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The prime minister’s commitment to “fighting against the burning injustice that if you’re born poor, you will die on average nine years earlier than others”1 is welcome and achievable. As her government has acknowledged,2 half of this difference in life expectancy is due to the higher rates of smoking among the least affluent, so major improvements can …

Background A growing body of knowledge exists to guide efforts to improve the organisation and delivery of health care, most of which is based on work carried out in hospitals. It is uncertain how transferable this knowledge is to primary care. Aim To understand the enablers and constraints to implementing a large-scale quality improvement programme in general practice, designed to improve care for people with chronic obstructive pulmonary disease. Design and setting A qualitative study of 189 general practices in a socioeconomically and ethnically-mixed, urban area in east London, UK. Method Twelve semi-structured interviews were conducted with people leading the programme and 17 in-depth interviews with those participating in it. Participants were local health system leaders, clinicians, and managers. A theoretical framework derived from evidence-based guidance for improvement programmes was used to interpret the findings. A complex improvement intervention took place with social and technical elements including training and mentorship, guidance, analytical tools, and data feedback. Results Practice staff wanted to participate in and learn from well-designed collaborative improvement projects. Nevertheless, there were limitations in the capacities and capabilities of the workforce to undertake systematic improvement, significant problems with access to and the quality of data, and tensions between the narrative-based generalist orientation of many primary care clinicians and the quantitative single-disease orientation that has characterised much of the quality improvement movement to date. Conclusion Improvement guidance derived largely from hospital-based studies is, for the most part, applicable to improvement efforts in primary care settings, although large-scale change in general practice presents some particular challenges. These need to be better understood and addressed if improvement initiatives are to be effective.

Health technology assessment needs to relate to contemporary questions which concern public health-care systems: how to keep people healthy, how to focus on the needs of those with chronic disabilities and integrate care between the hospital and the community, how to encourage and audit effective teamwork, and how to establish a consensus about what is effective and affordable. Clinicians have an ethical responsibility to practice efficiently and economically, for profligacy in the care of one patient may mean that another is treated inadequately. For similar reasons, clinicians need to play a full role in the management of services. Advice from health technology assessment is vital and needs to be accurate, relevant, timely, clear, and accessible. As well as being concerned about what works, we need also to eliminate from practice what does not. Regular audit and appraisal of practice against the evidence base should be useful in this respect. Alternative approaches to management, such as the provision of care as opposed to aggressive treatments, need to be evaluated, and health technology assessment needs to consider how services are delivered, not just specific treatments.

In 1739 Samuel Johnson wrote an essay on the life of Dr Hermann Boerhaave, Professor of Physic at the University of Leiden, who died in 1738. Boerhaave, born 11 years after Harvey's death, could be said to have been influenced by Harvey in that he favoured experimental natural philosophy as the gateway to scientific medicine. He was denied entry into the church because he was accused wrongly of being a follower of the philosopher Baruch Spinoza, regarded as a heretic because he criticised established religious practices; this in spite of strongly supporting the love of God and humanity. Boerhaave decided to become a physician as he was, in Johnson's words, 'equally qualified for a profession, not indeed of equal dignity or importance, but which must undoubtedly claim the second place amongst those which are the greatest benefit to mankind'. It is this claim that I wish to examine. Can we still claim this regard for our profession? Is the medicine we practise, and the way we practise, of the greatest benefit to mankind, and how do we ensure that it is?

