Volume 188 Issue 1

Hand hygiene should be the highest priority In this issue of the Journal there is yet another article showing that methicillin-resistant Staphylococcus aureus (MRSA) can easily be found on environmental surfaces — this time on identity badges and lanyards (→ What's hanging around your neck? Pathogenic bacteria on identity badges and lanyards).1 This adds to an increasing array of items such as neckties, stethoscopes, pens, computer keyboards and coats that can be colonised by pathogenic bacteria (although usually only in low numbers). While it is helpful to know all the places we may find MRSA, these types of studies really just confirm what should be blindingly obvious — that MRSA readily disseminates within our health care environment. Thus, the hands of health care workers will frequently come into contact with MRSA. The real issue with the control of MRSA is not the need for more information on environmental contamination, but the need to use the abundant information we already have to curtail the principal way that MRSA spreads in hospitals — via the hands of health care workers.2-4 Our inability to adequately address the key issues2 means that, increasingly, others will intervene, sometimes with mistaken emphasis and priorities. The United Kingdom has just mandated a “bare below the elbows” dress code in its hospitals.5 This means no more coats or even wristwatches, despite a lack of evidence that these items play a major role in transmitting MRSA. The UK Prime Minister has called for better cleaning of wards, in the belief that this is the key to controlling MRSA.5 While there is some merit in these proposals, they are focusing on elements that are minor compared with the most important one — how best to stop MRSA spreading via hands. We already know more than enough to control MRSA.2 If we use regular hand hygiene procedures with alcohol/disinfectant solutions we can reduce serious infections caused by MRSA. Better screening policies will identify people carrying MRSA and help to keep them away from those not already carrying the organism. If we wear appropriate gowns and gloves when dealing with patients (especially those known to have MRSA), then clothing and other inanimate articles will less often become contaminated with MRSA. Having more single rooms in hospitals and reducing overcrowding in emergency departments and other areas will make it easier to separate patients with MRSA from those without. We need to follow “isolation” rules, such as preventing staff from bringing their own stethoscopes or other equipment into a room where a patient with MRSA is being cared for. If we use hand hygiene procedures before and after seeing each patient, even if our hands have been in contact with MRSA on an inanimate surface, any MRSA organisms should be killed before our hands transmit them to patients. The question is, how do we change our current work practices and behaviour to ensure that these important elements are followed, not just some of the time but all the time? We don’t need more environmental-type studies without clinical endpoints. We need studies in which we intervene and show that the interventions reduce the number of people infected with MRSA.3,4 Surprisingly, there are few such studies, which is likely a reflection of how we regard quality improvement (QI) programs. QI research is not “sexy”. It is often difficult to attract funding for QI studies and get them published, because the realities of clinical practice mean that it is frequently hard to control all variables. Nevertheless, it is peer-reviewed QI programs with successful interventions that are most likely to lead to long-term reductions in MRSA infections. MRSA is a major and increasing problem worldwide. Unfortunately, the extent of infections caused by MRSA is not measured consistently or accurately (and often not at all). Timely data are not readily available for the vast majority of Australian hospitals. In England, it was mandated in April 2001 that all MRSA bacteraemia episodes be notified.6 Data from individual hospital trusts are now accessible on the Internet.7 While making the data available has generated disagreements,8,9 this intervention coincided with the first sustained year-by-year fall in the number of MRSA bacteraemia episodes (from 7700 in 2003–04 to 6378 in 2006–07). In Australia, over 4500 episodes of health care-related S. aureus bacteraemia occur per year.10 Of those, about 2000 episodes involve MRSA, with a 35% mortality rate. We need the health care profession to better define the extent of disease caused by MRSA and other serious pathogens using practical and robust outcome measures.7,11 Data from a broad range of institutions need to be made available to enable meaningful comparisons, so that institutions with higher rates of infection can learn from their colleagues with lower rates. Hospital managers need to be part of this process. We also need to ensure that we not only measure what is going on, but, more importantly, do something about it.11 It is possible for us to achieve much better control of MRSA. Denmark, The Netherlands and Western Australia, for example, have kept the number of health care-acquired MRSA infections down to low levels.2 We know what the problem is. What we appear to lack is an understanding of human behaviour and the political and medical will to really do something about it. It is time to change. We have been missing the big picture for too long.

