Gastric cancer is the second most common cause of cancer death in the world. Helicobacter pylori infection is now a well-accepted cause of this malignancy; in some parts of the world, up to eighty percent of all gastric cancers are at least in part caused by H. pylori infection. H. pylori infection typically starts in childhood as an inflammatory process in the stomach. The changes in the gastric microenvironment facilitate gastric cancer over time. Among infected individuals, genotype of H. pylori, coincident environmental exposures, and genetic factors of host seem to play roles in determining who will get gastric cancer and who will not. Unfortunately, it remains unknown whether treatment of H. pylori prevents gastric cancer. Thus, screening for H. pylori to prevent cancer is not yet widely recommended. Some consensus groups, however, have recommended screening for and treating H. pylori infection in individuals with family histories of gastric malignancy. In high-risk countries, screening programs for early gastric cancer itself may improve therapeutic outcome for this highly lethal disease.

Background: Positron emission tomography (PET) with 18-fluorodeoxyglucose (FDG) is a potentially useful but expensive test to diagnose solitary pulmonary nodules.

Objective: To evaluate the cost-effectiveness of strategies for pulmonary nodule diagnosis and to specifically compare strategies that did and did not include FDG-PET.

Design: Decision model.

Data Sources: Accuracy and complications of diagnostic tests were estimated by using meta-analysis and literature review. Modeled survival was based on data from a large tumor registry. Cost estimates were derived from Medicare reimbursement and other sources.

Target Population: All adult patients with a new, noncalcified pulmonary nodule seen on chest radiograph.

Time Horizon: Patient lifetime.

Perspective: Societal.

Intervention: 40 clinically plausible combinations of 5 diagnostic interventions, including computed tomography, FDG-PET, transthoracic needle biopsy, surgery, and watchful waiting.

Outcome Measures: Costs, quality-adjusted life-years (QALYs), and incremental cost-effectiveness ratios.

Results of Base-Case Analysis: The cost-effectiveness of strategies depended critically on the pretest probability of malignancy. For patients with low pretest probability (26%), strategies that used FDG-PET selectively when computed tomography results were possibly malignant cost as little as $20 000 per QALY gained. For patients with high pretest probability (79%), strategies that used FDG-PET selectively when computed tomography results were benign cost as little as $16 000 per QALY gained. For patients with intermediate pretest probability (55%), FDG-PET strategies cost more than $220 000 per QALY gained because they were more costly but only marginally more effective than computed tomography-based strategies.

Results of Sensitivity Analysis: The choice of strategy also depended on the risk for surgical complications, the probability of nondiagnostic needle biopsy, the sensitivity of computed tomography, and patient preferences for time spent in watchful waiting. In probabilistic sensitivity analysis, FDG-PET strategies were cost saving or cost less than $100 000 per QALY gained in 76.7%, 24.4%, and 99.9% of computer simulations for patients with low, intermediate, and high pretest probability, respectively.

Conclusions: FDG-PET should be used selectively when pretest probability and computed tomography findings are discordant or in patients with intermediate pretest probability who are at high risk for surgical complications. In most other circumstances, computed tomography-based strategies result in similar quality-adjusted life-years and lower costs.

How successful are HIV prevention programs? Which HIV prevention programs are most cost effective? Which programs are worth expanding and which should be abandoned altogether? This book addresses the quantitative evaluation of HIV prevention programs, assessing for the first time several different quantitative methods of evaluation.

The authors of the book include behavioral scientists, biologists, economists, epidemiologists, health service researchers, operations researchers, policy makers, and statisticians. They present a wide variety of perspectives on the subject, including an overview of HIV prevention programs in developing countries, economic analyses that address questions of cost effectiveness and resource allocation, case studies such as Israel's ban on Ethiopian blood donors, and descriptions of new methodologies and problems.

Background & Aims: Gastrin is a putative promoter of colorectal carcinomas. The aim of this study was to evaluate the temporal relationship between gastrinemia and development of colorectal malignancy.

Methods: We conducted a nested case-control study among 128,992 subscribers to a health maintenance program who had participated in a multiphasic health checkup between 1964 and 1969. Serum had been frozen since the checkup and the cohort followed up for cancer. Of 1881 incident colorectal carcinoma cases, 250 were randomly selected; 1 control without cancer was matched to each case by age, sex, education, and date of serum collection. Stored sera were tested for Helicobacter pylori immunoglobulin G and for gastrin and glycine-extended gastrin.

Results: Verified cases included 166 colon cancers, 58 rectal cancers, and 9 with cancer in both locations. A mean of 15.3 years had elapsed between serum collection and diagnosis of cancer. Median gastrin levels were similar in cases and controls (41.7 vs. 40.7 pg/mL). However, a gastrin level above normal was associated with increased risk for colorectal malignancy (odds ratio, 3.9; 95% confidence interval, 1.5-9.8). If this association is causal, 8.6% of colorectal cancers could be attributed to high serum gastrin level.

Conclusions: Hypergastrinemia is associated with an increased risk of colorectal carcinoma.

OBJECTIVE: To compare the probability of cancer in a solitary pulmonary nodule using standard criteria with Bayesian analysis and result of 2- [F-18] fluoro-2-deoxy-D-glucose-positron emission tomographic (FDG-PET) scan.

SETTING: A university hospital and a teaching Veteran Affairs Medical Center.

METHODS: Retrospective analysis of 52 patients who had undergone both CT scan of the chest and a FDG-PET scan for evaluation of a solitary pulmonary nodule. FDG-PET scan was classified as abnormal or normal. Utilizing Bayesian analysis, the probability of cancer using "standard criteria" available in the literature, based on patient's age, history of previous malignancy, smoking history, size and edge of nodule, and presence or absence of calcification were calculated and compared to the probability of cancer based on an abnormal or normal FDG-PET scan. Histologic study of the nodules was the gold standard.

RESULTS: The likelihood ratios for malignancy in a solitary pulmonary nodule with an abnormal FDG-PET scan was 7.11 (95% confidence interval [CI], 6.36 to 7.96), suggesting a high probability for malignancy, and 0.06 (95% CI, 0.05 to 0.07) when the PET scan was normal, suggesting a high probability for benign nodule. FDG-PET scan as a single test alone was more accurate than the standard criteria and standard criteria plus PET scan in correctly classifying nodules as malignant or benign.

CONCLUSION: FDG-PET scan as a single test was a better predictor of malignancy in solitary pulmonary nodules than the standard criteria using Bayesian analysis. FDG-PET scan can be a useful adjunct test in the evaluation of solitary pulmonary nodules.

Background & 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.