reviewed continually, and decisions made as to which worker takes responsibility. This results in low rates of referral to psychiatrists and low prescribing costs (especially for benzodiazepines). We believe that awareness of mental health factors may also enable us to have low referral rates in other specialties. Finally, Professor Sims does not mention the prevention of mental illness. Interested general practitioners are in a key position to detect hidden or early mental health problems. Having the resources, they tackle many of these problems without referral to a psychiatrist. Consultants should remember that primary health care teams, like patients, have different needs. Some may be good at treating varicose ulcers but poor at managing anxiety or vice versa. Consultant services therefore need to be flexible and educational and move out into health centres, thus strengthening the primary health care team and enhancing its capacity to cope. DEREK PHILLIPS Health Centre, Slaithwaite, Huddersfield HD7 5AB 1 Sims A. Even better services: a psychiatric perspective. BRM7 1991;302:1061-3. (4 May.)

SIR,-The initial response' to the articles on community care by Professors Andrew Sims2 and Elaine Murphy' was perhaps not surprising. Professor Murphy's views, heavily criticised in the subsequent correspondence, at least have the merit of appreciating that the politics of community care have been altered by Thatcherism and the Policy Studies Institute. The case for an increase in consultant manpower, which Professor Sims seems to have made the priority of his presidency of the Royal College of Psychiatrists, now looks isolated and outdated. Professor Sims's argument for the supremacy of the consultant psychiatrist in the multidisciplinary team is not accepted by other disciplines. Although the concept of a generic mental health professional has never gained official recognition, it could defuse wasteful interdisciplinary power struggles. I am not underestimating the importance of education and training, as Professor Murphy does. Many able people may be deprived of an adequate training in mental health because of vested disciplinary interests. Democratisation of the multidisciplinary team, though, does enable inexperienced workers to make their own

contribution. Neither Professor Sims nor Professor Murphy really considers the impact of the government's reforms on community care.4 In particular, the introduction of care management with supporting budgetary frameworks could alter provision considerably. Care managers will essentially act as brokers for services and are expected to assume some or all of the responsibility for purchasing services to implement a care programme. Once these arrangements are in place it may become clearer if the real issues have been underfunding, ring fencing of the community care budget, a sole agency for community care, and so on. Understandably, the future is uncertain, but I hope that the vision offered for community care is more than a choice between Professor Sims's plea for an increase in the strength of consultant psychiatrists and Professor Murphy's haphazard and flawed views. DUNCAN DOUBLE

Department of Psychiatrs, University of Sheffield, Northern General Hospital, Sheffield S5 7AU 1 Correspondence. Better mental health services.

1339-40. (1 June.)

BMJ 1991302:

2 Sims A. Eveni bettcr services: a psychiatric perspective. BAiJ 1991;302:1061-3. (4 May.)

1534

3 Murphy E. Community mental health services: a vision for the fttture. BM3' 1991;302:1064-5. (4 May.) 4 Department of Health. Caring for people. Communitt care in the next decade and beyond. London: HMSO, 1990.

SIR,-The correspondence' on community mental health services in response to articles by Professor Andrew Sims2 and Professor Elaine Murphy' is revealing in showing the attitudes of some doctors. The enthusiastic response to Professor Sims's plea for more consultant psychiatrists2 and the defensive attitude to Professor Murphy's article3 is just what many users of mental health services would expect from psychiatrists. As part of our work establishing contracts for mental health services, both in Newcastle and in other places around England, we have attempted to get a range of users to help plan and to comment on contracts. Although not perfectly representative, there is a clear message from clients, patients, and carers in several districts that their priorities for development do not include more consultant psychiatrists. They believe that the immediate need is for more social care along the lines outlined by Professor Murphy. It is interesting that Professor Sims bases his argument on the central importance of the doctorpatient relationship. He does not, however, cite any evidence that this is viewed as a central issue by patients. A recent unpublished study conducted in a children's cancer ward showed the high value that parents and patients place on social contact with a range of non-medical and non-nursing staff, including domestic staff, physiotherapists, and social workers. This is anecdotal evidence that, important as the doctor-patient relationship is, users often place a higher value on other forms of support. It is encouraging to note the complete agreement that community services are the way forward and that the medical profession is vigorously discussing the most appropriate form of provision. The views of users must not be overlooked in this debate, and we all need to improve the mechanisms by which clients and carers can participate in planning. INGRID BARKER

Newcastle Health Atuthority, Newcastle upon Tyne NE2 1EF RICHARD GLEAVE Health Services Management Unit, Newcastle University, Newcastle upon Tyne NEI 7RU 1 Correspondence. Better mental health services. BMJ7 1991;302: 1339-40. (1 June.) 2 Sims A. Even better services: a psychiatric perspective. B.M7 1991;302:1061-3. (4 May.) 3 Murphy E. Community mental health services: a vision for the

titture. BAUJ 1991;302:1064-5. (4 May.)