Peter J Collignon FASM, FRCPA, FRACP

Objective: To determine whether identity badges and lanyards worn by health care workers (HCWs) are capable of harbouring potentially pathogenic bacteria.Design, setting and participants: Cross-sectional study of 71 HCWs (59 clinical ward staff and 12 infection control staff) at Monash Medical Centre, a university teaching hospital. Samples from lanyards, identity badge surfaces and connections (eg, clips, keys, pens) were cultured. The study was conducted from July to August 2006.Main outcome measures: Presence of pathogenic bacteria on identity badges and lanyards; differences in bacterial counts on items carried by nurses and doctors.Results: A total of 27 lanyards were identified with pathogenic bacteria, compared with 18 badges. Analysing lanyards and badges as a combined group, seven had methicillin-resistant Staphylococcus aureus, 29 had methicillin-sensitive S. aureus (MSSA), four had Enterococcus spp and five had aerobic gram-negative bacilli. Lanyards were found to be contaminated with 10 times the median bacterial load per area sampled compared with identity badges. There were no significant differences between nurses and doctors in total median bacterial counts on items carried, but doctors had 4.41 times the risk of carrying MSSA on lanyards (95% CI, 1.14–13.75).Conclusion: Identity badges and lanyards worn by HCWs may be contaminated with pathogenic bacteria, which could be transmitted to patients. In view of this finding we suggest appropriate infection control interventions.

Despina Kotsanas BSc(Hons), MClinEpi · Carmel Scott BN · Elizabeth E Gillespie BN, MPubHealth · Tony M Korman MB BS, FRACP, FRCPA · Rhonda L Stuart MB BS, FRACP, PhD

Objective: To measure the safety and acceptability of providing written advice (WA) for selected patients referred to a haematology service, as an alternative to inpatient or outpatient assessment.Design, setting and participants: Review of the initial management and subsequent course of patients newly referred to a tertiary referral hospital in Christchurch, New Zealand, between 16 October 2003 and 8 June 2006. Structured questionnaires were sent to all referring doctors and patients recently managed with WA.Main outcome measures: Numbers and diagnoses of patients managed with WA, early assessment or delayed assessment; re-referral and treatment details; characteristics of WA letters; and opinions of referring doctors and their patients on the WA process.Results: 26% of new referrals (714/2785) were managed with prompt WA, while 16% (455/2785) received the alternative of delayed assessment. After a median follow-up of 23 months (range, 8–40 months), 13% of those managed with WA (91/714) were re-referred back to the same haematologists; 7% (52/714) were assessed in hospital and 2% (15/714) eventually required treatment. There were no deaths due to haematological causes. Over 90% of responding referring doctors said the WA process was rapid and effective, and 77% of recently managed patients were pleased to be treated by their own doctors.Conclusions: Using WA to manage a substantial minority of patients referred to haematologists can be rapid and safe. It is widely accepted by referring doctors.

Peter S Ganly PhD, FRACP, FRCPA · Helen Keeman · Ruth L Spearing FRACP, FRCPA · Mark P Smith FRACP, FRCPA · Nigel Patton MD, FRACP, FRCPA · Eileen G Merriman MB ChB, BMLSc · Steve S Gibbons FRACP, FRCPA

