CORRESPONDENCE * All letters must be typed with double spacing and signed by all authors. * No letter should be more than 400 words. * For letters on scientific subjects we normally reserve our correspondence columns for those relating to issues discussed recently (within six weeks) in the BMJ. * We do not routinely acknowledge letters. Please send a stamped addressed envelope ifyou would like an acknowledgment. * Because we receive many more letters than we can publish we may shorten those we do print, particularly when we receive several on the same subject.
The politics of change SIR,-Professor Rudolf Klein makes an interesting and valid point on the distinction between services and institutions.' Their interaction is complex and requires deeper analysis than a simple opposition of concepts. Two separate though related points need to be included in the discussion. Firstly, the dynamics of change have a variable time element. Too fast a rate of change causes unnecessary and counterproductive turbulence, with diminished output. True, an institution is important only if it can deliver services (and an institution can equally well be a management structure in the community as a teaching hospital in Central London). But an institution takes time to be built, to come into stream, and to deliver. If we unthinkingly neglect our institutions and let them decay we cannot instantaneously revive them when a future need becomes apparent. It took 10 years to build the district general hospital in which I spent my professional life; it took twice as long to achieve the arrangements for obstetric beds and services in west London, culminating in the closure of an isolated maternity hospital. An institution is more like an army regiment with a tradition than a commercial company whose board can be transformed overnight. In transitional times (and what times are not?) maintaining the morale and function of an institution is to preserve its potential for effective change and delivery of services in the future. The other point to be considered is the assumption that there will be a buyers' market as far as general practitioner budget holders are concerned. This may well become erroneous if more and more local hospitals fall by the wayside and larger hospitals create local monopolies. And this ignores the quasi-monopolistic position of hospitals in "remote" areas, whose nearest neighbour may be 80 km away. An equilibrium may well be struck at which most local general practitioner budget holders will find no sellers of hospital services except at prices well above the anticipated or planneo minimum. The marginal potential for increased capacity in neighbouring institutions if a major unit closes is another practical consideration. Without actual growth by the survivors it is hard to see how, for example, 60 000 casualty patients and 80000 outpatient attendances could be absorbed
by neighbouring hospitals. What is clear, whether we have information about contracts or not, is that the hospital service as a whole is underfunded for doing what it is doing at present, in the way that it is trying to do it at present. The government believes that changing the way things are done and organised will in the future free resources that will allow the service to do the things it is trying to do at present. They said that, of course, in 1983 with the Griffiths report, and I was one of those who believed that and tried
BMJ
VOLUME
302
1
JUNE
1991
to make it happen. The flavour of the decade is different now, with market forces as the engine of change. Managers now are forced to reduce what they are trying to do (by closing wards, redundancies, etc) through lack of resources, while trying to adapt to another new organisation that may in the future give them the resources to do what they are trying to do now. But if clinical departments shut down those services will no longer be available for purchase by general practitioners or health authorities and cannot be recreated overnight or necessarily be found elsewhere. R EBAN Goosey, Oxfordshire SN7 8PA I Klein R. The politics of change. BMJ 1991;302:1102-3.
(11 May.)
Duodenal ulcer, gastric acid, and Helicobacter pylon SIR,-Dr A R Axon bases his belief "that gastric acid is only one of several factors responsible for ulcer genesis"' partly on my 30 year old work that, "Though patients with duodenal ulcer do, as a group, have a high acid output, individual values show considerable overlap with those of many people with normal acid secretion."' This, however, is an incomplete picture of my hypersecretory model of duodenal ulcer3: not only do a third of patients with duodenal ulcers have peak acid output above the upper limit of normal but there was a lower limit of peak acid output of 15 mmol/h below which I found no patients with duodenal ulcer; this is comparable to the finding that no stomachs with less than 10' parietal cells were found at postmortem examination in patients with duodenal ulcer.4 This simple pathophysiological threshold model for duodenal ulcer had the corollary that any acid lowering drug or operation that reduced peak acid output and kept it below 15 mmol/h-whether it be partial gastrectomy, one of the various vagotomies, antacids, antimuscarinics, H2 blockers, or H+K' ATPase inhibitors-would allow a duodenal ulcer to be healed and kept healed, so that we can now heal and keep healed almost every peptic ulcer. Moreover, Hunt's group has not only strictly correlated healing of duodenal ulcers with the acid lowering effects of all antisecretory drugs5 but has refined the model so that, for example, all of an ulcer can be expected to heal within four weeks if intragastric pH is increased to pH 3 or above for 18-20 hours a day.6 Although this pathophysiology of duodenal ulcer has been clear and effective, however, it has no more been treating the underlying pathogenesis of such ulcers than has been insulin treatment of
diabetes mellitus. It is the pathogenesis ofduodenal ulcer that is now being elucidated in relation to Helicobacter pylon. H pylon should soon be eradicable by short treatment regimens, which will be Dr Axon's "permanent non-surgical cure" of duodenal ulcer provided that reinfection does not occur. J H BARON Department of Surgery, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 ONN 1 Axon AR. Duodenal ulcer: the villain unmasked? BMJ 1991; 302:919-21. (20 April.) 2 Baron JH. The relationship between basal and maximal acid output in normal subjects and patients with duodenal ulcer. Clin Sci 1963;24:357-70. 3 Baron JH. An assessment of the augmented histamine test in the diagnosis of peptic ulcer. Gut 1%3;4:243-53. 4 Baron JH. Aetiology. In: Wastell C, ed. Chronic duodenal ulcer. London: Butterworths, 1972:19-52. 5 Jones DB, Howden CW, Burget DW, Kerr GD, Hunt RH. Acid suppression in duodenal ulcer: a meta-analysis to define optimal dosing with anti-secretory drugs. Gut 1987;28:1120-7. 6 Burget DW, Chiverton SG, Hunt RH. Is there an optimal degree of acid depression for healing of duodenal ulcers? Gastroenterology 1990;99:345-51.
