Тексты по английскому языку / journal

яюProfiting from closure: the private finance initiative and the NHS

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Private investment is efficient when it maximizes the returns on capital. Public investment is efficient when it maximizes returns within the constraints of public policy goals, like meeting the population's healthcare needs. Given these different aspirations, what does partnership between the private and public sectors mean in practice? Specifically, what happens when private finance funds hospital redevelopment, as the private finance initiative attempts to do? In a BMA report published this week, Declan Gaffney and Ally son Pollock of St George's Hospital Medical School address this question in what is the most detailed independent study to date of the 14 private finance initiative schemes approved in June this year. Reliance on private investment, the authors say, inflates the scale of capital schemes to levels which far exceed more prudent public proposals as bidders try to improve their rate of return. This cost escalation puts new demands on public revenue, which in turn leads to the search for new economies and new subsidies. The economies inspire bed reductions and unpiloted innovations in healthcare provision, while the subsidies entail transfers from other health sectors and raids on the very public funds that private finance was meant to replace. Returns on capital come to predominate over other policy considerations, and the health service ends up paying more for less.

The figures are striking. From relatively modest beginnings, the estimated costs of the 14 schemes rose on average by 72% as investors proposed bigger schemes involving larger loans and more equity. In Swindon the cost rose by 229%. Hospital closures and bed reductions of 7% to 44% helped meet the cost by releasing land for sale and allowing economies to be made in the new buildings.

But asset sales and conjectured "efficiency savings" have proved inadequate to bridge the affordability problem which cost escalation had created, and a series of new subsidies have been introduced. Some health authorities increased their annual commitment, taking money from other schemes and from sectors, such as community services, most likely to bear the burden of cost shunting out of the hospital system. Regional offices translated block grant capital into revenue payments, which meant subsidizing privately financed projects out of the equipment and maintenance budgets of hospitals without privately financed schemes. In several cases equipment replacement was dropped from the deals even though equipment formed part of the estimated capital cost. And finally, the NHS Executive introduced a direct annual subsidy for the first 30 years of the private finance contract, a subsidy almost large enough in the case of Swindon to have paid for the original public scheme which the private finance initiative scheme had replaced (Ј42m compared with Ј48m).

The private finance initiative, says the report, has been bailed out and the cost borne by other parts of the health service. It has become not just a mechanism for reducing hospital services but also a costly burden. This state of affairs is unlikely to be exposed by the system of appraising the initiative, as that overlooks the costs which the scheme shifts out of the hospital sector on to others.

These are important findings. They suggest that the private finance initiative results in commercial returns unduly influencing the conduct of capital planning and the determination of asset size. In Edinburgh, for example, efficiency savings tied to the proposed new hospital imply patient throughput approaching 88 finished consultant episodes per bed per year compared with a national average for England that has leveled out at 54. There is no precedent in Britain for such levels of activity. The planning base, staffing, and resource implications of the new model of care on which the hospital depends are unclear and the practical arrangements remain unpiloted. This is not health-care planning as it is traditionally understood.

The Department of Health knows this, of course, so why is it prepared to accept the cost and the risk? The signs are that the private finance initiative offers a vehicle for another agenda that is gaining ground among NHS managers. Under this agenda, large-scale capital investment provides an opportunity to redesign the hospital sector. What are the problems to which large (and costly) capital investment is supposed to be a solution? In Birmingham, where the health authority started consulting last month on its own private finance initiative plan, the problems are said to be constantly increasing referrals to relatively expensive hospitals. Their solution involves reducing the size of the, hospital sector by half and substituting cheaper alternatives. This means building a new health infrastructure which is where the private finance initiative comes in.

What Birmingham's analysis omits to mention is the role of capital charges in the pressure felt by hospital budgets. Capital charges, which force hospitals to earn commercial returns, were introduced by the previous government to make transfer to private health provision that much easier. This rump of a privatization policy continues to influence the NHS asset base by encouraging ward and hospital closure in much the same way as the old window tax encouraged bricking up windows (D Mayston, paper in preparation). To pay for the privately financed project in Birmingham, the expected rate of return on redeveloped hospitals has been increased from the current 6% to 13°/o.3 So hospital costs are artificially inflated rather than hospitals simply being too expensive.

The problem for Birmingham and Edinburgh, and the other areas which are using capital spending to drive out labour from the hospital sector, is that no one is yet clear what sort of health service will result or whether it will save money. In the past the impact of capital charges was felt by chronically sick and elderly patients. The impact of the private finance initiative will be wider as early discharge and prevented admission have their effects across the board. How will these patients react when they are directed to cheaper alternatives and what sort of care can they expect to find there?



