objective was to determine the rates of transition from early to advanced gastric lesions in a population in Linqu County, China, where the GC rates are among the highest in the world. An endoscopic screening survey was launched in 1989-1990 among 3,399 residents aged 34-64 years with precancerous lesions diagnosed from biopsies taken from 7 standard locations in the stomach and from any suspicious sites. The cohort was subsequently followed, with endoscopic and histopathologic examinations conducted in 1994. Logistic regression analysis was used to estimate odds ratios (ORs) of progression to advanced lesions of various levels of severity as a function of age, sex and baseline pathology. The rates of progression were higher among older subjects, among men and among subjects with more extensive gastric lesions. 34 incident GCs were identified during the follow-up period. The ORs of GC, adjusted for age and sex, varied from 17.1, for those with baseline diagnoses of superficial intestinal metaplasia (IM), to 29.3, for those with deep IM or mild dysplasia (DYS) or IM with glandular atrophy and neck hyperplasia, to 104.2, for those with moderate or severe DYS, as compared with subjects with superficial gastritis (SG) or chronic atrophic gastritis (CAG) at baseline. Our prospective study of a high-risk population revealed sharp increases in the risk of GC and advanced precursor lesions according to the severity of lesions diagnosed at the start of follow-up. Int. J. Cancer, 83:615-619, 1999. Published 1999 Wiley-Liss, Inc.

Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer

Background & Aims: Reports in the literature regarding the relationship of Helicobacter pylori infection to gastric cancer are conflicting. The aim of this study was to identify the source of heterogeneity between studies. Methods: Meta-analysis of cohort or case-control studies with age- and/or sex-matched controls, providing raw data on H. pylori infection detected by serology, was used. Results: A fully recursive literature search identified 19 qualified studies with 2491 patients and 3959 controls. Test for homogeneity found a significant difference in odds ratio between patients with early and advanced gastric cancer (6.35 vs. 2.13; P = 0.01), patients with cardiac and noncardiac gastric cancer (1.23 vs. 3.08; P = 0.003), and population- and hospital-based controls (2.11 vs. 1.49; P < 0.001). The summary odds ratio for gastric cancer in H. pylori–infected patients is 1.92 (95% confidence interval [CI], 1.32–2.78), 2.24 (95% CI, 1.15–4.4), and 1.81 (95% CI, 1.16–2.84) for all studies, cohort, and case-control studies, respectively. H. pylori–infected younger patients have a higher relative risk for gastric cancer than older patients with odds ratios decreasing from 9.29 at age ≤29 years to 1.05 at age ≥70 years. H. pylori infection is equally associated with the intestinal or diffuse type of gastric cancer. Conclusions: H. pylori infection is a risk factor for gastric cancer. The heterogeneity of reported results is caused by differences in the selection of controls, patient age, and the site and stage of gastric cancer. GASTROENTEROLOGY 1998;114:1169-1179

Risk of stomach cancer in patients with gastric or duodenal ulcer.

It has been suggested that the risk of stomach cancer is increased when there is a history of gastric ulcer, but decreased in those with a history of duodenal ulcer. To provide further information on the issue, data from a case-control study of gastric cancer conducted in greater Milan, northern Italy, between 1985 and 1993, were examined. There were 746 cases of gastric cancer below the age of 75 and 2,053 controls admitted to hospital for acute, non-neoplastic, non-hormone-related diseases. A total of 76 (10.2%) cases and 84 (4.1%) controls reported a history of gastric ulcer, corresponding to a multivariate odds ratio (OR) of 2.6 (95% confidence interval, CI = 1.8-3.6). Fifty nine cases (7.9%) and 111 (5.4%) controls reported a history of duodenal ulcer, corresponding to an OR of 1.3 (95% CI = 0.9-1.8). The OR of gastric cancer was significantly above unity for the first five years after diagnosis of gastric ulcer (OR = 7.4, 95% CI 3.7-14.8), and declined thereafter. No consistent pattern of risks was observed after duodenal ulcer. The present data therefore confirm that the risk of gastric cancer is increased after gastric ulcer. They do not support, however, a reduced risk after duodenal ulcer. This may be due to variable baseline characteristics of the populations studied, or to the different role and impact of Helicobacter pylori and other determinants of duodenal ulcer and gastric cancer in various countries.