BACKGROUND: Nephropathy associated with vesicoureteric reflux (VUR) and urinary tract infection can result in end-stage renal failure, hypertension, or both. Whether long-term VUR contributes to these outcomes is unknown. We compared, in a randomised trial, medical with surgical management of children with bilateral severe VUR and bilateral nephropathy. METHODS: We stratified by age and glomerular filtration rate (GFR) 25 boys and 27 girls aged 1-12 years and randomly assigned them to medical or surgical management. At enrolment and 4 years' follow-up we estimated GFR from the plasma clearance of 51Cr-labelled edetic acid (EDTA), and did intravenous urography. We also did a metastable 99mTc-labelled dimercaptosuccinic acid (DMSA) assay and contrast cystography. The change in GFR at 4 years, expressed as a percentage change between enrolment and 4 years, was available for 26 of 27 patients in the medical and 24 of 25 in the surgical group. We assessed GFR in 48 patients 10 years after enrolment. FINDINGS: Mean GFR at enrolment was 72.4 mL/min per 1.73 m(2) (SD 24.1) in the medical and 71.7 mL/min per 1.73 m(2) (22.6) in the surgical group. The mean percentage change in GFR at 4 years was 2.4% (SE 4.5) versus 4.7% (5.0) in the medical and surgical groups, respectively. The difference in change in GFR at 4 years between the two groups was not significant (7.1%, 95% CI 6.4% to 20.6%). INTERPRETATION: Our data do not lend support to the view that the outcome for renal function is improved by surgical correction of VUR in children with bilateral disease.

This paper emphasises the need for a consistent identifier to be used to share information between agencies for children in the same way as for adults.

We studied 23 children with steroid-sensitive nephrotic syndrome (SSNS), 21 children with steroid-resistant types of nephrotic syndrome and 32 children with other types of nephritis. Our controls were 43 apparently healthy children. We measured the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and the low molecular weight (LMW) protein beta 2-microglobulin (B2M), retinol-binding protein (RBP), alpha 1-microglobulin (A1M) and urine protein 1 (UP1). Results for B2M were considered only for a urine pH greater than 6.0. Comparisons were made with urine albumin excretion, glomerular filtration rate (GFR) and tubular abnormalities in selected renal biopsy samples. We found that abnormalities of LMW protein excretion occurred in between 50% (B2M) and 88% (UP1) of all subjects. In children with SSNS, A1M (r = 0.73), UP1 (r = 0.65) and NAG (r = 0.54) excretion were significantly correlated with albumin excretion, but not RBP or B2M excretion. Increased fractional excretion of A1M, B2M and UP1 and increased plasma A1M were demonstrated in 9 children with SSNS, suggesting competition for tubular reabsorption with albumin, most marked for UP1. In the steroid-resistant nephrotic and nephritic syndromes, correlation with albumin was found for all proteins. In these subjects, RBP (r = 0.37), B2M (r = 0.42) and A1M (r = 0.28) were inversely correlated with GFR, but not UP1, NAG or albumin. We found that RBP excretion was significantly greater in the presence of severe tubular abnormalities in 11 children with recent renal biopsies, but not A1M, UP1 or NAG. We conclude that LMW proteinuria is common in children with glomerular disease, and does not necessarily imply a poor prognosis. Factors other than histologically proven tubular abnormality may account for elevated LMW protein excretion. RBP is the LMW protein most closely associated with structural abnormality and least affected by increasing albuminuria.

Academic Medical Centres (AMCs) translate laboratory research into clinical success. University College London Partnership (UCLP) is further designated to translate proven interventions into populatio

We studied glucose metabolism using the hyperglycemic technique in a cross-section of 23 children (15 pubertal, 8 prepubertal) with stable chronic renal failure as a possible cause of their poor growth. Linear growth was expressed as growth velocity standard deviation score (GVSDS). GVSDS correlated with glucose disposal rate but not with insulin sensitivity index in the pubertal (r = 0.87, P0.001) and prepubertal (r = 0.86, P0.02) children with chronic renal failure. Thirteen children were followed longitudinally during medical suppression of hyperparathyroidism with dietary phosphate restriction and high-dose phosphate binders. Following significant suppression of serum parathyroid hormone (PTH) levels back to the normal range (932 +/- 240 ng/l to 199 +/- 50 ng/l), GVSDS, glucose disposal rate and insulin secretion all increased significantly (p0.01), with no change in insulin sensitivity index and renal function. The changes in GVSDS correlated with the changes in glucose disposal rate (r = 0.86, P0.02) and with the changes in insulin secretion (r = 0.80, P0.01). However, the changes in GVSDS did not correlate with the changes in PTH. The hypothesis that insulin may be more important than PTH in the pathogenesis of growth failure in chronic renal disease deserves further investigation.

