Helicobacter pylori—Keeping it in the Family
abstracts & commentary
Synopsis: Intra-family transmission appears to be a significant factor in the spread of Helicobacter pylori and may contribute to instances of familial gastric cancer.
Sources: Goodman KJ, Correa P. Lancet 2000;355:358-362; El-Omar EM, et al. Gastroenterology 2000;118:22-30; Brenner H, et al. Gastroenterology 2000;118:31-35; Parsonnet J. Gastroenterology 2000;118:222-224.
In the first of these articles, goodman and correa studied the effect of family composition on Helicobacter pylori prevalence among rural Colombian children aged 2-9 years. A total of 684 children were screened for H. pylori using a urea breath test. The risk of infection was related to number of children in the family (odds ratio, 1.4 for 1 sibling; 4.3 for 4-5), birth order, age of other siblings, and age gap between siblings. They concluded that infection is transmitted most readily among siblings who are close in age, and most frequently from older siblings to younger ones.
The next two papers and the accompanying editorial (by Parsonnet) look at the implications of familial infection with H. pylori for the risk of gastric cancer. El-Omar and colleagues studied H. pylori status, gastric secretory function, and gastric histology among 100 first-degree relatives of patients with noncardia gastric cancer and compared them with controls. Relatives of gastric cancer patients had a higher prevalence of hypochlorhydria (27% vs 3%) and gastric atrophy (34% vs 5%) but the same prevalence of Helicobacter infection. However, in the relatives, these pathological and secretory abnormalities were found exclusively among those who were positive for H. pylori. Eradication of H. pylori resolved gastric inflammation in all and atrophy and hypochlorhydria in 50%. They concluded that relatives of patients with gastric cancer have an increased prevalence of precancerous gastric abnormalities, but this increase is confined to those with H. pylori infection. Consequently, they propose that prophylactic eradication of the infection should be offered to such subjects. Brenner and colleagues compared the prevalence of H. pylori infection among those with and without a parental history of gastric cancer in a sample of 1351 males and females aged 30-74 years in Germany. H. pylori prevalence was higher (69%) among those with a positive parental history of gastric cancer than in those without (44%). They concluded that familial aggregation of gastric cancer can be explained at least partly by familial clustering of H. pylori infection. The accompanying editorial discusses the implications of the latter two studies.
Comment by Eamonn M. M. Quigley, MD
Despite its prevalence and public health implications, the mode of transmission of H. pylori infection remains in debate. Goodman and Correa provide important evidence to support an important role for person-to-person transmission of this infection. The precise mode of transmission cannot be defined from their study but there are some grounds to suspect a role for fecal-oral transmission. The next two articles both suggest that familial clustering of gastric cancer may be explained, in large part, by familial clustering of H. pylori infection. Brenner et al actually documented a higher rate of H. pylori infection among the children of gastric cancer patients, while El-Omar et al found the same rates among gastric cancer relatives and controls. The latter group suggested that it was the response to the infection, rather than the infection per se, that differentiated the relatives. They found that they were much more likely to develop the premalignant states of achlorhydria and atrophy. In her editorial, Parsonnet suggested that, these findings notwithstanding, Helicobacter, and infection acquired in childhood in particular, is the principal explanation for familial occurrence of gastric cancer. All in all, these important studies emphasize the role of intrafamilial spread in H. pylori infection and its clinical consequences. One can certainly conclude that relatives of gastric cancer patients should be screened and the infection eradicated if detected. Whether, as Parsonnet asks, one should offer the same to those, described by Goodman and Correa, who have acquired the infection in childhood continues to be debated. (Dr. Quigley is Professor, Department of Medicine, National University of Ireland, Cork, Ireland.)
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