Helicobacter pylon infection and gastric cancer SIR,-Dr D Forman and colleagues concluded that there was a higher specific Helicobacter pylon IgG concentration in patients who subsequently developed gastric cancer than in controls.' They were unable to suggest possible mechanisms by which H pylon infection could induce gastric carcinoma.

We have recently shown the immunohistochemical expression of growth regulatory peptides in gastric mucosa in 56 subjects (paper submitted for publication). Epidermal growth factor has a potential for oncogenic action in the stomach.' We have shown that it is present in greater density in or near the proliferative zone in inflamed antral mucosa than in uninflamed antral mucosa. H pylon was present in 82% of patients with antral inflammation compared with 34% of patients without antral oc!tritis-figures similar to those found in other studies.' Moreover, there is an association

between expression of epidermal growth factor and the presence of lymphocytes, but not neutrophils, in the inflamed mucosa. Possibly lymphocytes may induce expression of epidermal growth factor in gastric epithelial cells by release of cytokines.4 We believe, therefore, that if H pylorn indeed has a role in gastric carcinogenesis the infection may induce gastric neoplasia indirectly as a result of increased expression of epidermal growth factor in the gastric epithelium. JANUSZ JANKOWSKI Gastrointestinal Unit, Ninewells Hospital, Dundee DDl 9SY 1 Forman D, Newell DG, Fullerton F, Yarnell JWG, Stacey AR, Wald N, et al. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. BM, 1991;302:1302-4. (I June.) 2 Tahara E, Yasui W, Ochiai A, Yamamoto T, Hata J, Yokozakio H, et al. Interaction between epidermal growth factor and its receptor in progression of human gastric carcinomas. Prog Cancer Res Ther 1988;35:536-9. 3 Ormand JE, Talley NJ, Shorter RG, Conley CR, Carpenter HA, Fich A, et al. Prevalence of Helicobacter pylori in specific forms of gastritis. Dig Dis Sci 1991;36:142-5. 4 Correa P. Chronic gastritis (non specific). In: Whitehead R, ed. Gastroinlestinal and oesophageal pathology. Edinburgh: Churchill Iivingstone, 1989:402-21.

Helicobacter pylon infection and duodenal ulcer SIR,-Dr A R Axon's editorial on duodenal ulcer succinctly reviews the evidence that convinces many that Helicobacter pylorn is an important agent in duodenal ulcer disease.' Furthermore, he reiterates the views of the working party convened by the World Congress of Gastroenterology that attempts to eradicate H pylori should be made only in patients with peptic ulcers in whom management problems arise and that in these patients triple treatment-namely, bismuth and two antibiotics (usually amoxycillin or tetracycline and metronidazole)-should be used. The working party itself went on to recommend that "H pylorn therapy should be reserved for those groups of patients where it has been shown unequivocally to have an advantage over the currently available cytoprotective and acid suppressive drugs."2 Regrettably, this rational and well thought out policy has not been adopted by Gist-brocades, the major retailer of bismuth salts in this country. In recent promotional literature put out in support of this bismuth preparation the company recommends that patients with ulcers that relapse or who require maintenance treatment should receive treatment with bismuth for eight weeks and metronidazole or tinidazole for two weeks. Undoubtedly, this regimen will produce better eradication rates than a regimen of bismuth alone, but the results are likely to be less satisfactory than those obtained with the triple treatment regimen advocated by the working party of the World Congress of Gastroenterology, which concluded that "the indiscriminate use of antibiotics is to be discouraged" and "if H pylort therapy is undertaken, the most effective treatment regimen should be employed. The Working Party recommends a triple combination." Furthermore, the promotional literature in question does not include evidence that dual treatment is beneficial in healing and reducing relapse of ulcers. Although there is some limited evidence that this is so, the case is far from proved.' Eradication of H pylori may not be the only factor responsible for the effectiveness of treatment regimens in duodenal ulcer as antibacterial agents seem to have some efficacy in peptic disease probably independent of any effect on H pylon.4 The main concern about using dual treatment regimens-namely, bismuth and metronidazole or tinidazole-is the risk of the development of resistant H pylori/. At present, in most European countries about 20% of H pylon organisms are

