disease is highly prevalent. Much of the advice on malaria was equally inaccurate. Only 32% were correct in their recommendations of antimalarials while some of those surveyed looked beyond the boundaries of today’s medicine in recommending “malaria shots”. 8% mentioned additional precautions (water purification, insect repellents, and antidiarrhoeal agents) but perhaps the most helpful advice was from the representative of a country with a civil war who urged us not to go there for that reason. We found considerable improvement between the two surveys. 60% gave correct information or referred the caller to other sources compared with 46% 9 years ago.1 However, diplomatic representatives are still not an ideal source of pretravel advice. The travelling public will get the best advice from health-care professionals in travel clinics and public health units. Robyn T Shafer, Jason Correia, Vishal Patel, *J S Keystone Tropical Disease Unit, Toronto Hospital, University of Toronto, Ontario M5G 2C4, Canada
Keystone J, Sawyer L. Travel advice from embassies and consulates of developing countries. Can Med Assoc J 1987; 136: 693.
Case for reforming Human Fertilisation and Embryology Authority SIR—Anybody who doubts the need for reform of the UK Human Fertilisation and Embryology Authority (HFEA) should read carefully the letter from the chairman of the HFEA in your issue of July 20 (p198).1 Of course, the HFEA “provide[s] information” for Parliamentary questions; that is its job. My criticism2 was that HFEA was unable to give “precise” information, and Deech1 concedes that “unfortunately the wrong figure was given”, claiming this inaccuracy was immediately identified and corrected. However, in answer to Parliamentary questions during March, 1996, on embryo creation during 1991–94, the Secretary of State for Health gave inaccurate figures, not once but three times, and to my knowledge this information has still not been provided satisfactorily. Further questions (N45 and N46) asked how many of the embryos created before August, 1991, and still in existence in August, 1991, had been used for research, treatment cycles, or freezing or had been destroyed. The reply was “This information is not available”. The legal cases on embryo destruction which are being built up around this period will no doubt benefit from this lack of information. The HFEA chairman suggests I falsely accused the body she chairs as “careless” when I referred to the authority’s dismissal of French studies on embryo freezing. The HFEA’s report of July 19, 1995, on the storage period for embryos, states (para 25) that “The conclusions of a French study of behavioural changes in mice born from frozen embryos have been withdrawn by the authors”. The conclusions were never withdrawn. The French scientists wrote to the Ministry of Health and to Deech herself at the HFEA, and after this correspondence an addendum had to be made to para 25 with apologies to the French scientists. HFEA, like the unfortunate frozen embryos, is also subject to a 5-year review. Comment on Reproductive Ethics was not invited to contribute to this review (another case of “careless dismissal”?) but we will continue to ensure that reform of the HFEA is as radical as possible. Josephine Quintavalle CORE (Comment on Reproductive Ethics), PO Box 4593, London SW3 6XE, UK
Deech R. What to do with spare embryos. Lancet 1996; 348: 198. Quintavalle J. What to do with spare embryos. Lancet 1996; 347: 1489.
Helicobacter pylori screening and gastric cancer SIR—Parsonnet and colleagues (July 20, p 150)1 demonstrate that screening for and treatment of Helicobacter pylori infection is potentially cost-effective in the prevention of gastric cancer and that 660 patients would be treated for each case of cancer prevented. While we agree with the first statement we cannot agree with the second. We observed that 96% (49/51) of patients operated on for gastric cancer in Turin were infected by a specific strain of H pylori, one that carries the cytotoxinassociated gene A (cagA).2 Only 18% of the general population in Turin is infected by such a strain, as judged by studies of antibody to cagA protein in the sera of 555 patients admitted to our hospital’s emergency care department.3 Since 2·3% of males in Turin die of gastric cancer before age 74,4 we estimate that one in eight males infected by a cagA-positive strain of H pylori will die from this malignancy before that age. An association between increased risk of stomach cancer and anti-cagA has also been reported for Japanese-Americans.5 It would thus be much more costeffective to test for anti-cagA, and cure those testing positive, than to test for any H pylori infection. If the treatment of a cagA-positive infection prevents 30% of attributable gastric cancer, we would need to treat only about 25 individuals in Turin for each case of cancer prevented. *Antonio Ponzetto, Tito Soldati, Maurizio De Giuli *Department of Gastroenterology, Ospedale San Giovanni Battista, I-10126 Torino, Italy; Department of Surgery, Ospedale Molinette, Torino; and Department of Surgical Oncology, Ospedale San Giovanni Antica Sede, Torino
Parsonnet J, Harris RA, Hack HM, Owens DK. Modelling costeffectiveness of Helicobacter pylori screening to prevent gastric cancer: a mandate for clinical trials. Lancet 1996; 348: 150–54. Covacci A, Censini S, Bugnoli M, et al. Molecular characterization of the 128 kDa immunodominant antigen of Helicobacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci 1993; 90: 5791–95. Ponzetto A, De Giuli M, Sanseverino P, et al. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst 1996; 88: 465. Zanetti R, Crosignani P, eds. Cancer in Italy: incidence data from cancer registries 1983–1987. Torino: Lega Italiana per la Lotta Contro i Tumori, 1992. Blaser MJ, Chyou PH, Nomura, et al. Age at establishment of Helicobacter pylori infection and gastric carcinoma, gastric ulcer and duodenal ulcer risk. Cancer Res 1995; 55: 562–65.
SIR—Clinical trials of Helicobacter pylori eradication to prevent gastric cancer, the focus of Parsonnet and colleagues’ paper (July 20, p 150),1 may well have to randomise at least 100 000 individuals in aggregate and follow them up for one or two decades. Even if chronic infection with H pylori is as strongly related to gastric cancer as smoking is to lung cancer, eradication of the infection might take many years to produce a large proportional reduction in gastric cancer. With smoking, cessation at age 60 produces a reduction of less than 50% in lung cancer mortality during the first decade after stopping, but produces more than a 50% reduction during the second decade.2 If, by analogy, the reductions in gastric cancer during the first and second decades after allocation to H pylori eradication are taken to be 25% and 50%, respectively, then a trial in the UK of H pylori eradication at age 60 might have to randomise at least 100 000 individuals to achieve statistically reliable results. Without any intervention about 1000 of them would die of gastric cancer within 20 years (400 in the first decade and 600 in the second). Analogy with tobacco suggests that the findings during the first decade of a gastric cancer prevention trial might or might not be statistically convincing (as the result suggested by this analogy would be about 150 vs 200 deaths
Vol 348 • September 14, 1996