Letters

In reply: We thank Jureidini and Tonkin for their comments. In relation to their criticism of the study by Emslie et al,1 intention-to-treat analysis is the accepted standard. In relation to the study by Keller et al,2 their criticism about the criteria for response has already been answered elsewhere. (Criteria were defined in the report as a final Hamilton Rating Scale for Depression [HAM-D] score that was ≤ 8 or a reduction from baseline of ≥ 50%. Dual criteria were selected because the scores at entry could range from a minimum of 12 [set by protocol] to a maximum of 53 [highest scores for the 17-item HAM-D]. Limiting response to either a 50% reduction or a specified cut-off point would impede patients at the lower end of the ranges from meeting the criterion.3) The concern about the absence of differences in change scores on the HAM-D cannot be resolved, as mean change in scores and standard errors of the means were not reported. However, 63.3% (57/90) of subjects taking paroxetine (P = 0.02 versus placebo) achieved a HAM-D total score of ≤ 8 at endpoint. With respect to the size of difference in response rate to active treatment versus placebo, the results of trials involving selective serotonin reuptake inhibitors (SSRIs) in children and adolescents are similar to those reported in adults (ie, SSRIs achieve a response in about 20% more participants than placebo,4 which is similar to the 26% difference between cognitive behavioural therapy and various control conditions5). Consistent with these results, the US Food and Drug Administration has recently approved fluoxetine to treat children and adolescents aged seven to 17 years for major depression. We believe that there are sufficient new treatment data (including a study,6 published since the submission of our article, showing fluoxetine's superiority over placebo in symptom improvement and in remission rates) to warrant revision of the 1997 guidelines. Depression affects one in 20 Australian teenagers, few of whom will access specialist mental health services.7 Contrary to the view of Jureidini and Tonkin, we believe general practitioners must provide treatment for young people suffering depression. A strength of the National Health and Medical Research Council guidelines is that they offer comprehensive advice to promote thoughtful assessment and management of depression in young people.

Raphael TW Chan · Joseph M Rey · Philip L Hazell

To the Editor: I do not believe that Dinnen's comments1 should be so easily dismissed as suggested by the academics proposing that general practitioners should do questionnaires,2,3 at least in New South Wales. I write this as barely a month has passed since a most damning report was released by a NSW Parliamentary Inquiry into Mental Health Delivery. A prime example of arrogance and loss of contact with the reality of clinical services by academia and administration is that, during the demise of mental health services in NSW, the services have been forced to complete a new 30-page admission process for every admission. Just what was needed by registrars spending hours trying to find beds for seriously mentally ill patients! The gulf between academia and administration on the one hand and real clinical services on the other is now huge in NSW, at least in mental health services. No one outside real clinical services has any credibility or right to demand doctors, let alone hard-pressed GPs, engage in dubious and very likely useless research projects without very special funding to support the project. I found the K10 questionnaire extraordinarily simplistic compared with a Mental State Examination (MSE). Surely, if there is concern, doctors should be encouraged to revise how the MSE is carried out, and not encouraged to adopt "cookbook" medicine.

Brian M Boettcher

To the Editor: As a general practitioner I was gratified to see Dinnen's letter1 in which he questioned the "urgent need" for GPs to use more questionnaires for depression management. Reading the professorial reply,2 I despair. As more and more specific health promotions are introduced (eg, Asthma 3-Step Plans, Diabetic Care protocols, Health Assessments, Care Plans) we have to consider not just our patient's problems, but which forms to fill out or numbers to put down to fulfil Health Insurance Commission requirements or be correctly remunerated. By the time a depressed patient is sitting in my room, he or she wants to be correctly diagnosed and treated, not to be given a form to fill out. In my opinion, to hand a form to a depressed patient who has tearfully told me his or her problems is an insult. We do not (yet) expect patients to fill out a checklist for heart failure. As to the suggestion that the form be filled out in the waiting room, how is this to be done? Should the patient be sent out again with form in hand? Privacy concerns do not allow reception staff to hand out such forms, and the waiting room is not the best place to fill them out if they are needed. In reality, the GP is likely to give the patient a form and then go have a coffee or make a telephone call. No psychiatrist will ever receive a referral from me based on a K10 score. I may, however, mention that my patient still has suicidal impulses, cries a lot, has trouble sleeping and cannot concentrate at work. That should be easy enough for anyone to understand.