Pharmaceutical companies must believe there are benefits from advertising, but just what these benefits are, and how they are measured, is not clear Pharmaceutical company executives must believe that advertising is effective. Otherwise, pharmaceutical advertising would be illegal under the Australian Corporations Act 2001 (Cwlth), which requires that company staff rationally believe their business judgements to be in the best interests of their corporation.1 However, Henderson and colleagues’ study in this issue of the Journal may have found an advertising delivery channel that does not work (→ The effect of advertising in clinical software on general practitioners' prescribing behaviour).2 They compared prescribing by general practitioners exposed to advertisements in clinical software with prescribing by unexposed GPs during 2003–2005. Despite a large sample size and carefully controlling for many possible confounders, they did not detect any significant difference in prescribing for six of the seven drugs studied. Interestingly, there was significantly less prescribing of one drug by exposed GPs — possibly a false-positive finding arising by chance, but this is the first ever published evidence that pharmaceutical advertising may sometimes unintentionally reduce sales. Opinions about the effectiveness of advertisements (one-way persuasive messages from an identified sponsor) have varied over the past 100 years. Founder of one of the first department stores in the United States, John Wanamaker, may have lamented that “half the money I spend on advertising is wasted; the trouble is I don’t know which half”.3 A pharmaceutical marketing textbook asserts that advertising alone does not increase sales, but is cost-effective for increasing awareness of new drugs.4 According to this text, advertising has a small but useful role, because it synergistically boosts the effectiveness of other promotional methods, including drug representatives. By contrast, advertising executive Pierre Garai asserted that “advertising which does not work does not continue to run. If experience did not show beyond doubt that the great majority of doctors are splendidly responsive to current [prescription drug] advertising, new techniques would be devised in short order.”5 This suggests that advertising becomes more effective over the years by a trial-and-error process akin to evolution by natural selection. Recently, marketing academic Dick Wittink concluded that medical journal advertising produced competitive returns on investment in many situations.6 In 2007, it is not clear how effective advertising is, or how accurate companies have become at measuring its effectiveness. The findings of Henderson and colleagues2 are consistent with many hypotheses. It is possible that advertising has an effect that their study failed to detect. There may have been an unknown confounder, or an effect that was too small to be detected but still large enough to provide adequate return on investment. The study focused on drugs that had been available for more than a year but advertising is more effective for introducing new drugs.4 The study measured market share, but advertising may increase market size. Competitors who did not advertise in clinical software may have promoted their drugs with other equally effective methods. Advertising to GPs in the exposed group may have saved promotional resources that were used to target GPs in the control group in other ways. Perhaps advertising in clinical software really is ineffective. This is plausible because these advertisements impinge on the doctor–patient relationship in a way many find annoying, and some find repugnant.7 Doctors are habituated to medical journal advertisements, but may give advertisements delivered through a new channel more attention and thus more scrutiny, rendering them less effective.8,9 Perhaps any additional advertising that targets doctors will have little impact because expenditure on pharmaceutical promotion may now be high enough to run into the law of diminishing returns.10 Maybe advertising is sometimes counterproductive. For example, some doctors may react against advertisements they dislike. During a consultation, when patients also see an advertisement on the computer screen, the doctor may choose an unadvertised drug to avoid having it appear that the decision was biased. However, there would still be a bias (but in the opposite direction) that would be problematic if the advertised drug was the best treatment. If any type of drug promotion is ineffective, then it wastes money earned from the high prices paid by patients and taxpayers that are supposed to provide incentives for research. If pharmaceutical executives come to believe that advertising in clinical software is ineffective, they will be required to cease investing in it. This would have major repercussions for the clinical software industry where, currently, the software maker who accepts advertising revenue dominates the market. However, the pharmaceutical industry may want to persist with this very new advertising channel. Companies might decide to allow time for more effective techniques to evolve. They may pay for ineffective advertising just to keep the channel open in case it works during new drug launches. Advertisements in clinical software could become more effective in a few years when doctors have become habituated to them, and so give them less attention.8,9 Perhaps the companies’ real aim is not short-term sales, but to gain influence over future decision-support functions within clinical software that could have considerable impact on prescribing in the long term. Like Wanamaker, we may never really know if advertisements in clinical software in 2003–2005 were just a waste of money or not. If pharmaceutical executives are motivated and able to determine the true effectiveness of advertisements in clinical software, then these advertisements will either become extinct or evolve to become more influential, for good or ill for all concerned.

Peter R Mansfield BM BS

Objective: To assess the effect of pharmaceutical advertising embedded in clinical software on the prescribing behaviour of general practitioners.Design, participants and setting: Secondary analysis of data from a random sample of 1336 Australian GPs who participated in Bettering the Evaluation and Care of Health, a national continuous cross-sectional survey of general practice activity, between November 2003 and March 2005. The prescribing behaviour of participants who used the advertising software was compared with that of participants who did not, for seven pharmaceutical products advertised continually throughout the study period.Main outcome measures: Prescription for advertised product as a proportion (%) of prescriptions for all pharmaceutical products in the same generic class or group.Results: GP age, practice location, accreditation status, patient bulk-billing status and hours worked were significantly associated (P < 0.05) with use of advertising software. We found no significant differences, either before or after adjustment for these confounders, in the prescribing rate of Lipitor (adjusted odds ratio [AOR], 0.90; P = 0.26); Micardis (AOR, 0.98; P = 0.91); Mobic (AOR, 1.02; P = 0.89); Norvasc (AOR, 1.02; P = 0.91); Natrilix (AOR, 0.80; P = 0.32); or Zanidip (AOR, 0.88; P = 0.47). GPs using advertising software prescribed Nexium significantly less often than those not using advertising software (AOR, 0.78; P = 0.02). When all advertised products were combined and compared with products that were not advertised, no difference in the overall prescribing behaviour was demonstrated (AOR, 0.96; P = 0.42).Conclusion: Exposure to advertisements in clinical software has little influence on the prescribing behaviour of GPs.