The influence of delayed graft function on renal allograft survival has been studied in a review of 322 renal transplants performed at one pediatric institution. The appearance of the first radionuclide renal scan was used to indicate early function in patients receiving their first cadaveric allograft. Patients whose first radionuclide renal scan showed both good renal perfusion and good function (n = 52) were compared with those whose scans demonstrated good perfusion but no function (n = 32). the actuarial graft survival of those with no function was significantly worse (P.05). The difference in graft survival was not solely due to grafts lost in the early posttransplant period. Analysis of serial serum creatinine estimations suggests a process of continued inexorable nephron loss in some patients whose grafts showed a delay in achieving function.

The European Society for Paediatric Nephrology (ESPN) was founded 25 years ago. The progress of paediatric nephrology in Europe since then has been considerable, but we now face a number of problems. The care of the child with kidney disease is often expensive and more needs to be done to examine the cost effectiveness of the management of the child with kidney disease. International co-operation can also foster clinical research to determine the effectiveness of treatment through the institution of controlled trials and outcome studies. Particular problems are posed by the need to integrate the countries of Eastern Europe that have changed from command to market economies over the last year. In many instances there is no shortage of doctors, nurses and hospital beds but there is a need to change administrative and academic structures and to introduce appropriate technology. It is suggested that this may be assisted by twinning units. The integration of Europe requires that the role of the paediatric nephrologist in different countries needs to be examined, and appropriate training to fulfil these responsibilities needs to be agreed. Different countries obviously have different ways of organising and providing services for children with kidney disease. Kidney failure is rare in childhood and there are economic and academic advantages from close collaboration, both with adult nephrology services and with other paediatric specialities. Where it is intended to integrate children's hospitals into large multidisciplinary university hospitals for economic reasons, it is nonetheless necessary to make sure that the requirements of children are properly recognised and the requirements of the European Charter for children in hospital are met.(ABSTRACT TRUNCATED AT 250 WORDS)

Successful management of acute renal failure (ARF) in children, particularly infants, requires knowledge of the functional characteristics of the kidney during development and understanding of the metabolic balance of the growing child. The newborn kidney is immature containing only 17% of its adult cellular complement; at 6 months postnatally cell division is complete and further growth is due to an increase in cell size. Nephron formation is complete before birth but superficial cortical nephrons are not functionally mature; at birth the more mature juxtamedullary nephrons contribute a greater proportion of total glomerular filtration than in the adult. There is a proportional increase in juxtamedullary blood flow but total renal blood flow is low because of the high renal vascular resistance. Glomerular filtration rate (GFR) at birth averages about 20 ml/min/1.73 m2 body surface area but the rapid postnatal increase in renal blood flow is associated with a rapid rise in GFR to 48 ml/min/1.73 m2 at one month and to 80 ml/min/1.73 m2 by 6 months of age (1).

We studied 13 children subjected to elective tonsillectomy, 6 of whom (study patients) received supplemental intravenous isotonic saline during and after operation, and 7 of whom (controls) did not. Clinical and biochemical evidence of hypovolaemia was present in the control but not in the study patients. Plasma antidiuretic hormone (ADH) and urine osmolality were higher in controls (p less than 0.005 and p less than 0.05 respectively). Plasma sodium concentration and osmolality were similar in the two groups. We conclude that hypovolaemia is the principal stimulus to ADH release following surgery and that, in addition to replacement of observed losses of blood and other fluids by fluids of appropriate composition, hypovolaemia should be prevented by the administration of maintenance quantities of isotonic fluid, rather than exacerbated by fluid restriction, in patients in whom oral fluid intake is interrupted for more than a brief period. Hypotonic and sodium free fluids should be avoided because of the risk of hyponatraemia.