Heidi Andersen-Dalheim

To the Editor: I read with great interest about your search in dictionaries for the word "pathography".1 Pathography2 originates from reflections on genius and its possible association with insanity, a question that has occupied experts in many fields since Socrates, Plato and Aristotle. The first psychiatric scientific treatise concerning this question was contributed by Moreau de Tours in 1859.3 Inspired by him, Cesare Lombroso, in 1863, coined the famous expression genio et follia, and contributed many, albeit somewhat uncritical, pathographies. The term pathography was first used about 1899 by the German psychiatrist Paul Julius Möbius, who contributed with several seminal pathographies, including Rousseau, Goethe, Schopenhauer and Nietzsche. Among other famous pathographers should be mentioned Freud, W Lange, Jaspers, Birnbaum and Kretschmer. Pathography can be defined4 as . . . historical biography from a medical, psychological and psychiatric viewpoint. It analyses a single individual's biological heredity, development, personality, life history, and mental and physical pathology, within the socio-cultural context of his/her time, in order to evaluate the impact of these factors upon his/her decision-making, performance and achievements. No preconceived format can be assumed as the method depends on the nature of the various available materials and on the specific inquiry. A prerequisite for plausible pathographical results is a thorough knowledge and understanding of psychopathology, and of the borderland between normal and abnormal mental life, combined with a capacity for [sober] historical judgement. . . . The pathographical method is applicable to any personality, sick or sound, provided that sufficient biographical sources are available. The pathographical result is a facet but often an indispensable one. Subjects of pathography have traditionally been famous people in all areas of human achievement. Pathography is also indispensable in assisting historians, political scientists and other groups in their quest for a better understanding of events where leaders or other "very important persons" have played a significant role, and where personality or illness, physical or mental, has been decisive, at times with far-reaching consequences for nations.5,6 History is replete with such examples.

Johan A Schioldann

To the Editor: In the abstract of his article on asthma prevention with dietary manipulation,1 Mellis states that "we know" that the major modifiable dietary environmental risk factors for childhood asthma are not having been breastfed and low intake of omega-3 fatty acids. In his discussion of the evidence, Mellis suggests that breastfeeding may be protective and, importantly, acknowledges the controversy. He further states (in the abstract) that observational studies have shown a reduction in childhood asthma in children who eat fish regularly (that is, have a high intake of omega-3 fatty acids), similar to those who were exclusively breastfed for three months. However, he provides no references for these observational studies, and nor does he discuss any specific evidence in support of including omega-3 fatty acids for reducing childhood asthma. While there are some suggestions of such an association, the evidence is extremely limited compared with the extensive literature on the potential for the protective effect of breastfeeding. Further, there are substantial methodological issues associated with the few studies that do exist, not the least of which is the measurement of the relevant dietary parameters. Australian studies have suggested a protective influence of at least two fish meals per week on bronchial hyperresponsiveness in 7–11-year olds2 and of eating oily fish3 on the prevalence of childhood asthma. However, neither of these studies had the capacity to measure omega-3 fatty acid nor fish intake in a valid way. These limitations were acknowledged by the authors of the studies, and have been noted by others;4 they need to be included in any discussion of a putative protective effect. It should also be noted that the biological plausibility of such an association has been challenged.4 There are many valid reasons for promoting the consumption of omega-3 fatty acids, but shouldn't we wait for the outcome of the randomised clinical trial currently under way before accepting the statement that "we know" that a low intake of these fatty acids increases the risk of childhood asthma?

Jill L Sherriff

In reply: Sherriff is correct in pointing out that the studies showing protection from bronchial asthma (and bronchial hyperresponsiveness) are based on consumption of fish meals rather than a direct measure of omega-3 fatty acid intake. This protection has been observed consistently in cross-sectional studies of New South Wales primary school children. Thus, the level of evidence is at best Level III, albeit using a proxy for omega-3 fatty acid intake. Results of a randomised-controlled trial of omega-3 fatty acid supplementation currently under way in western Sydney are now in the public arena at 18-month follow-up.1,2 At this early stage, it is uncertain who has genuine asthma rather than other wheezing syndromes. Nevertheless, the group who received omega-3 fatty acid supplementation have differences in rates of wheeze compared with those not supplemented.1,2 For example, the rate of "ever" having had wheeze was 52.6% in the controls versus 42.8% in the supplemented group (absolute risk reduction, 9.8%; number need to treat, about 10). In the table of recommendations in my article,3 I carefully pointed out that supplementing infants with omega-3 fatty acid is something to "consider" rather than strongly recommending it. It should also be noted the level of evidence is low (Level III). Stronger recommendations will depend on the long-term results of randomised trials, such as the western Sydney trial.1,2 In summary, at this stage the only strong dietary recommendations which can be made are: not to use strict elimination diets during pregnancy (Level I evidence); and to consider using lactobacillus probiotic supplements. The evidence for lactobacillus is Level II (from a single randomised controlled trial), although the protection shown is for atopy rather than asthma. Clearly, the children in the lactobacillus study will need further follow-up, and the trial will need to be repeated in other populations. All of this highlights the need for better-quality studies in the area of primary prevention of asthma, based on dietary factors during pregnancy or early infancy.