Preventing RhD haemolytic disease of the newborn

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In 1994 we saw the 25th anniversary year of the worldwide introduction of anti-rhesus (D) immunoglobulin prophylaxis, one of the most successful prophylactic programmes in medical history. In 1977, 110 cases of stillbirth or neonatal death due to RhD haemolytic disease were registered in Britain; by 1992, this figure seemed to have dropped to nine cases. In this issue of the BMJ, however, Whitfield and colleagues show that this is a serious underestimation. Extrapolation of their Scottish figures suggests that there are 50 deaths a year due to RhD haemolytic disease in Britain. They conclude that the discrepancy is due to underreporting because deaths due to early abortion (before 24 weeks) and late neonatal death (second to fourth week of life) are not included in official figures.

The policy introduced in 1969 was to give anti-D immunoglobulin to RhD negative women only after the birth of a RhD positive infant or after a sensitising event in pregnancy, such as antepartum haemorrhage. The question now is whether the policy should be extended so that all pregnant women who are RhD negative receive an antenatal dose of anti-D immunoglobulin. More than half the deaths in Whitfield's study were due to sensitis Wion of the mother between the 28th and 40th week of her first pregnancy. Routine antenatal prophylaxis with anti-D immunoglobulin would largely have prevented sensitisation in the first pregnancy, and neonatal death after a subsequent pregnancy. Another paper in this issue reports that introducing a programme of antenatal prophylaxis in Derbyshire reduced the sensitisation rate from 1.12% of women at risk to 0.28%, a finding that is consistent with previous work. This paper also shows that the shift from hospital to community based antenatal care did not reduce the programme's success. The lower incidence of sensitisation might also have been due to a heightened awareness among general practitioners of the need to give anti-D immunoglobulin to women with antepartum haemorrhage; the number of such events doubled during the period under study.

There are two reasons why RhD immunisation and sensitisation of pregnant women still occurs. Firstly, because not all women receive anti-D immunoglobulin when they should, and, secondly, because small, undetected leaks of fetal blood into the maternal circulation can occur during the third trimester of pregnancy. Both issues were extensively discussed in April during a consensus conference organised by the Royal College of Physicians of Edinburgh and the Royal College of Obstetricians and Gynaecologists. Contributors were worried that current guidelines for prophylaxis with anti-D immunoglobulin were not being followed. Potentially sensitising events during pregnancy such as blunt abdominal trauma and antepartum haemorrhage require that the mother is protected by an injection of anti-D immunoglobulin, preferably after a Kleihauer test or equivalent to asses the size of the fetomaternal bleed. Kleihauer tests may be difficult to perform and standardise but health professionals should at least recognise sensitising events and consider giving anti-D immunoglobulin "blind" if testing is not available. Pregnant women who are RhD negative should also be educated about the condition, so that they recognise the need for treatment should a sensitising event occur.

The conference agreed that the second cause of RhD immunization - fetomaternal bleeding during the last trimester - would be largely eliminated by giving anti-D immunoglobulin antenatally in one of two possible dose schedules: two doses of 500 IU, one at 28 weeks and the other at 34 weeks, or one dose of 1000 IU given between 28 and 30 weeks. Both options are effective. Antenatal programmes are cost effective if reserved for women in their first pregnancy, as they were in the Derbyshire study.

Although the conference consensus panel considered that this jestriction could not be justified on ethical or economic grounds, it seems that the tremendous global shortage of anti-D immunoglobulin may prevent extension of antenatal prophylaxis to all pregnant women at risk. The shortage of anti-D immunoglobulin from voluntary RhD negative donors is a major concern worldwide. The risk of transmitting viruses with the immunising RhD positive red cells cannot be completely eliminated and has caused the ithdrawal of many voluntary donors. Most countries now accept immunoglobulin preparations from commercial sources, prepared from paid donors' blood, and these seem to be safe. Once human monoclonal anti-D immunoglobulin is available, shortage will be a thing of the past; but, while it is being developed and tested, the need for immunised donors will continue well into the next century, and the debate about how best to use this scarce resource will continue.



Helicobacter pylori and its interaction with risk factors for chronic disease

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In this issue Brenner and colleagues-document the effects of lifestyle on Helicobacter pylori infection in 447 patients in a German rural practice (p 1489). They found that the H pylori infection rate appeared to be reduced by alcohol consumption (?100 g per week), increased by coffee drinking (?3 cups per day), and non-significantly increased by smoking. In the past, when idiopathic gastric hyperacidity was considered to be the chief cause of dyspeptic symptoms, smoking, coffee, and alcohol were often implicated as exacerbating the condition and advice given to eliminate these habits. Increasingly since 1984, however, when Warren and Marshall hypothesised that campylobacter-like organisms were the cause of peptic ulcer disease, there has been a need to re-evaluate the role of these traditional risk factors. This need has been addressed by Brenner et al with some seemingly unexpected results.

