From a cohort of 128,992 persons followed since the mid-1960s at a health maintenance organization, 186 patients with gastric carcinoma were selected as case patients and were matched according to age, sex, and race with 186 control subjects without gastric carcinoma. Stored serum samples collected during the 1960s were tested for IgG antibodies to H. Pylori by enzyme-linked immunosorbent assay. Data on cigarette use, blood group, ulcer disease, and gastric surgery were obtained from questionnaires administered at enrollment. Bardhan Udry Development Microeconomics Pdf Books. Tissue sections and pathology reports were reviewed to confirm the histologic results. The mean time between serum collection and the diagnosis of gastric carcinoma was 14.2 years.

Of the 109 patients with confirmed gastric adenocarcinoma (excluding tumors of the gastroesophageal junction), 84 percent had been infected previously with H. Pylori, as compared with 61 percent of the matched control subjects (odds ratio, 3.6;95 percent confidence interval, 1.8 to 7.3). Tumors of the gastroesophageal junction were not linked to H. Pylori infection, nor were tumors in the gastric cardia. Pylori was a particularly strong risk factor for stomach cancer in women (odds ratio, 18) and blacks (odds ratio, 9). A history of gastric surgery was independently associated with the development of cancer (odds ratio, 17; P = 0.03), but a history of peptic ulcer disease was negatively associated with subsequent gastric carcinoma (odds ratio, 0.2; P = 0.02).

Neither blood group nor smoking history affected risk. GASTRIC carcinoma is estimated to be the world's second most common cancer.

Although the dramatic decline in the incidence of gastric carcinoma in the United States and Western Europe over the past 50 years has led some to proclaim an 'unplanned triumph,' in much of Latin America and Asia the incidence remains very high., Because the incidence of gastric carcinoma can change dramatically from place to place and from one generation to the next, it has been hypothesized that its incidence is determined largely by environmental rather than genetic factors. From studies of migrants, it has further been inferred that the risk is increased by exposure to environmental factors in childhood. One specific histologic type of gastric adenocarcinoma, the so-called intestinal type, is particularly prone to the regional and temporal variations of an environmentally related malignant condition,; the decrease in the incidence of stomach cancer in the United States has resulted primarily from a decline in the intestinal type of disease. The incidence of the less common histologic type of adenocarcinoma, the diffuse type, varies less over time and according to geographic location, although it too has decreased in recent years.

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Association of the diffuse type with blood-group A has suggested a genetic component to its genesis. Until recently, research on environmental causes of gastric carcinoma focused primarily on diet. The recent identification of Helicobacter pylori (formerly Campylobacter pylori ) in chronic inflammatory conditions of the stomach, however, has stimulated interest in its potential role in carcinogenesis. Pylori has been linked to chronic atrophic gastritis, an established precursor of the intestinal type of gastric carcinoma., It is not surprising then that several areas in the United States and other parts of the world that are associated with a high risk of gastric carcinoma also have a high prevalence of H. Pylori infection, even among young children. High rates of infection have also been found in patients with cancer or precancerous conditions, and a case–control study found that patients with gastric carcinoma had a relative risk of H. Pylori infection of 2.7 relative to healthy control subjects.

One study linked H. Pylori with the intestinal type of disease more specifically. These cross-sectional and retrospective investigations, however, provide only circumstantial evidence for a causal association between H. Pylori and gastric carcinoma. A sequence more consistent with cause and effect — i.e., infection preceding cancer — has not been established.