Craig M Mellis

To the Editor: The publication of the main results of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), and the accompanying editorial, triumph the role of thiazide diuretics as first-line management for hypertension.1,2 It brought to mind the lines from the nursery rhyme Old Mother Hubbard — "And when she went there, the cupboard was bare." Simple frequency analysis of diuretic antihypertensive medications listed in the Australian Medicines Handbook (1998 and 2003) revealed that the total number of thiazide diuretics available as monotherapy in 1998 was six (bendrofluazide chlorothiazide, chlorthalidone, hydrochlorothiazide, methyclothiazide and indapamide), and in 2003 three (bendrofluazide, chlorthalidone and indapamide).3,4

Mark R Nelson

To the Editor: It has been known for a long time that washing soda (crystalline sodium carbonate) is effective for removing fluid from joint effusions. The crystals are simply wrapped in a tea towel, crushed with a rolling pin and wrapped around the joint overnight. In the morning the sodium carbonate is rock solid and the joint effusion has markedly improved. I was discussing with one my patients her problem of gross upper-limb lymphoedema after surgery and radiotherapy for breast cancer to the axilla. She went home and made an appropriate pack of sodium carbonate, which she wears overnight. She can now use her arm throughout the day. Obviously, the lymph fluid reaccumulates because her lymphatic system is well and truly obstructed. This patient spoke to several other patients in the Day Centre at the Monash Medical Centre, who tried this in addition to other exercises for lymphoedema, and they have found it to be extraordinarily effective. One woman had gross oedema of her hand, which rendered it useless: she simply immersed her hand in a solution of sodium carbonate and thus dialysed the fluid from her hand. Thereafter she could use her hand for 12 hours before significant amounts of fluid reaccumulated. While this is obviously not the perfect solution to lymphoedema in patients with breast cancer, anything that may help them is worth noting. Perhaps a suitable linen device could be made which would cover the whole arm at night. Evidence for the use of this simple dialysis treatment is currently anecdotal. It might be appropriate to design a clinical trial to determine whether this method has potential in treating this extremely troublesome form of lymphoedema.

Graeme N Brodie

To the Editor: Although liver flukes (genus, Fasciola) are parasites of livestock, human infection is a significant global health problem,1 albeit seldom seen in Australia.2 Infected livestock contaminate waterways with parasite eggs, leading to infection of snails that shed metacercariae on to vegetation, such as watercress.1,3,4 Adult parasites reside in and damage the bile ducts.1,3 Liver flukes could cause disease if introduced into the food chain.1 We report the first case in Australia of liver fluke infection (fasciolosis) in a patient with no history of farm or livestock contact. She probably acquired the disease from eating watercress purchased at a Melbourne market four to five months before symptom onset. Computed tomography of the liver in a woman with fasciolosis Low density lesions (arrowed) following intrahepatic ductal branches in the right lobe of the liver were consistent with Fasciola parasites causing biliary obstruction. A 35-year-old woman presented in August 1998 with fever and right upper quadrant abdominal pain. Blood examination showed eosinophilia (2.5 x 109/L; reference range [RR], < 0.6 x 109/L]). Liver function tests gave normal results apart from elevated serum aspartate aminotransferase levels of 48 U/L (RR < 41 U/L). Abdominal computed tomography showed multiple low density lesions in the right lobe of the liver, with diameter up to 3 cm (Box). A fine needle aspirate showed no evidence of malignancy. Blood tests four weeks later revealed increasing eosinophilia (3.5 x 109/L) and worsening liver function (serum levels: alanine aminotransferase, 163 U/L [RR, 7–56 U/L]; alkaline phosphatase, 126 U/L [RR, 30–120 U/L]; γ-glutamyl transferase, 98 U/L [RR, 5–45 U/L]). A parasitic infection was suspected, but four faecal samples and serological tests for hydatids, Schistosoma, Strongyloides and Entamoeba spp. were negative. Coprological diagnosis of fasciolosis can be problematic, as eggs may be released intermittently and in small numbers, especially in low-intensity infection.1 Enzyme-linked immunosorbent assay (ELISA) using Fasciola hepatica antigen, performed at Westmead Hospital, Sydney, was borderline positive. However, ELISA for IgG4 antibodies against recombinant F. hepatica cathepsin L5 antigen, performed at Monash University, Melbourne, was strongly positive. The patient was treated with two doses of triclabendazole (12 mg/kg body weight per dose) on successive days in October 1998. Abdominal pain subsided within two weeks, her appetite was restored, and eosinophil count and liver function normalised within four weeks. Computed tomography two months after treatment showed a reduction in size of the liver lesions. The patient remained well six months later. This case demonstrates that fasciolosis may present to urban medical practitioners in Australia. Ingestion of watercress is an important clue to the aetiology.2 Serological diagnosis is possible before eggs appear in faeces using a new specific ELISA test that detects the IgG4 response to cathepsin L antigen.5

Andrew J Hughes · Terry W Spithill · Rebecca E Smith · Craig S Boutlis · Paul DR Johnson