There are reasons why alcohol, coffee, and smoking might have little effect on, or even increase, the hostility of the gastric environment to H pylori. The acid gastric pH prevents most organisms from thriving or even surviving in the stomach. H pylori, however, has an electropositive internal milieu; twice the number of basic amino acids, argenine and lysine, as Haemophilus influenzae and Escherichia coli, and powerful urease activity, with the ability to produce both ammonia and factors that inhibit parietal cell acid production. All these attributes make survival of H pylori in the stomach less influenced by the reduction in pH which may accompany coffee, smoking, and alcohol consumption.

Alcohol and smoking tend to increase the rate of gastric emptying. However, H pylori has at least five different adhesins to attach itself to gastric epithelial cells. These, together with the fact that the surface lipopolysaccharide of H pylori is several orders of magnitude less immunoganic thanbther enteric bacteria, may allow it to adhere to the gastric mucosal surface and create a quasi "stagnant loop syndrome" despite adequate luminal flow. These functions have been highlighted by the recent complete sequencing of the H pylori gene. One of the remaining questions is why alcohol is effective in the face of this powerful bacterial genetic machinery. Is it the time honoured antiseptic effect of alcohol, to which H pylori has developed no defence?

H pylori infection is the most common human chronic bacterial infection, affecting half the population and associated with duodenal and gastric ulceration, chronic active and atrophic gastritis, gastric carcinoma, and mucosa associated lymphoid tissue lymphoma. As well as the risk of cancer, Brenner et al draw attention to the role of H pylori in cardiovascular disease in a fashion similar to Chlamydia pneumoniae. They speculate that the beneficial effect of low alcohol consumption on coronary heart disease may relate to its ability to reduce H pylori infection. A corollary might be that smoking and coffee consumption contribute to the risk of coronary heart disease by increasing susceptibility to H pylori infection. Furthermore, since coffee raises serum cholesterol concentrations unless it is filtered to remove the offending diterpenes, will filtered coffee lacking deterpenes still promote H pylori infection? Should we screen patients at high risk of coronary heart disease for H pylori? If so, can we use the more generally available IgG test requiring simply a serum sample or should a C urea breath test be the standard? Finally, will alcohol consumption be advised to help eliminate H pylori?

Brenner et al outline the possible positive effect of alcohol and the negative effect of coffee on the elimination of H pylori. H pylori is important because of its association with a broad range of diseases. However, in view of its high prevalence, other factors, including genes and environment, are likely to be pivotal in the pathogenesis of disease. The high prevalence of this bacteria also raises the question of routine screening and, if so, which test to use. In addition, should changes in lifestyle to reduce H pylori infection be encouraged - for example, green tea and saki rather than coffee in Japan? Certainly, these data are the closest we have had to support St Paul's injunction to "take a little wine for thy belly's sake." The emphasis, however, may be on "little" - that is, 1-2 drinks daily. Above this level, despite the continued lower risk of coronary heart disease, the risk of cancer, stroke, and all cause mortality rises. Finally, recent publications from the health professionals study of 47806 men found no increased risk of duodenal ulcer associated with coffee, smoking, or alcohol but a negative association with dietary fibre and vitamin A. We require more studies before we are confident in giving advice on this important and complex topic.



Discussion

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Our study corroborates the finding that women who have a low birth weight infant are more likely to give birth to another low birth weight infant dian women who have had infants of normal birth weight. The most likely cause is related to maternal genes or the intrauterine environment. A decline in social status was found to be a comparatively strong predictor of low birth weight, which suggests that fetal growth is reduced under poor social circumstances. All results were adjusted for gestational age, and the effect was also seen in the subgroup of outcome children born at term in the unexposed cohort. In the exposed cohort the effect of a decline in social status was larger for newborn infants with a birth weight of 2000 g.

In the unexposed cohort a decline in social status was more closely associated with low birth weight than social status at the time of birth of the index child. The odds ratio of 1.24 in the exposed cohort represents an increase from 20% to almost 25% in the risk of having another low birth weight infant when compared with couples for whom none of the indicators of risk changed. The odds ratio of 2.32 in the unexposed cohort is a similar increase in excess risk (from 4.5% to 10%). The findings from the two cohorts are therefore similar on an additive scale, but the association was significant only in the unexposed cohort

Many expect that lone mothers are at a higher risk of having a low birth weight infant, but including cohabitation status in the analysis did not change the risk associated with social mobility in either cohort.