Six children (aged 3 years 11 months to 15 years 9 months) with end-stage renal failure and anaemia (mean haemoglobin 7.1 g/dl, range 6.3-7.7 g/dl) on thrice-weekly haemodialysis were treated with recombinant human erythropoietin (rHuEPO), given as an intravenous bolus in an escalating dose regime after dialysis. All responded with an increase in reticulocyte count and haemoglobin concentration in a mean time of 11 weeks (range 9-13 weeks) and at a dose of 100 or 150 units/kg thrice weekly. The dose of rHuEPO was then adjusted to maintain the haemoglobin concentration within the lower half of the normal range for the child's age and sex. The mean haemoglobin after 12 weeks treatment was 10.9 g/dl (range 8.5-12.1 g/dl) and after 24 weeks, 10.5 g/dl (range 7.9-13.3 g/dl). Four children had no further need for blood transfusion and are thus no longer at risk of blood-borne infection, iron overload and sensitisation to HLA histocompatibility antigens. Serum ferritin fell in the three patients with evidence of iron overload; the three with low or normal iron stores at the onset of treatment maintained erythropoiesis with oral iron supplementation. HLA antibodies decreased in all patients. The only serious complication encountered was thrombosis of vascular access in one child. No child became seriously hypertensive or developed cerebral symptoms. The benefits of rHuEPO therapy for children with end-stage renal failure are potentially considerable and with careful monitoring, the risks low.

SOCIETY FLIES BLIND WHEN IT COMES TO HEALTH CARE. The value of treatments to patients, in particular with respect to health gain, is not routinely measured. As a result, reforms focus less on improving health and value to patients and more on cost minimization; consequently, such reforms are led by administrators, not physicians. Physicians are disgruntled and disenfranchised, and perversities result such as, in the United States, cost shifting and other forms of dysfunctional competition. The way forward is for physicians to seize the initiative, take as their goal improved value of care to patients, organize medical practice around medical conditions and care cycles, and measure riskadjusted outcomes and costs, all within a competitive health system. Positive-sum competition for value to patients will result that only physicians can deliver. Tinkering with financial incentives in the system will never be enough. In a reduced form, this is the main argument advanced by Porter and Teisberg for reforming and improving the US health care system. However, there are important similarities in England’s National Health Service (NHS). While reducing overall cost growth is not a problem due to the (relatively) large real-term increases in the global fixed budget over the last 7 years, health reforms in England have been in the main led by politicians and implemented by managers, with the physician community largely on the sidelines, antagonized or marginalized. Measuring risk-adjusted clinical outcomes is not widely implemented, prompted by public outrage (for example, following well-publicized failures in cardiac surgery) as much as by professional leadership. The financial bottom line, rather than health gain, tends to drive local reconfigurations in service. To improve the health care system, physicians should take a firm lead: a large portion of the activities most likely to have an impact on improving outcomes and quality are embedded in the care setting provided by physicians interacting directly with patients. However, it is unlikely that physicians will rise to the leadership needed, at least in the NHS, and some of the “false solutions” rejected by Porter and Teisberg are necessary and worthwhile candidates for future reforms. In this Commentary, we explain why, and describe how some of these “false solutions” are being used to reform the NHS to achieve better value for patients.

