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Helicobacter pylori and gastric cancer: time for mega-trials?

J. Danesh

Published 1999 in British Journal of Cancer

ABSTRACT

The first report of an association between chronic infection Helicobacter pylori, a spiral bacterium of the stomach, and gas cancer appeared in 1991 and in 1994 the International Agenc Research of Cancer declared H. pylori a human ‘carcinogen (IARC Working Group, 1994). Five years after that rep however, the causal role of H. pylori in gastric cancer remain controversial, with risk estimates ranging from ninefold (We and Forman, 1996) to no important association at all (Cresp Citarda, 1996). Recent quantitative reviews, by contrast, sug that H. pylori infection is likely to be only a moderate risk fact for gastric cancer (Danesh, 1999 a, 1999b). Reliable epidemiological evidence on H. pylori and gastric cancer is still relatively sparse. Although the number of c reported in prospective studies has increased by threefold 1994, there are now a total of only about 800 cases in ten pub prospective studies. A synthesis of these studies indicates th H. pylori is two or three times more common in people with gas cancer than in others (Figure 1). Doubts persist, however, abo extent to which inadequate adjustment for possible confoun factors, such as smoking and markers of poverty, and the pre tial publication of studies with more extreme results might have to exaggerated estimates. The biological plausibility of a ca association is suggested by strong correlations reported betwe H. pylori infection and putatively precancerous gastric lesions (suc atrophic gastritis and intestinal metaplasia) (Kuipers et al, 1 Sakaki et al, 1995) and by the production of lesions that rese human gastric cancer in Mongolian gerbils following long-te experimental infection (Watanabe et al, 1998). Even if a two threefold relative risk were established, however, it would explain the sharp variations in gastric cancer mortality betw populations (e.g. 20-fold higher in certain parts of China than in USA) (Peto, 1990) or between past and present (e.g. the fiv decrease in Scotland between 1950 and 1990) (Swerdlow 1998). Moreover, although H. pylori infects men and women abo equally and is strongly associated with duodenal ulceration, ga cancer is twice as common in men and may be inversely asso with duodenal ulceration (Howson et al, 1986; Hansson e 1996). Clearly, if H. pylori is a cause of gastric cancer, there m be some other major cause(s) of the disease. To assess the role of the infection in gastric cancer m precisely would require larger studies than hitherto, especial

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