Hi some cases poor health may have triggered a decline in social status,22"24 and health conditions rather than the change in social status may have caused low birth weights. These factors would, however, explain but a small part of the association since only severe diseases trigger a decline in social status in Denmark, which has an extensive social support system. Most women with health poor enough to initiate a decline in social status would probably also have low fertility and therefore not be considered in this study. Changes in social status have not previously been associated with low birth weight, but unemployment and low social status have been linked with poor reproductive outcome in several studies.

The impact of paternal factors on birth weight remains unclear, but maternal half siblings have a much higher correlation for birth weight than paternal half siblings,3 H and this is supported by our findings of little effect on birth weight of a change in partner. A change in male partner is not, however, expected to change the distribution of birth weight. If a paternal effect is randomly distributed, the average difference in birth weight between the two pregnancies would be expected to be unaffected by a change in male partner, but the correlation coefficient would be expected to be lower for those who change partner, which is what this study found.

Only limited data were available on environmental exposures, and these factors are probably more important in fetal growth man those that could be captured in this study. Area of residence is, for example, only a proxy measure for some environmental exposures such as clean drinking water or air pollution. A decline in social status may be related to lack of compliance in medical care, and smoking or other factors that are linked with growth retardation may be related to downward social mobility, as they are for low social status.12 This study does not permit identification of the actual determinants responsible for low birth weight that may be related to a decline in social status.

Our study analysed a large cohort and was carried out without loss to follow up. The data are of good quality with regard to the timing of pregnancies, paternity, birth weight, residence, and job tides. Further research should identify changes in proximal fetal growth factors influenced by changes in social status. Women in poor social conditions should be given special attention during antenatal care.



Methods

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The study was carried out in four practices in the area covered by the Lambedi, Southwark, and Lewisham Family Health Service Authority in southeast London between September and December 1994. This authority had lower than average prescribing levels compared with the rest of England." The practices were chosen on the basis of their prescribing analysis and cost (PACT) data, to include two high prescribing and two low prescribing practices (relative to the other practices covered by the same family health service authority). All the practices were non-fundholding group practices, two of them receiving high levels and two of them low levels of deprivation payments.

We chose surgery sessions to represent different days of the week and times of day. At the beginning of each chosen session, the researcher gave a questionnaire to the doctor. This asked for the patient's name or computer number, the diagnosis or presenting problem, the doctor's perception of whether the patient wanted a prescription, whether the doctor felt pressurised to write a prescription, whether a prescription was written (and if so, the details of the drugs), and whether the prescription was "strictly indicated on purely medical grounds." The 15 participating doctors completed a questionnaire for each patient immediately after the consultation.

The researcher also approached each adult patient in the waiting room and asked them to complete a questionnaire while waiting to see the doctor. An oral explanation of the study was accompanied by a written explanation for the patient to keep. The questionnaire asked for the patient's name or computer number, the symptom or presenting problem, prior drug treatment for this or other conditions, expectations of receiving a prescription that day, exemption status for prescription charges, and demographic characteristics. Expectations of a prescription were assessed with two questions to identify both ideal expectation and actual expectation. The first asked if the patient was hoping that the doctor would give them a prescription that day, and the second asked if the patient expected that the doctor would actually give them a prescription. Questionnaires were not given to the patients who had already completed one, to those who could not speak English, to those who saw the doctor immediately, or to those who refused. Completed questionnaires were returned to the researcher in sealed envelopes.

At the end of surgery the researcher matched the patients' and doctors' questionnaires, and the responses were then coded. Symptoms and diagnoses were coded according to the International Classification of Primary Care. A 10% sample of matched questionnaires was checked for accuracy of coding. Information about the doctors' qualifications was added to the database from the medical register.

The response rate was calculated by dividing the number of matched pairs of questionnaires by the total number of consultations in the chosen surgery sessions, having excluded those who did not attend, those who had already completed a questionnaire, and, in one practice, those who were known by the practice staff not to speak English. This is likely to be an underestimate as it was not possible to confirm apparent non-attenders in one practice, and some non-English speakers may not have been identified. Characteristics of responding patients were compared with the age and sex of non-respondents and with the demographic characteristics of the resident population of the inner London boroughs of Lambeth, Southwark, and Lewisham from the 1991 census.