THE RECURRENCE OF SEVERE ACUTE RESPIRATORY SYNdrome (SARS) in China during 2004 has highlighted the continuing threat to human health from infectious disease outbreaks. A zoonosis caused by a novel coronavirus, SARS first emerged among humans in the southern Chinese province of Guangdong during November 2002. By March 2003, SARS had spread to neighboring Hong Kong and from there to Toronto, Ontario, and many other areas in a matter of days. The World Health Organization (WHO) has reported that by July 2003 when the epidemic had waned, in Hong Kong there were 1755 probable cases of SARS with 300 deaths (17%) and in Canada there were 251 probable cases with 43 deaths (17%). Most Canadian cases and all deaths were in the Toronto area. Both areas had serious difficulties managing the outbreak, and several inquiries into public health and epidemic management have since been performed. We led the panels that first reported on SARS and public health in each jurisdiction. Both panels worked through the summer of 2003 and issued their reports within a week of one another in early October 2003. Herein, we compare our findings, highlight common conclusions, and suggest some general lessons that may be applicable to other areas.

Information about a patient's health is recorded in order to provide for that patient's care. Most patients will not think about the other uses for their data and many assume that the information they provide will go no further than the health care professionals who have been caring for them. Information collected about patients is essential for developments in our understanding of health and health care. Most patients will be happy to allow their data to be used for these purposes, once this has been explained. Health care professionals have an obligation to ensure that patients know when identifiable data about them are to be used and to get their agreement about making disclosures. We know that this is not easily achieved; doctors, nurses and others providing care are already over-stretched. Patients may be anxious about their condition and treatment. They may not, for a variety of reasons, read leaflets or letters sent or given to them. This does not mean our obligations to respect patients by keeping them informed and seeking their agreement can be ignored. Openness about how health care professionals work and partnership with patients are essential to the continued trust of the public in the professions. The challenge is not to answer the question whether we need consent but rather how we can best obtain it.

At present, NHS managers are highly constrained, suffering excessive regulation and central control. More autonomy for trusts would mean fewer directives and less performance management. Giving trusts a new organisational form, such as a public interest company or foundation hospital, might be reinvigorating and would not involve further reorganisation. These new freedoms should be accompanied by new accountabilities, not solely to politicians but to independent NHS regulators, local communities and patients. Devolved power and greater patient choice could produce a more responsive NHS. Its potential needs to be explored through experimentation and evaluation.

Red cell morphology was examined by light microscopy in 122 urine specimens from 99 patients with haematuria in an attempt to define the site of origin. Altogether 84% of glomerular bleeding and 91% of non-glomerular bleeding was correctly assigned according to diagnoses determined by renal biopsy in 51 patients and clinically in 48. The test should be interpreted with caution as both false positive and false negative results were observed, some in the same individual with unchanged pathology at different times. No advantage of phase contrast over bright field microscopy was apparent even when examining uncentrifuged urines.

Eleven boys, mean age 15.3 years (range 13.2-17.5), with pubertal delay in association with steroid therapy for steroid-sensitive nephrotic syndrome and following renal transplantation were treated with oxandrolone 2.5 mg daily for a mean of 0.50 years (range 0.34-0.61). Mean growth velocity increased from 3.9 cm/year (range 1.1-6.3) to 6.1 cm/year (range 2.0-14.4) and was maintained at 6.1 cm/year (range 0.4-10.2) (P less than 0.05). However, there was no significant difference in growth between the treated boys and age- and puberty-matched controls. Elevation of blood cyclosporin A and creatinine levels occurred in the transplant patients. Oxandrolone may initiate a pubertal growth spurt in patients taking steroid therapy for renal disease, but should be used with extreme caution because of potential side-effects.

This paper summarises a symposium concerned with the provision of care for children with kidney disease in developing countries. Better organisation of services is required to prevent waste of resources, with the emphasis on team work between professionals, shared care with local health care personnel remote from the paediatric nephrology unit and good communications. Families need to be educated and provided with appropriate information so that they can care for their child at home. Technology should be simple and robust and the staff using it should be fully trained to maintain it in use. Therapies should be definitive where possible, because long-term supervision of treatment is often difficult. Effective but inexpensive medications should be used where possible. Twinning of developing and richer countries is valuable to transfer technology, help with training and assist in care through the development of personal contacts.