To the Editor: Collins and colleagues1 reported a case of bacteraemic community-acquired MRSA (CAMRSA) infection that they believed to be the first reported in Australia. One of us (G N) published a reference to a case of septicaemia and osteomyelitis in Brisbane caused by CAMRSA in 2000.2 This severe case occurred in a previously healthy 16-year-old boy with no risk factors for MRSA infection who, after prolonged ventilatory and inotropic support and vancomycin therapy, required a long period of rehabilitation. A further two cases of septicaemia occurred in Ipswich and will soon be published as part of a study of CAMRSA conducted in 2000–2001.3 We recently encountered another case involving a previously well 23-year-old man who presented to the emergency department with a large abscess on his upper lip and extensive cellulitis of the surrounding face and neck, and with left-sided pleuritic chest pain and associated fevers and rigors. The patient denied previous antibiotic use or contact with healthcare facilities at any time in the past. There was no history of injecting drug use or trauma. Staphylococcus aureus was isolated from blood cultures, and resistance to oxacillin and susceptibility to erythromycin, clindamycin, tetracycline, gentamicin, ciprofloxacin, fusidic acid, rifampicin, and vancomycin was shown. Specimens from operative debridement of the facial abscess yielded S. aureus with the same susceptibility pattern. Chest x-rays showed extensive consolidation of the left lower lobe and an associated loculated pleural effusion. Clinical, radiological, and echocardiographic evaluations did not reveal another focus of infection. The patient was treated with intravenous vancomycin for three weeks followed by oral clindamycin, with complete clinical resolution. It is now clear that CAMRSA infection may result in severe, life-threatening sepsis. The possibility of pneumonia associated with CAMRSA is of particular concern. A 1999 report from Minnesota and North Dakota documented four deaths in children from CAMRSA, including two with necrotising pneumonia.4 A further two fatal cases of necrotising pneumonia caused by CAMRSA were recently reported from France.5 The strains involved in all of these cases carry the gene for Panton-Valentine (P-V) leukocidin, a staphylococcal toxin that has been shown to be strongly associated with cases of severe superficial abscesses and necrotising pneumonia.6 As the strain of CAMRSA most commonly encountered in Eastern Australia also carries the P-V leukocidin gene (Professor J Etienne, Faculty of Medicine, Claude Bernard Lyon 1 University, personal communication), doctors should be aware of the possibility of severe community-acquired pneumonia caused by this organism.

Graeme R Nimmo · E Geoffrey Playford

To the Editor: Kuchar et al1 describe a patient who received an implantable defibrillator discharge after a single ingestion of loratadine. We are concerned that their conclusion — that this patient "probably" had drug-induced torsade de pointes — is incorrect. Review of the intracardiac electrograms from this patient (shown in Box 2 of their article) with known monomorphic ventricular tachycardia (VT; shown in their Box 1) shows a relatively fixed rate of the VT without the large variations in cycle length consistent with torsade de pointes. While there are no established guidelines for determining torsade de pointes based on intracardiac electrograms, it is clear that during monomorphic VT electrocardiograms can show variability in amplitude and orientation. Consistent with the early stages of monomorphic VT,2 the first three electrograms have a different orientation compared with the remaining electrograms, which are largely similar. Unfortunately, as the transition from supraventricular rhythm to tachycardia was not shown, it cannot be ascertained whether the tachycardia began with a pause-dependent mechanism, an important criterion to help diagnose torsade de pointes.3 Given that this patient's implantable defibrillator intracardiac electrograms do not show a continually changing electrogram pattern, that the cycle length is relatively constant, and that there is a lack of documented QT prolongation, there is no evidence of the patient's arrhythmia being torsade de pointes. Incidentally, it is unclear whether these electrograms were recorded before (as specified in the discussion) or after defibrillator discharge (title of Box 2). It is well documented that a defibrillator discharge can have significant effects on the recording of intraventricular electrograms. Most likely, this patient, with documented pre-existing monomorphic VT (their Box 1[b]), had an episode of VT (not torsade de pointes) appropriately treated by the implanted defibrillator, probably having no direct relationship with loratadine. Notably, their Box 3 shows torsade de pointes in another patient, not receiving loratadine. In summary, Kuchar et al1 correctly state that there have been no documented episodes of torsade de pointes after ingestion of loratadine. Similarly, their report does not appear to document an episode of torsade de pointes.

Philip T Sager · Enrico P Veltri

In reply: We agree that there are no guidelines defining torsade de pointes based on intracardiac electrograms, but there are several reasons why the likelihood of torsade de pointes (as opposed to any other arrhythmia) in our patient is high. The electrogram shows the arrhythmia just before delivery of direct current shock, this being about 30 minutes after the patient took her first ever dose of loratadine. There are marked variations in electrogram morphology, despite minimal variation in RR interval, in a short strip of recording in this patient with documented QT prolongation. Further, she had no history of monomorphic ventricular tachycardia, no inducible monomorphic ventricular tachycardia at electrophysiologic examination, and no evidence of structural heart disease. Neither was a mechanism for supraventricular arrhythmia identified. The absence of initiating beats showing pause-dependence is unfortunate, but this is not provided by the generation of device implanted in this patient. Hence, we believe the word "probable" is an apt description for the observation made.