Victims of Creutzfeldt-Jakob disease prompt code of conduct

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The Australian government is to enforce a code of conduct for medical experiments in the wake of a $A10m (4.4m pounds) compensation payout to victims of Creutzfeldt-Jakob disease (CJD) transmitted by treatment. The minister for health, Dr Carmen Lawrence, has asked the National Health and Medical Research Council's health ethics committee to draft standards to make doctors accountable for mistakes. "I think the days when doctors could say, whether they were in this field or another, 'We know what's good for you and we'll judge the risk and the benefits,' are gone. The patient deserves to be fully informed about the benefits and the risk as they are known at the time."

Earlier this month the government announced the package of services aimed at helping over 2400 patients who were treated with human pituitary hormones between 1967 and 1985. The package will offer medical help to those who have contracted the disease and counselling to everyone who was treated with the growth hormone.

A recent report by Professor Margaret Allars found that the doctors and bureaucrats who administered the programme had breached state and federal laws. She found that doctors had also stretched guidelines, breached ethics, and condoned the often illegal harvesting of glands from dead bodies to extract human growth hormone and a human pituitary gonadotrophin for infertile adults.

Dr Lawrence said that despite the "moral culpability" of some administrators of the programme, legal advice was that no disciplinary action could be taken. She said that the only remedy for medical negligence was through the state's medical board or civil court proceedings. "There was perhaps far too much medical enthusiasm and not enough constraint on their activities."

The president of the Australian Medical Association, Dr Brendon Nelson, said that the new code of conduct was in the public interest. "The patients need to know whether they want to take the risks and doctors need to be accountable," he said.

However, many CJD support groups are not satisfied with the payout. Joanne Coldwell, spokeswoman for the southern Sydney support group, said that the money covered only medical and counselling services and not suffering or humiliation. "That is like saying to a rapist that you will give him compensation to counsel his victim," she said. The coordinator for the New South Wales CJD Support Group, Suzanne Solvyns, said: "Although new ethical guidelines are proposed, the only way to stop doctors using people experimentally again is to make the administrators of medical programmes accountable."



Chernobyl damaged health, says study

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People who cleaned up after the nuclear disaster at Chernobyl have an increased incidence of cardiovascular and gastrointestinal disease and cancers of the stomach and lung, according to the first epidemiological study of the incident. They seem not to have an increased risk of leukaemia. "It is as if they are suffering from accelerated aging," said Dr Alexei Nikiforov, director of the Russian Centre of Ecological Medicine, at a recent international meeting on radiological risk in Paris. "They have roughly the same diseases as anybody else, but the diseases occur with higher frequency and in a more acute manner."

The term "liquidators" is used to describe the 500000 to 600000 people, mostly young men, who cleaned up after the accident at Chernobyl eight years ago. Some of them worked for only a few hours on highly radioactive sites such as the reactor's roof, while others worked for weeks or months in less contaminated areas. Little is known about how much radiation the liquidators received, and most of them returned home without any medical follow up.

The Russian Ministry of Defence agreed to make military records available to Dr Nikiforov only last year. Dr Nikiforov's centre identified about 75000 former liquidators who now live in the St Petersburg region and selected two cohorts for study: 14000 men exposed to doses of radiation that can be fairly well estimated and 22000 soldiers, who, unlike civilians, were followed up by doctors.

The study is not completed-the data have not been fully quantified, and it has not been determined whether the increase in disease can be attributed to the effects of radiation. But Dr Nikiforov points out that the type of disease seen in the liquidators is different from that observed after the nuclear bomb explosions at Hiroshima and Nagasaki 45 years ago. Among Japanese survivors the excess of solid tumours was observed about 30 years after exposure while the rise in cardiovascular disease became apparent only in recent years. An increased incidence of leukaemias, however, was observed during the first 10 years after the bombing.

At an earlier meeting, also in Paris, Dr Angelina Neagu, head of neurology at the Ukrainian Centre of Radiation Medicine, reported a doubling of spontaneous abortions and congenital anomalies in several districts affected by the Chernobyl disaster.

Jacques Lochard, director of the Nuclear Protection Evaluation Centre in Paris, said that experience with serious natural or industrial catastrophes shows that before people return to normal they need to come to terms with the accident and its consequences. But this stage has not been reached in the Ukraine because people still believe that they are living in constant danger.

Legislation introduced in the Ukraine in 1991 recognises four categories of "victim" of radiation for the purposes of compensation.

Victims are given a card that entitles them to various compensations, including free public transport, reduced rent, early retirement, and money or coupons to be used in special stores. This has created resentment and ghettos, perpetuating the "post-accident crisis."

"We have a lot to learn from the way the Chernobyl crisis has been handled," said Lochard. He said that one of the objectives of the studies, which will continue with the support of the World Health Organisation and the European Union, is to establish emergency plans to face an unlikely, but not impossible, large scale nuclear accident elsewhere.