Joan Henderson BAppSc(HIM)(Hons) · Graeme Miller MB BS, PhD, FRACGP · Ying Pan BMed, MCH · Helena Britt BA, PhD

Complementary and alternative medicines (CAMs) are being used increasingly in Australia, often in conjunction with conventional medicines.1 While the demand for CAMs is growing, the regulatory framework is weak. The electronic lodgement facility, introduced in 1996, has made it easier to place new CAMs on the Australian Register of Therapeutic Goods (ARTG). Concern about the regulation of CAMs has been growing among organisations such as CHOICE.2 Here, we review the regulatory requirements for CAMs, compare weight-loss products listed on the ARTG with registered pharmaceutical products, analyse complaint procedures and advocate policy change. We have focused on weight-loss products because of widespread concern about an obesity “epidemic”, extensive advertising of the products and the large number on the market. Regulation of therapeutic goods in AustraliaIn 1989, the federal Parliament passed the Therapeutic Goods Act 1989 (Cwlth), which created the ARTG. The ARTG has two parts: one for “registered goods” and the other for “listed goods”. Some goods captured by the Act are classified as “exempt goods” and are not entered in the ARTG (ss. 9A, 18). Box 1 shows the differences between the various categories of therapeutic goods. “Registered” medicines are considered to be of relatively higher risk and are individually evaluated by the Therapeutic Goods Administration (TGA) for quality, safety and efficacy before market entry. “Listed” medicines are considered to be of relatively lower risk (Box 2).3 Most, but not all, CAMs are listed medicines.4 Initially, the TGA did not require sponsors to have evidence to support claims made about their products. In 1999, concern that improbable therapeutic claims were being made about CAMs led to the introduction of a requirement that sponsors hold substantiating evidence.5 Further, since a report by the Expert Committee on Complementary Medicines in the Health System, a random sample of about 20% of new listings is said to be assessed each year for compliance with TGA requirements.6 Both these measures have been introduced to increase monitoring of CAMs. In 1991, the government introduced fees and charges to industry for services provided by the TGA, such as ARTG applications, good manufacturing practice inspections and annual licensing. The aim was to achieve 50% cost recovery. In 1998, the government determined that 100% of costs would be recovered.7 Illustrative TGA fees (at 1 July 2007) were $170 200 for registering and evaluating a new prescription medicine (a new chemical entity); $990 for registering and evaluating an over-the-counter product or CAM (plus $6570–$46 000, depending on the number of pages of data submitted); and $540 for listing a medicine. The annual charge for a registered (non-biological) prescription medicine was $3030; for a registered over-the-counter product, conventional or CAM, $920; and for a listed medicine, $690.7 Sponsors self-assess their medicines as being listable using the web-based electronic listing facility (ELF) of the ARTG. The ELF system automatically checks that the ingredients entered are consistent with those allowed in listed medicines and asks the sponsors to certify that they hold evidence to support the indications (and thus claims) made. Sponsors may pick either a coded indication such as “May aid or assist weight loss . . .” or a custom indication entered as free text in a memo field. More than one entry into either field is allowed. After payment of a fee, the ELF system automatically generates an “AUST L” number and a certificate of listing. Since the introduction of the ELF, the time taken to list a product has been reduced from around 5 months to 10 days or less for about 90% of applications.8 Complaints from the public about listed products need to be submitted to various authorities, as summarised in Box 3.9 In February 2007, the Australian Government reintroduced a provision of the Therapeutic Goods Advertising Code, which had existed before August 2005, prohibiting health care professionals from endorsing therapeutic goods in advertisements to consumers. This provision took effect from 8 March 2007, but allowed existing advertisements to continue for either 2 years after approval (eg, in print) or 1 year if approval had not been required (eg, Internet advertisements).10 An example: weight-loss productsIn Australia, both listed and registered weight-loss products are available. To determine the numbers of each and compare them, we asked the TGA to search the ARTG for registered or listed products with the indication “weight loss”, or similar, for the period 1996 to 2006. We then supplemented the list by searching the shelves of pharmacies and health food shops and Australian Internet sites. Because of problems encountered, the TGA made available a subset of the ARTG database so that we could refine their search for weight-loss products. For the registered and listed products found, we compared the therapeutic claims with the published evidence. The website of the Therapeutic Goods Advertising Code Council was used to identify complaints and select illustrative case studies. Products identifiedThe initial search output received from the TGA failed to show some registered weight-loss