Dennis L Kuchar · Bruce D Walker · Charles W Thorburn

To the Editor: We welcome Ring and Brown's editorial comment1 on the Public Report Card 2002 No More Excuses,2 produced by the Australian Medical Association's Task Force on Indigenous Health. We hope that drawing attention to the poor outcomes of Indigenous Australians will catalyse Federal and State governments to take action, particularly as international comparisons demonstrate the likelihood of success. Australia's poor performance in relation to its Indigenous people is a complex phenomenon, involving political, sociocultural and historical factors, as well as health factors. Levels of ill health among Indigenous communities in post-colonial Australia, Canada and New Zealand are particularly disturbing from a global health perspective, as they persist despite the relative affluence and excellent health status enjoyed by the general population in these nations. One of the difficulties in assessing progress is the lack of high-quality data for comparative purposes. The types of indicators of Indigenous health in common use in Australia, Canada and New Zealand range from central indicators (such as the age-standardised rate ratios for Aboriginal people) to secondary indicators (such as change in the prevalence and incidence of chronic diseases, like diabetes, in Aboriginal communities). It would be useful to develop additional indicators that more closely reflect Aboriginal community knowledge models and values.3 Existing indicators emphasise outcomes rather than opportunities for early intervention, such as early childhood development and youth resilience. Finally, there need to be greater attempts to explore how to use and compare international experiences to help Indigenous people most effectively. The Memorandum of Understanding between the Canadian Institutes of Health Research, the Medical Research Council of Australia, and the Health Research Council of New Zealand may provide a framework for international collaboration.4

Paul Bauert · Elizabeth McMaugh · Carmel M Martin · Janet K Smylie

To the Editor: Our recent study of patients' priorities for asthma care1,2 provides additional evidence supporting the concerns of Wilson and Robertson in their editorial questioning the possible overuse of inhaled corticosteroids.3 We have reported a qualitative study of 62 individuals who presented to an emergency department at either a central city, suburban or rural hospital, in which we explored individuals' perceptions about their asthma, its care and the impact of asthma on their lives.1,2 We also asked participants to complete a questionnaire on the use of medications and sought to amplify this information by further probing the use of medications in our qualitative data collection. Of the 82% of participants in our study currently using inhaled corticosteroid medication (51), 30% (16) were taking 1000 μg of fluticasone or equivalent daily and another 19% (10) were taking more than 1500 μg or equivalent. Current product information for fluticasone suggests a maximum dose of 1000 μg twice daily, whereas National Asthma Council (NACA) guidelines recommend that 500 μg fluticasone or equivalent daily may be the upper limit of useful effect.4,5 We also asked patients how long their medication lasted. Eleven (18%) stated that inhaled corticosteroid devices lasted three weeks or less. Use above recommended doses did not only occur for inhaled corticosteroids, but also for symptom controller medications. Twenty-four (35%) of the 31 (50%) patients receiving this medication reported that a device lasted three weeks or less, indicating use above usual recommended doses. Most patients in our study voiced concerns about the cost of asthma and drug side effects; some adjusted their medication use to manage these issues.1 In such individuals, high use or overuse of preventive and controller medication would increase both costs and side effects, partly explaining these patients' concerns. Doctors may be overprescribing inhaled corticosteroid medication because there is a discrepancy between dosages recorded in published drug information and newer recommendations for optimal inhaled corticosteroid dose.4,5 Our findings show that, in some patients, the risks associated with the use of inhaled corticosteroids are likely to be compounded by using them at higher doses than those recommended. Doctors need to be aware of this in managing patients with asthma who have severe symptoms, in whom overuse, rather than underuse, is likely to be a problem.

Dianne P Goeman · Susan M Sawyer · Michael J Abramson · Kay Stewart · Francis C K Thien · Rosalie A Aroni · Jo A Douglass

To the Editor: Halasz and Vance1 are correct to point out that there is a diversity of causes that can contribute to a child exhibiting symptoms of attention-deficit hyperactivity disorder (ADHD), as defined in the Diagnostic and statistical manual of mental disorders (DSM-IV).2 In their article, they describe a child who meets the DSM-IV criteria for diagnosis of ADHD and in addition has been affected by environmental factors including poor bonding (due to maternal depression), domestic violence and parental separation. The child also exhibits developmental disability, as exemplified by delayed language development. The message is that, by explaining his symptoms in terms of his early experiences and his developmental disability, a diagnosis of ADHD can be excluded. Children with ADHD frequently come from families with disharmonious parental relationships. This may be associated with ADHD in one of the parents, perhaps the violent father in the case described. As clinicians our aim is to ameliorate symptoms as promptly and effectively as possible, and I am frequently impressed by the dramatic improvement that stimulant medication can make to a child's functioning both at school and within the family, with follow-on improvements in mood and self-esteem. Behavioural interventions and family therapy are important adjuncts to medication, but families such as the one described can be difficult to work with and this can limit the effectiveness of such interventions. A carefully monitored one-month trial of stimulant medication, with behavioural rating scales completed by the class teacher, may be appropriate in cases such as the one described. On the other hand, to deny a child a trial of stimulant medication on the basis of adverse early experiences and developmental disability may be to keep from the child the treatment that would help most.