We studied 40 children with a history of vesicoureteric reflux (VUR) without evidence of renal scarring, 93 children with a history of VUR and renal scarring and 10 children with previous urinary tract infections in whom the urinary tract was radiologically normal. Urine retinol-binding protein (RBP), albumin and N-acetyl-beta-D-glucosaminidase (NAG) were measured in each child. All were free from infection at the time of the analysis. Urinary RBP and NAG levels were significantly elevated (P0.001) in the group of children with renal scarring. Elevated RBP levels were detected in 51% of children with bilateral renal scarring compared with 7% of children with unilateral scarring. Urine RBP excretion increased progressively according to the type of scarring, best determined by the type of scarring of the less affected kidney. In children with renal scarring, elevated NAG levels were seen mostly in the 65 children with bilateral scarring and severe reflux. Urine albumin excretion was elevated in 10 children, 9 with bilateral scarring, all of whom had elevated RBP excretion. Urine protein excretion was unaffected by the presence or absence of persisting VUR. There was a strong negative correlation between glomerular filtration rate and RBP excretion (r = -0.69). We conclude that evidence of tubular dysfunction is common in children with bilateral renal scarring and usually precedes any glomerular protein leak. Tubular dysfunction may be the consequence of relative nephron hyperperfusion in the presence of bilateral scarring.

Recent reforms to the NHS in England seem to make integration of care harder rather than easier. But Chris Ham, Jennifer Dixon, and Cyril Chantler argue that integration is not incompatible with competition and that it is essential for more efficient care

Although red cell morphology has been used to localise the site of haematuria in the urinary tract, the cause of red cell deformity is still speculative. We have conducted experiments in vitro using venous red cells which indicate that hypochromia depends mainly upon sodium concentration and occurs when this falls below 75 mmol/l. We simulated the passage of red cells through the renal tubule by sequentially treating them with fluids of composition similar to those in different tubular segments, and produced anisocytosis and hypochromia but not the typical "bizarre deformity"--the hallmark of glomerular haematuria. We conclude that dual injury is required to produce the "typical" dysmorphic red cells in glomerular haematuria. First, mechanical damage caused by passage of red blood cells through the glomerular basement membrane followed by a second, osmotic, injury sustained by red cells during passage through the hypotonic tubular segment.

A study of long-term outcome of 78 subjects who had had Henoch-Schonlein nephritis during childhood (at a mean of 23.4 years after onset) shows that severity of clinical presentation and initial findings on renal biopsy correlate well with outcome but have poor predictive value in individuals. 44% of patients who had nephritic, nephrotic, or nephritic/nephrotic syndromes at onset have hypertension or impaired renal function, whereas 82% of those who presented with haematuria (with or without proteinuria) are normal. 17 patients deteriorated clinically from an initial assessment in 1971; 7 of these had apparently completely recovered in 1976. 16 of 44 full-term pregnancies were complicated by proteinuria and/or hypertension, even in the absence of active renal disease. These findings indicate that childhood Henoch-Schonlein nephritis requires long-term follow-up, especially during pregnancy.

Diurnal variation in leucocyte cystine and the effects of equimolar single doses of oral phosphocysteamine and rectal cysteamine were studied in eight patients with cystinosis, aged 1.8-16.5 years. No significant diurnal variation in leucocyte cystine was found. Absorption of cysteamine was reduced after rectal administration compared with the oral dose: mean (SD) peak concentration 17.2 (6.3) mumol/l v 36.4 (5.5) mumol/l at 40 min and mean (SD) area under the curve 22.3 (14.3) v 59.4 (33.1) mumol/h/l. Oral phosphocysteamine significantly reduced the mean (SD) leucocyte cystine from 8.09 (0.47) to 3.26 (1.48) nmol 1/2 cystine/mg protein at three hours. At 12 hours the mean leucocyte cystine was significantly lower than the pretreatment concentration. Rectal cysteamine did not significantly reduce the mean leucocyte cystine concentration. In conclusion, phosphocysteamine suspension may be administered every 12 hours. Rectal cysteamine administration is feasible but higher doses are required before efficacy can be judged.

