The risk of gastric cancer is known to be increased in patients with a positive family history, and this familial disposition may be a result of genetic and environmental factors. Helicobacter pylori infection is an important environmental risk factor for gastric cancer, especially when the inflammation involves the body region of the stomach as much as or more than the antral region. Various degrees of atrophy and impaired acid-secretory function usually accompany this type of inflammation pattern. Both are long-recognized abnormalities associated with gastric cancer. However, little is known about the role of H. pylori infection as a risk factor for gastric cancer in patients with a family history of this type of cancer. El-Omar and associates examined the prevalence of atrophy and hypochlorhydria in first-degree relatives of patients with gastric cancer and the association of these precancerous abnormalities and H. pylori infection.
Records of all patients with gastric cancer over a four-year period were reviewed, and those with documented noncardia gastric adenocarcinoma were identified. A total of 100 first-degree adult relatives of 40 gastric cancer index patients were recruited for the study, as were two control groups. The first control group was recruited for an acid secretion study and consisted of demographically similar healthy volunteers who had no family history of gastric cancer. The second group was recruited for histologic comparison and consisted of patients undergoing endoscopy for dyspepsia who had no evidence of esophagitis, ulcer disease or cancer. All cancer relatives and the first control group were screened for H. pylori using a C-urea breath test, and all underwent acid-secretory studies. All cancer relatives and the second control group underwent upper gastrointestinal endoscopy to obtain gastric biopsy specimens from the antral and body regions, and blood studies to determine H. pylori IgG serology. All cancer relatives who tested positive for H. pylori infection were treated with eradication therapy.
The prevalence of H. pylori infection was similar in cancer relatives and the first control group, 63 and 64 percent, respectively. However, cancer relatives with H. pylori infection had significantly lower levels of acid output and significantly more hypochlorhydria and atrophy than did the members of either control group with H. pylori infection. There was no difference in acid secretion or in atrophy between cancer relatives and members of either control group who were H. pylori-negative. One year after eradication of H. pylori infection, acid secretion levels were restored to normal, and atrophy declined in 50 percent of cancer relatives who had hypochlorhydria. Antral and body inflammatory scores on biopsy were initially significantly higher among the cancer relatives and the second control group who were H. pylori-positive, but these scores decreased markedly one year after eradication of infection.
The authors conclude that relatives of patients with gastric cancer have an increased prevalence of gastric atrophy and hypochlorhydria; both abnormalities are associated with increased risk for noncardia gastric cancer. The incidence of these precancerous abnormalities appears to be confined to persons with H. pylori infection, although these abnormalities do not develop in every person with infection. Eradication of H. pylori infection in relatives of patients with gastric cancer is important because it may reduce their cancer risk.