Alison Poulton

In reply: We believe the core symptoms of attention-deficit hyperactivity disorder (ADHD) in children reflect a behavioural "final common pathway" of developmental risk factors,1 which can include transgenerational associations of core symptoms, as Poulton notes. Current scientific evidence suggests both genetic and environmental contributions, such as verbal and visuospatial executive dysfunction2 and/or early patterns of attachment deficits.3 Increased levels of parental psychopathology, associated with (in the child) deficiencies in problem solving, affect regulation, emotional communication and secure attachment, may contribute to the child's symptoms. For this reason, we advocate that medical management be based on a thorough assessment, to ensure that appropriate psychological interventions (eg, parent and teacher management training) are offered alongside psychostimulant medication. In a recent speech at a scientific meeting of the Faculty of Child and Adolescent Psychiatry, Dr A Mawdsley, a distinguished child psychiatrist, expressed his belief that "prescribing medication in the absence of a careful emotional state assessment is inferior medical practice". He went even further to state that "prescribing medication in the absence of a behavioural modification program should be considered medical negligence".

George Halasz · Alasdair LA Vance

To the Editor: I wish to draw attention to a draconian anomaly in the National Health Act 1953 (Cwlth). All GPs encounter patients "shopping" for narcotics and/or tranquillisers. The Doctor Shopper phone line (which enabled GPs to rapidly obtain information from the Health Insurance Commission to identify non-genuine patients) was a boon in guiding GPs' management of such situations. Concern over the new private sector amendments to the Privacy Act 1988 (Cwlth) led to an examination of the legal standing of the Doctor Shopper phone line, and it has now been cancelled. Concerned GPs are now limited to requesting that a "patient" sign a voluntary release of their Pharmaceutical Benefits Scheme record. This tells the "patient" that they have been rumbled, and they move on to the next practice on their list. If they have signed the Privacy Release Form, then the GP will receive a printout of the drugs they have received under the Pharmaceutical Benefits Scheme in the previous six months. This is accompanied by a letter informing the doctor that he or she "cannot make a record of, divulge or communicate to any person, any information with respect to the affairs of the person whose information has been released. To do so attracts a penalty of $5000 and/or imprisonment for a period not exceeding two years". So, under the provisions of the National Health Act (subsection 135A), even putting this information in the medical records of a multidoctor practice would appear to be illegal. It is clearly illegal to warn other doctors outside the practice. There is no corresponding legislation which affects doctor shoppers. So the "right-doers" can finish up in jail, while the "wrong-doers" can, with impunity, continue to play their dissembling, time-consuming, and sometimes harassing, games.

Max Kamien

To the Editor: We are writing to add our wholehearted support to the plea made by Carapetis et al1 for a simplified ethical approval process for multicentre studies. We are conducting two national case-controlled studies of cancer in Australia, funded by grants from the National Institutes of Health and the Department of Defense in the United States, as well as the National Health and Medical Research Council (NHMRC). Our ability to achieve full population coverage was a major competitive advantage in terms of securing international funding. However, to realise this objective, we have spent more than a year obtaining ethics approval from the myriad institutions controlling access to patients and the public. We have been required to make more than 60 separate ethics applications, lodging about 550 copies of the proposal (a total of 40 000 sheets) at a cost of more than $7000 for paper and printing alone. When labour is included the cost of the initial submissions escalates to $16 000 (excluding substantial investigator time). Other costs include the extraordinary requirement of one ethics committee in Victoria that an investigator from Queensland personally attend a 10-minute interview at which no substantive issues were raised. The ethical benefit of this investment must be questioned when the majority of changes required by committees have dealt with minor issues such as grammatical style that have little to do with patient protection. Inevitably, such directives are inconsistent across institutions. It is thus impossible to comply with all requests while maintaining a standard set of study documents. These problems are accentuated for the increasing number of Australian researchers relying on overseas funding. For example, regulatory authorities in the United States insist that all ethics committees reviewing US-funded projects involving humans must have US federal approval to do so. In our experience, few Australian hospital ethics committees have this approval. Therefore, in addition to fulfilling standard institutional ethics requirements, we have also had to help several committees go through the lengthy process of securing US accreditation simply to approve our study! For all the above reasons, we strongly believe that Australian researchers and patients would be best served by a single national ethics committee for large multicentre studies. This would also reduce the enormous burden currently placed on the individual committees. In the meantime, we thank Breen and Hacker2 for their reminder to institutional ethics committees that the NHMRC national statement "empowers ethics committees to minimise unnecessary duplication".