BMJ VOLUME 302

22 JUNE 1991

resistant to nitroimidazoles. Indiscriminate use of drug regimens without known efficacy, and no facilities to monitor the H pylori state or sensitivities, seem likely to encourage the development of resistant organisms to the level of 80% seen in parts of Africa -a level that is believed to be due to the frequent use of metronidazole in these populations.; Although dual or perhaps even single regimens mav in the future be useful in treating H pylori infection, it seems premature and unwise to advocate wide use of regimens that do not have proved efficacy and may have drawbacks.

study supports a case against the value of eradication of H pylon. Dr Heatley's concern over resistance is praiseworthy, but until we have the ideal single medication we must surely aim for eradication with such treatment as is already available. Waiting submits a patient to a lifetime of an unnecessary disease. JANE BARRETT

Gist-brocades, West Bvfleet, Weybridge, Surrey KT 14 6RA

R V HEATLEY

Department o Mtedicine, St James's University Hospital, tecds LS9 7TF I Axon AR. Duodenal ulcer: the villain unmasked? BMJ 1991; 302:919-21. (20 April.) 2 lrytgat GNJ, Axon ATR, [)ixon MF, Graham DY, Lee A, Marshall BJ. Helicobacter pylori: causal agent in peptic ulcer disease? In: Working partsP reports. World congresses of gastro-

enterologv. Oxford: Blackwell Scientific, 1990:36-45. 3 Marshall BJ, Goodwin CS, Warren JR, Murray R, Blinkow ED, Blackbottrn SJ, ei al. Prospective double-blind trial of duodenal ulcer relapse after eradication of Campylobacter pylorn. Lancet 1988;ii: 1437-41. 4 Quintero D)iaz M, Sotto Escobar A. Metronidazole versus cimetidine ita treatment of gastroduodenal ulcer. Lancet 1986;i: 907. 5 Satoh H, (Guth PH, Grossman MI. Role of bacteria in gastric ulceration produced by indomethacin in the rat: cytoprotective action of antibiotics. Gastroenterology 1983;84:483-9. 6 O'Riordan T, Mathai E, Tobin E, McKenna D, Keane C, Sweetaey E, et al. Adjuvant antibiotic therapy in duodenal ulcers treated with colloidal bismuth subcitrate. Gut 1990;31: 999-1002. 7 Glupczynski Y, Burette A, De Koster E, Nyst J-F, Deltenre M, Cadranel S, et al. Metronidazole resistance in Helicobacter

I Tytgat GNJ, Axon ATR, Dixon MF, Graham DY, Lee A, Marshall BJ. Helicobacter pylorn: causal agent in peptic ulcer disease? In: Working party reports. World congresses of gastroenterology. Oxford: Blackwell Scientific, 1990:36-45. 2 Wyatt JI. Campylobacter pylorn, duodenitis and duodenal ulceration. In: Rathbone BJ, Heatley RV, eds. Campylobacter pylon and gastroduodenal disease. Oxford: Blackwell Scientific, 1989:117-24. 3 Rauws EAJ, Tytgat GNJ. Cure of duodenal ulcer associated with eradication of Helicobacter pylorn. Lancet 1990;335: 1233-5. 4 Axon ATR. Duodenal ulcer: the villain unmasked? BMJ 1991;302:919-21. (20 April.) 5 O'Morain C. Peptic ulcer disease. Inrsh Doctor 1989 Jan 15:

350-3. 6 Smith AC, Price AB, Borriello P, Levi AJ. A comparison of ranitidine and tripotassium dicitrato-bismuthate (TBD) in relapse rates of duodenal ulcer. The role of campylobacter pylorn (CP). Gastroenterology 1988;94:A43 1. 7 Coghlan JG, Gilligan D, Humphries H, McKenna D, Dooley C, Sweeney E, et al. Campylobacter pyloridis and relapse of duodenal ulcers. Lancet 1987;ii: 1 109-1 1. 8 Marshall BJ, Goodwin CS, Warren JR, Murray R, Blincow ED, Blackborn SJ, et al. Prospective double-blind trial of

duodenal ulcer relapse after eradication of campylobacter pylori. Lancet 1988;ii: 1437-42.