SIR, -The evidence that Helicobacter pylori has a role in the aetiology of duodenal ulcer comes from the West,' and yet most patients who are infected with H pylon live in the developing world, where most of the population is infected. IgG antibodies are found in 70-80% of those tested, and infection is acquired at an early age.3 Even among a group of 40 asymptomatic volunteers H pylon infection was present in 80%.4 Despite this high prevalence of H pylon infection duodenal ulcer is often less common than in the West.5 6 If it is suggested that H pylon causes duodenal ulcer in the West it must also be explained why the organism does not cause duodenal ulcer in the developing world. Though evidence for a role in the aetiology of duodenal ulcer in the West is accumulating, the case is far from proved in the developing world: at best H pylon can have only a minor role in combination with other factors. CHRIS HOLCOMBE Department of Surgery, Charing Cross Hospital, London W6 8RF 1 Axon AR. Duodenal ulcer: the villain unmasked? BMJ 1991; 302:919-21. (20 April.) 2 Megraud F, Brassens-Rabbe M-P, Denis F, Belbouri A, Hoa DQ. Seroepidemiology of Campylobacter pylorn in various populations. J Clin Microbiol 1989;27:1870-3. 3 Holcombe C, Tsimiri S, Eldridge J, Jones DM. Prevalence of antibody to Helicobacter pylori in children in northern Nigeria. RevEspEnferm AparDig 1990;55:39. 4 Holcombe C, Kaluba J, Lucas SB. Non-ulcer dyspepsia in Nigeria: a case control study. Trans R Soc Trop Med (in press). 5 Tovey Fl, Tunstall M. Duodenal ulcer in black populations in Africa south of the Sahara. Gut 1975;16:564-76. 6 Holcombe C, Okolie H. Duodenal ulcer in the northern savannah of Nigeria. TropDoct 1991;21:16-8.
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The politics of change SIR,-Professor Rudolf Klein makes an interesting and valid point on the distinction between services and institutions.' Their interaction is complex and requires deeper analysis than a simple opposition of concepts. Two separate though related points need to be included in the discussion. Firstly, the dynamics of change have a variable time element. Too fast a rate of change causes unnecessary and counterproductive turbulence, with diminished output. True, an institution is important only if it can deliver services (and an institution can equally well be a management structure in the community as a teaching hospital in Central London). But an institution takes time to be built, to come into stream, and to deliver. If we unthinkingly neglect our institutions and let them decay we cannot instantaneously revive them when a future need becomes apparent. It took 10 years to build the district general hospital in which I spent my professional life; it took twice as long to achieve the arrangements for obstetric beds and services in west London, culminating in the closure of an isolated maternity hospital. An institution is more like an army regiment with a tradition than a commercial company whose board can be transformed overnight. In transitional times (and what times are not?) maintaining the morale and function of an institution is to preserve its potential for effective change and delivery of services in the future. The other point to be considered is the assumption that there will be a buyers' market as far as general practitioner budget holders are concerned. This may well become erroneous if more and more local hospitals fall by the wayside and larger hospitals create local monopolies. And this ignores the quasi-monopolistic position of hospitals in "remote" areas, whose nearest neighbour may be 80 km away. An equilibrium may well be struck at which most local general practitioner budget holders will find no sellers of hospital services except at prices well above the anticipated or planneo minimum. The marginal potential for increased capacity in neighbouring institutions if a major unit closes is another practical consideration. Without actual growth by the survivors it is hard to see how, for example, 60 000 casualty patients and 80000 outpatient attendances could be absorbed
by neighbouring hospitals. What is clear, whether we have information about contracts or not, is that the hospital service as a whole is underfunded for doing what it is doing at present, in the way that it is trying to do it at present. The government believes that changing the way things are done and organised will in the future free resources that will allow the service to do the things it is trying to do at present. They said that, of course, in 1983 with the Griffiths report, and I was one of those who believed that and tried
BMJ
VOLUME
302
1
JUNE
1991
to make it happen. The flavour of the decade is different now, with market forces as the engine of change. Managers now are forced to reduce what they are trying to do (by closing wards, redundancies, etc) through lack of resources, while trying to adapt to another new organisation that may in the future give them the resources to do what they are trying to do now. But if clinical departments shut down those services will no longer be available for purchase by general practitioners or health authorities and cannot be recreated overnight or necessarily be found elsewhere. R EBAN Goosey, Oxfordshire SN7 8PA I Klein R. The politics of change. BMJ 1991;302:1102-3.