David C Whiteman · Penelope M Webb · David M Purdie · Adèle C Green

To the Editor: Both adult and paediatric hospital emergency departments (EDs) are subject to inappropriate use.1,2,3 Some families use the ED as a primary care provider,4,5 often claiming that they have no regular general practitioner.6 Such families may experience poorer overall health.7,8 We hypothesised that providing such families with information about GPs in their area and emphasising the benefits of having a GP responsible for their long term healthcare might: facilitate the establishment of ongoing relationships between patients and GPs; and encourage families to use GPs more as their primary source of care. We conducted a controlled trial (week-on, week-off randomisation) of families identified as having no regular GP who presented to the Royal Children's Hospital ED over four months. Information about the GPs interested in seeing children was located on a computer database. Medical staff were able to search for a GP whose surgery was close to the patient's street address. Families were provided with detailed information about the GP's practice (eg, opening times, languages spoken, etc). Parents were given a list of GPs and a map showing the locations of their surgeries, together with a letter of introduction; the families decided which GP they would attend. Families in the control group were just treated as usual. Families were then contacted after two months to see if they had visited a GP and whether regular contact had been established. Over the four months, 216 families were enrolled; 96 were allocated to the intervention group. Despite our active encouragement, the ED medical staff provided the intervention material to families in the intervention group on just 49% of occasions. We found that, two months after the initial ED visit, intervention-group families were no more likely to have established an ongoing relationship with a GP than control families (46 [38.3%] and 41 [42.7%], respectively; P = 0.5), irrespective of whether or not they received the intervention material. In summary, this single intervention was not sufficient to alter healthcare-seeking behaviour of families with no regular GP. It seems the motivation to obtain a GP lies with the family. Thus, it would seem necessary to design and deliver an intervention that addresses the beliefs of families about the roles of various facets of the healthcare system. With time and work pressures, ED medical staff may not be in the best position to provide such intervention.

Michael K Marks · Daniel Steinfort · Peter LJ Barnett

In reply: We agree with Johnson and Lassere about the value of longitudinal studies, especially clinical trials, in assessing healthcare benefits and costs. They are critical to informing clinical practice and health policy. If it were possible to conduct these studies across a wide variety of settings, representing the range of "real life" practice, then there would be little need for epidemiological modelling. However, this is not possible. Clinical trials (with or without cost components) will only ever be conducted over relatively short durations, on circumscribed populations and under tightly controlled conditions. A key, but often overlooked, issue is whether the results of studies are externally valid (generalisable). Indeed, the evidence base that dictates clinical practice and health policy should comprise data that are both internally and externally valid. We do not suggest that epidemiological modelling replace longitudinal studies (in fact, modelling depends critically on robust prospective data); rather, it complements these studies by providing a means to assess their external validity. We are also mindful of the limitations of epidemiological modelling, as outlined in our article,1 and acknowledge the importance of ensuring rigour in the methods. Our article dealt with generating the data needed for sound economic evaluation, by taking into account the long-term benefits, risks and costs of treatment strategies, and "real-life" health service conditions. This is distinct from the issue of whether "conditional listing" on the Pharmaceutical Benefits Scheme should be implemented for drugs that are yet to be proven cost-effective.

Danny Liew · John J McNeil · Anna Peeters · Stephen S Lim · Theo Vos

To the Editor: In a recent letter in the Journal,1 Rodger writes that breast screening is unlikely to affect overall mortality and notes that this "gives the lie to the conclusions of Olsen and Gøtzsche's overview, which are based only on overall mortality". English is not my first language, but according to my English–English dictionary "give the lie to" means either "to disprove" or "to accuse of lying", and a related adjective is "mendacious". In actual fact, however, in our Cochrane Review,2 we carefully analysed both breast cancer mortality and all-cancer mortality. We found breast cancer mortality to be an unreliable outcome that is biased in favour of screening. For deaths ascribed to any cancer, including breast cancer, we found a relative risk of 1.02 (95% CI, 0.95–1.10) for the two trials with medium-quality data,3-5 and a relative risk of 1.00 (95% CI, 0.91–1.10) for the only trial with poor-quality data that reported all-cancer mortality.6 If it were true that screening reduced breast-cancer mortality by 30%, as some Swedish researchers have claimed,7 then the expected relative risk for all-cancer mortality should not be greater than 0.95. These findings should raise concern rather than complacency. Another, recent indication that things are not what they purport to be is provided by the results of the large Two-County study. A Swedish overview of the randomised trials reported a 10% reduction (95% CI, 0.73–1.11; absolute reduction, 5.0/1000 to 4.5/1000) in breast-cancer mortality for one of the two counties,8 whereas the authors of the Two County study reported a 24% reduction (95% CI, 0.62–0.93; absolute reduction, 5.7/1000 to 4.3/1000),9 with the same type of statistics, within the same age group of women (40–74 years), and after a similar follow-up (1.2 v 1.3 million women-years). The conclusion in our Cochrane Review is: "The currently available reliable evidence does not show a survival benefit of mass screening for breast cancer (and the evidence is inconclusive for breast cancer mortality)." I would not have expected Rodger, as an editor of the Cochrane Breast Cancer Group that approved and published our Cochrane Review, to talk about "giving the lie" to our results.