The incidence of duodenal ulcer in developing countries is far from uniform, and areas of high as well as low incidence have been identified." 12 Unfortunately, we lack information about the incidence of gastric metaplasia in such countries, but it seems reasonable to suggest that differing genetic and environmental factors could depress output of gastric acid in certain populations and in turn lower the incidence of gastric metaplasia. In the absence of metaplasia duodenal H pylon infection cannot occur and ulcers do not develop even if there is a high prevalence of H pylon' infection in the stomach. Though the essential truth of Schwartz's dictum of "no acid, no ulcer" cannot be denied," we advocate greater awareness of another old dictum proposed by Konjetzny in 1924- "an ulcer does not develop in a healthy mucosa. "'4 The natural course of duodenal ulcer can be fundamentally altered only by restoring the duodenal mucosa to health. Permanent eradication of H pylon would eliminate chronic inflammation both there and in the stomach, while measures that permanently reduce output of gastric acid, like vagotomy, are likely to reverse gastric metaplasia and lead to restoration of a small intestinal-type surface epithelium.'5 The absence of gastric metaplasia would also eliminate the risk of further duodenal inflammation without necessarily affecting the H pylorn state. Patients with persistent gastritis associated with H pylon, however, will remain at risk of gastric ulcer and possibly, in the longer term, at increased risk of gastric cancer.'6 M F DIXON J I WYATT

pylori. Lancet 1990;335:976-7.

***We sent Dr Heatley's letter to Gist-brocades; its medical director replies as follows: SIR,-Dr Heatley's quotation of the working party's recommendations is, unfortunately, incomplete. Eight lines on, entirely consistent with the earlier statement, is: "Where there is no history of NSAID [non-steroidal anti-inflammatory drug] therapy and the duodenal ulcer is Hp [Helicobacter pylorn related, eradication therapy should be considered."' In a book coedited by Dr Heatley the incidence of H pylon' in duodenal ulcer is given as 95%.' Thus eradication treatment should be considered for 95% of cases of duodenal ulcer. Far from disagreeing with the working party's recommendations, Brocades is endeavouring to provide general practitioners with a workable eradication regimen. According to the working party, eradication rates with colloidal bismuth subcitrate plus metronidazole or tinidazole range from 53% to 85%. The same source gives rates with triple treatment of 65-94%. Triple treatment carries a heavy burden of adverse events. In one study 21% of patients withdrew owing to this and were excluded from analysis.' In the "real world" a still higher drop out rate could be expected. The concern about resistance to nitroimidazoles should not be ignored, but neither should the risk of resistance developing in a patient unable to complete a course of triple treatment because of side effects. Dr A R Axon's editorial also raises the concern that failure of compliance contributes to resistance.4 The pathogenicity of H pylon does not change with the development of resistance, neither should it present a management problem with the availability of maintenance treatment. I believe that the correlation between eradication of H pylon and lack of ulcer relapse is now unequivocal ` an4 widely accepted as such. The studies quoted by Dr Heatley do not assess H pylon state and do not investigate the effect of treatment on relapse. The second study, in rats, found that bacitracin, neomycin, and polymyxin B prevented, by an unknown cytoprotective mechanism, ulcers induced by non-steroidal anti-inflammatory drugs. Again, H pylon state was not assessed. Neither