Long-term steroid therapy has a depressant effect on hypothalamo-pituitary pulsatile secretion of growth hormone (GH), and this results in an attenuated pubertal growth spurt. Oxandrolone and recombinant human GH improve growth rates in children taking long-term steroid therapy for renal disease, but there are potential side effects. Treatment with recombinant human erythropoietin improved the growth of three prepubertal, but not three pubertal haemodialysis patients.

We have reported the syndrome of FJGN in numerous kindreds as well as isolated young subjects of either sex (reviewed in 1). The latter have generally had a strong family history of gout and sometimes renal disease. Subsequent investigations have invariably revealed FJGN in other seemingly healthy family members. The hallmark of the disorder has been a grossly reduced fractional uric acid clearance [FEur] for the young age, sex and renal function, as discussed elswhere in this Symposium (Cameron).

Enzyme-linked immunosorbent assays (ELISA) have been developed for the measurement of beta 2-microglobulin (B2M), retinol-binding protein (RBP), alpha 1-microglobulin (A1M) and urine protein 1 (UP1) in children. Results from random urine samples in 43 children (31 for B2M) are, when corrected for urine creatinine (geometric mean (range)): B2M 9.8 (6.0-40.7) micrograms/mmol, RBP 8.1 (less than 1-24.5) micrograms/mmol, A1M 0.4 (0.1-2.2) mg/mmol and UP1 17.8 (less than 2-309.4) micrograms/mmol. Fractional excretions (FE) in 23 children (14 for B2M) are (geometric mean (range)): FEB2M 0.04% (0.02-0.10%) and FEUP1 0.10% (0.01-1.21%). Results in overnight urine collections are also presented. Our results extend existing data for normal ranges in adults to include children and provide data on UP1 concentrations.

In 1902, Guthrie described an English family in which 12 of 15 members from two generations had “idiopathic” hematuria. He reported that in every affected individual the hematuria increased intermittently, usually in association with fever, malaise, headaches, backaches and pains in the legs. Precipitating factors included infections (often of the upper respiratory tract) and exposure to extremes of temperature. Urinalysis also revealed proteinuria in most cases

This is not a happy Christmas for our profession or indeed for many doctors. Doctors work extremely long hours under difficult conditions and many are demoralised by lack of resources and constant criticism. We feel proud of the advances in medical science and find it difficult to understand when patients complain because our efforts are not always effective. Much of the recent poor publicity has originated from the reporting of cases before the General Medical Council. It is ironic that these demonstrations of self regulation should lead to criticism of the system of self regulation by both the public and politicians. Now the government is introducing legislation to ensure the quality of clinical services and to make the profession more accountable. Last year Professor Roy Porter published a history of medicine entitled The Greatest Benefit to Mankind, which was Samuel Johnson's accolade to the medical profession.1 Porter points out that we are healthier than ever before yet more distrustful of doctors and the “medical system.” As he writes, such ambiguity is not new, but we need to attempt to understand it. Much of medicine and medical practice has changed during the past generation. Modern medicine is complicated and often uncertain. For example, babies born at less than 28 weeks' gestation are now routinely ventilated and, though more survive, around a quarter of those who do have disabilities and 10% are severely handicapped.2 Given that about 1% of pregnancies result in premature delivery are we sure that parents are fully informed of …

Demand for complementary and alternative medicine is high despite limited evidence. Linda Franck and colleagues believe that a thorough review by NICE would benefit the NHS and patients, but David Colquhoun argues that it cannot afford to re-examine evidence that has shown little benefit

EDITOR—In 2000 we attended a meeting to discuss how to improve healthcare delivery within the NHS.1 One of the recommendations was that patients, except in special circumstances, should receive copies of all letters, case summaries, or care plans written by doctors or other clinicians. We also suggested that with the patient's approval such material should be stored on a central server. The suggestion was accepted and …