Peter C Gøtzsche

In reply: In his letter, Gøtzsche is clearly under the misapprehension that, in using the figure of speech "gives the lie to", I am accusing him of lying. Nothing could be further from the truth. As he quotes, I applied that phrase to his conclusions. In my Australian Oxford Dictionary1 to "give the lie to" can mean — and it is this meaning that I was applying — "serve to show the falsity of a supposition". I was replying to Gough's response2 to my editorial3 on breast screening. He clearly showed that breast screening was unlikely to reduce overall mortality. I agree. I believe, therefore, that Olsen and Gøtzsche are wrong in supposing that analysis on the basis of breast cancer mortality is inappropriate, and that only overall mortality should be considered. Gough argues for this better than I can. Being an editor of the Cochrane Breast Cancer Group does not require me to accept every supposition or conclusion in a Cochrane review. The whole point in publishing a scientific paper — as part of the Cochrane Library or in a peer-reviewed journal — is to open it, after appropriate review, to public scrutiny, scientific comment and even criticism. Their Cochrane review4 has succeeded in achieving all of this.5 Lastly, I reiterate my comments in the editorial3 that mammographic breast screening detects breast cancers that are "smaller, less likely to involve nodes and, if node positive, more likely to involve fewer nodes." In other words, if the TNM (tumour–node–metastasis) system means anything, there is a better prognosis with such breast cancers than with those detected clinically. Perhaps Gøtzsche needs to add a clinical oncology perspective to his undoubted expertise in the finer details of trial methodology analysis.

Alan Rodger

Comment: The expression "give the lie to" has shifted its emphasis over the centuries, from the very direct "accuse (someone) of lying" to the much more abstract "show or imply (something) to be false". Some modern dictionaries, such as the Macquarie Dictionary (1997) and Merriam-Webster (2000), still give both meanings; others, such as the New Oxford Dictionary (1998), only the second. Large British and American databases, such as the British National Corpus, show that the phrase is usually used abstractly: one "gives the lie to" propaganda/a claim/an argument/a theory — whether in the context of academic discussion or political debate. The validity of an intellectual position is questioned, not the integrity of the person(s) associated with it. Yet, the simplicity of the phrase "give the lie to" probably gives the lie to the complexity of the challenge it expresses.

Pam Peters

To the Editor: The articles by Reid1 and Paterson,2 former bureaucratic leaders of the New South Wales and Victorian health systems, respectively, on the process for developing the 2003–2008 Australian Health Care Agreements (ACHAs) are disappointing. They offer few original conceptual insights or clear proposals. Reid's dream is that the 2003–2008 ACHAs will see "a new expression of national health policy on which funding decisions can be based". However, he presents only old ideas, such as "ACHAs will need to extend beyond public hospital issues to incorporate primary care", and, on the perennial cost-shifting between the two levels of government, "clearer lines of financial management of care and appropriate incentives are needed". Reid laments that the focus of all previous agreements has been "narrowly limited to one aspect of healthcare . . . the maintenance of universally accessible public hospital care free of charge". Paterson does propose something radical, and the core of his proposals is that "the payer must stand behind the patient and not between the patient and the provider". The way to Paterson's "outcome-enabled health system" is to "relieve the constraints that bind inputs and distort the 'production' system". Does he mean we need more doctors and nurses, or does he mean substitutes should perform some of their current activities? Patterson proposes more investment in "information and communications technology" to facilitate a gradual move to "patient-based funding". Does this mean capitation, medical savings accounts, or is he proposing non-insurable copayments? Whatever it means, there will be "no outcome-driven healthcare until the system recognises the whole patient", and this will only be achieved with "electronic patient record systems in routine and ubiquitous daily use by providers". Given their experience as senior health system administrators, it is a pity neither Reid nor Paterson provides any explicit suggestions that recognise the key factor that will determine the outcome of the ACHAs. This is the policy gridlock that any federal system almost inevitably imposes. A recent issue of the Journal of Health Politics, Policy and Law was devoted to health politics and policy in a federal system. The editor, Petersen, concludes with a view relevant to Australia: "You can love it, you can hate it, but . . . federalism thwarts uniformity and universalism, frustrates responsiveness and policy analysis, limits large scale innovation while churning more localized mills of idea generation and promotion, and offers a permanent employment plan for health policy researchers".3 Parts of Australian health arrangements certainly need an overhaul. An example is general practice. This sector, differently organised and financed, could deliver much more to the community, the rest of the healthcare system, the Federal Government and to general practitioners themselves. Change in this sector would not depend on improbable cooperation between levels of government, and would be more manageable than the multifarious whole-of-system reforms about which Reid and Paterson speculate.

William Coote

To the Editor: In their article describing an outbreak of Bordetella pertussis infection, Spearing and colleagues report an adult contact who was infected with B. pertussis and was treated with roxithromycin.1 In our experience, this is common practice in Australia, where roxithromycin is a frequently used macrolide antibiotic. We are currently preparing a systematic review (registered with the Cochrane acute infections group) of the effectiveness of antibiotic therapy for treating pertussis. We have found no studies of the effectiveness of roxithromycin for either treatment or contact prophylaxis for pertussis infection. B. pertussis is sensitive in vitro to roxithromycin but 2–4-fold less so than to erythromycin. While relying on the class effect of macrolides in eradicating B. pertussis and using roxithromycin in preference to erythromycin because of its lower side-effect profile may seem logical, there is no evidence to support this practice. In contrast, there is at least one study showing the efficacy of clarithromycin as an alternative to erythromycin for the treatment of pertussis.2

R John Massie · Sultan Altunaji · Renata Kukurozovic · Nigel Curtis