(11 May.)
Duodenal ulcer, gastric acid, and Helicobacter pylon SIR,-Dr A R Axon bases his belief "that gastric acid is only one of several factors responsible for ulcer genesis"' partly on my 30 year old work that, "Though patients with duodenal ulcer do, as a group, have a high acid output, individual values show considerable overlap with those of many people with normal acid secretion."' This, however, is an incomplete picture of my hypersecretory model of duodenal ulcer3: not only do a third of patients with duodenal ulcers have peak acid output above the upper limit of normal but there was a lower limit of peak acid output of 15 mmol/h below which I found no patients with duodenal ulcer; this is comparable to the finding that no stomachs with less than 10' parietal cells were found at postmortem examination in patients with duodenal ulcer.4 This simple pathophysiological threshold model for duodenal ulcer had the corollary that any acid lowering drug or operation that reduced peak acid output and kept it below 15 mmol/h-whether it be partial gastrectomy, one of the various vagotomies, antacids, antimuscarinics, H2 blockers, or H+K' ATPase inhibitors-would allow a duodenal ulcer to be healed and kept healed, so that we can now heal and keep healed almost every peptic ulcer. Moreover, Hunt's group has not only strictly correlated healing of duodenal ulcers with the acid lowering effects of all antisecretory drugs5 but has refined the model so that, for example, all of an ulcer can be expected to heal within four weeks if intragastric pH is increased to pH 3 or above for 18-20 hours a day.6 Although this pathophysiology of duodenal ulcer has been clear and effective, however, it has no more been treating the underlying pathogenesis of such ulcers than has been insulin treatment of
diabetes mellitus. It is the pathogenesis ofduodenal ulcer that is now being elucidated in relation to Helicobacter pylon. H pylon should soon be eradicable by short treatment regimens, which will be Dr Axon's "permanent non-surgical cure" of duodenal ulcer provided that reinfection does not occur. J H BARON Department of Surgery, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 ONN 1 Axon AR. Duodenal ulcer: the villain unmasked? BMJ 1991; 302:919-21. (20 April.) 2 Baron JH. The relationship between basal and maximal acid output in normal subjects and patients with duodenal ulcer. Clin Sci 1963;24:357-70. 3 Baron JH. An assessment of the augmented histamine test in the diagnosis of peptic ulcer. Gut 1%3;4:243-53. 4 Baron JH. Aetiology. In: Wastell C, ed. Chronic duodenal ulcer. London: Butterworths, 1972:19-52. 5 Jones DB, Howden CW, Burget DW, Kerr GD, Hunt RH. Acid suppression in duodenal ulcer: a meta-analysis to define optimal dosing with anti-secretory drugs. Gut 1987;28:1120-7. 6 Burget DW, Chiverton SG, Hunt RH. Is there an optimal degree of acid depression for healing of duodenal ulcers? Gastroenterology 1990;99:345-51.
SIR, -The evidence that Helicobacter pylori has a role in the aetiology of duodenal ulcer comes from the West,' and yet most patients who are infected with H pylon live in the developing world, where most of the population is infected. IgG antibodies are found in 70-80% of those tested, and infection is acquired at an early age.3 Even among a group of 40 asymptomatic volunteers H pylon infection was present in 80%.4 Despite this high prevalence of H pylon infection duodenal ulcer is often less common than in the West.5 6 If it is suggested that H pylon causes duodenal ulcer in the West it must also be explained why the organism does not cause duodenal ulcer in the developing world. Though evidence for a role in the aetiology of duodenal ulcer in the West is accumulating, the case is far from proved in the developing world: at best H pylon can have only a minor role in combination with other factors. CHRIS HOLCOMBE Department of Surgery, Charing Cross Hospital, London W6 8RF 1 Axon AR. Duodenal ulcer: the villain unmasked? BMJ 1991; 302:919-21. (20 April.) 2 Megraud F, Brassens-Rabbe M-P, Denis F, Belbouri A, Hoa DQ. Seroepidemiology of Campylobacter pylorn in various populations. J Clin Microbiol 1989;27:1870-3. 3 Holcombe C, Tsimiri S, Eldridge J, Jones DM. Prevalence of antibody to Helicobacter pylori in children in northern Nigeria. RevEspEnferm AparDig 1990;55:39. 4 Holcombe C, Kaluba J, Lucas SB. Non-ulcer dyspepsia in Nigeria: a case control study. Trans R Soc Trop Med (in press). 5 Tovey Fl, Tunstall M. Duodenal ulcer in black populations in Africa south of the Sahara. Gut 1975;16:564-76. 6 Holcombe C, Okolie H. Duodenal ulcer in the northern savannah of Nigeria. TropDoct 1991;21:16-8.
1333