BMJ

VOLUME

302

22

JUNE

1991

SIR,-We were interested in the letters prompted by Dr A T R Axon's article on the role of Helicobacter pylon in duodenal ulceration. ' Dr J H Baron argues that duodenal ulcers do not develop when the output of gastric acid is below 15 mmol/h and that ulcers will heal if outputs below this threshold can be maintained by any of the current antiacid treatments.2 In emphasising the part played by acid output he also acknowledges that simply lowering acid output does not remove the duodenal ulcer diathesis and accepts a role for H pylori in the underlying pathogenesis of such ulcers. On the other hand, Mr C Holcombe points to the low incidence of duodenal ulceration in some developing countries despite the high incidence of gastritis associated with H pylon' and concludes that H pylon can play only a minor part in the aetiology of such ulcers.3 Mr Holcombe seems to have overlooked the fact that H pylon infection itself is not proposed as the cause of duodenal ulcers in the West. H pylon do not attach to small intestinal surface epithelium and can colonise the duodenum and provoke an inflammatory response only in the presence of gastric metaplasia. Thus gastric metaplasia in the duodenum forms a necessary link between gastritis associated with H pylori and the active chronic duodenitis that underlies peptic duodenal ulceration.4 Patients with H pylon gastritis but without gastric metaplasia will not develop a duodenal ulcer, and vice versa. Small foci of gastric metaplasia can be found in duodenal biopsy specimens from up to 60% of "healthy" volunteers in the US' and The Netherlands,6 while significant metaplasia (>5% of the surface epithelium) has been found in 20%7 to 34%1 of patients with dyspepsia. The prevalence of gastric metaplasia in subjects positive and negative for H pylori is the same, but its extent is greater in subjects positive for the organism.8 There is accumulating evidence that gastric metaplasia is induced by acid.9 Thus we can speculate that subjects with an acid output above a certain threshold whose duodenal mucosa is subjected to an increased acid load will acquire gastric metaplasia as a defence response. A threshold of 15 mmol/h is consistent with previous data comparing gastric metaplasia with production of acid. '

Departments of Pathology, General Infirmary and St James's Hospital, Leeds 1 Axon AR. Duodenal ulcer: the villain unmasked? BMJ 1991; 302:919-21. (20 April.) 2 Baron JH. Duodenal ulcer, gastric acid, and Helicobacter pylori. BMJ 1991;302:1333. (1 June.) 3 Holcombe C. Duodenal ulcer, gastric acid, and Helicobacter

pylorn. BMJr 1991;302:1333. (1 June.) 4 Wyatt JI. Campylobacter pylori, duodenitis and duodenal ulceration. In: Rathbone BJ, Heatley RV, eds. Campylobacter pylon and gastroduodenal disease. Oxford: Blackwell Scientific, 1989:117-24. 5 Frierson HF Jr, Caldwell SH, Marshall BJ. Duodenal bulb biopsy findings for patients with non-ulcer dyspepsia with or without Campylobacter pylorn gastritis. Modern Pathology 1990;3:27 1-5. 6 Kreuning J, Bosman FT, Kuiper G, van del Wal AM, Lindeman J. Gastric and duodenal mucosa in "healthy" individuals. An endoscopic and histopathological study of 50 volunteers. J Clin Pathol 1978;31:69-77. 7 Andersen LP, Holck S, Elsborg L, Justesen T. The Helicobacter (Campylobacter) pylorn-colonized duodenal mucosa and gastric metaplasia. APMIS 1991;99:244-8. 8 Wyatt JI, Rathbone BJ, Sobala GM, Shallcross T, Heatley RV, Axon ATR, et al. Gastric epithelium in the duodenum: its association with Helicobacter pylorn and inflammation. 7 Clin Pathol 1990;43:981-6. 9 Tatsuta M, lishi H, Yamamura H, Yamamoto R, Taniguchi H. Enhancement by tetragastrin of experimental induction of gastric epithelium in the duodenum. Gut 1989;30:31 1-5. 10 Patrick WJA, Denham D, Forrest APM. Mucous change in the human duodenum: a light and electron microscopic study and correlation with disease and gastric acid secretion. Gut 1974;15:767-76. 11 Tovey Fl, Tunstall M. Duodenal ulcer in black populations in Africa south of the Sahara. Gut 1975;16:564-76. 12 Tovey Fl. Peptic ulcer in India and Bangladesh. Gut 1979;20: 329-47. 13 Schwartz K. Uber penetrierende Magen- und Jejunalgeschwure.

Beitrage zurKlinischen Chirurgie 1910;67:%-128. 14 Konjetzny GE. Zur chirurgischen Beurteilung der chronischen Gastritis. Archivffur klinischen Chirurgie 1924;129: 139-71. 15 Wyatt JI, Rathbone BJ, Dixon MF, Heatley RV. Campylobacter pylon and acid induced gastric metaplasia in the pathogenesis of duodenitis.J Clin Pathol 1987;40:841-8. 16 Forman D, Newell DG, Fullerton F, Yarnell JWG, Stacey AR, Wald N, et al. Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation. BMJ 1991;302:1302-5. (1 June.)

SIR,-Interest in the role .of Helicobacter pylori in duodenal ulcer disease is growing.' Several clinical investigators may wish to repeat and extend our study of relapse of duodenal ulcer after successful eradication of H pylori.2 1535