products, such as orlistat (Xenical [Roche]) and sibutramine (Reductil [Abbott]). It also failed to show many listed CAMs that were being actively promoted for weight loss. Some of these problems resulted because the ELF system allowed sponsors of listed products to enter information into the ARTG in free text without verification by TGA staff. Some non-standard indications had been used for weight-loss products (such as “thermogenic”, “body sculpting”, “reduce carb cravings”), which made a complete search for such products difficult, if not impossible. Our own search found over 1000 new weight-loss products listed on the ARTG from 1996 to 2006. New listings generally increased over the period, from 45 in 1996 to 144 in 2006. Most contained multiple ingredients (herbs, vitamins, minerals). Homoeopathic products are not included on the ARTG. Over the same period, 10 conventional medicines for weight loss were registered with the ARTG, each containing one ingredient, (orlistat, diethylpropion, phentermine, sibutramine). All these substances are officially scheduled poisons, and products containing them are registered for the management of obesity, unless the product is for export. Those containing orlistat and sibutramine have been fully evaluated. Phentermine-containing medicines were “grandfathered” on to the ARTG because they were already on the Australian market when the Act took effect in February 1991. Diethylpropion is no longer marketed. The safety and efficacy of these agents has been comprehensively reviewed.11 Thus, sponsors could decide not to market products they had placed on the ARTG or to take them off the market but leave them on the ARTG. Taking into account these limitations, we found about 100 times as many listed weight-loss products on the ARTG as registered products. It is not possible to be too specific about numbers because there were confounding factors, such as the inclusion in the listed goods part of the ARTG of prescription-only medicines that were destined for export. In our opinion, the indications for weight-loss products listed on the ARTG (and thus their promotional claims) were often not in accord with the limited scientific evidence available. Furthermore, the number of such listed products is increasing each year at a much greater rate than registered products. It is possible that this has been influenced by the decision not to evaluate listed products for efficacy and also the lower fees for listing a product compared with registration. A typical weight-loss productAn example of a publicly available, listed weight-loss product is shown in Box 4. We are unaware of publicly available evidence from clinical trials to support the therapeutic claims made for this product or for many other listed (and homoeopathic) weight-loss products. Several systematic reviews have evaluated the commonly included ingredients and have concluded that, at best, more definitive clinical trials are required before conclusions can be drawn.12,13 While these products are of relatively low risk, some herbal ingredients can cause harm by themselves and also by interacting with conventional medicines; both kinds of event may be under-reported.14,15 The Complaints Resolution Panel found that the claims made about the illustrated product, Xantrax (Hershel-Beck Laboratories), breached the Therapeutic Goods Advertising Code as they were misleading and likely to arouse unwarranted and unrealistic expectations of product effectiveness.16 In our experience, it usually takes 3 to 4 months for submitted complaints to be adjudicated by the Complaints Resolution Panel and several more months before the results are made public. Meanwhile, promotional campaigns continue. In addition, the sanctions imposed appear ineffectual, as shown by the fact that some companies repeatedly breach the Therapeutic Goods Advertising Code. For example, from March 2004 to November 2007, the sponsor of Xantrax, Cat Media Pty Ltd, has had at least 28 complaints about its products, 22 of which have been upheld.16,17 In 2006, the Panel received over 350 complaints, more than twice the number received in 2005. Of these, 170 have been finalised and 100 are still being processed, 60 concerning homoeopathic products and which were referred to the TGA, and 22 referred to other bodies. The system is clearly overloaded and under-resourced. We submitted complaints over 6 months ago that have yet to be addressed. We submitted complaints over 12 months ago that have been referred to other jurisdictions, about which we have heard no more; meanwhile, promotion continues. ImplicationsIn 2003, the Expert Committee on Complementary Medicines in the Health System was established to reassure the public about the safety and quality of CAMs. The Committee said (Finding 4.1.1) that the “Government needs to take a more active role in ensuring that consumers have access to reliable information about complementary medicines, and the skills to interpret information and make informed decisions”.6 In 2005, the government responded to the expert committee report by accepting, noting or supporting all but one of the 49 recommendations. The TGA established the Complementary Medicines Implementation Reference Group to oversee the implementation and has provided progress reports.18 Despite the widespread use of CAMs, many consumers are unaware that listed medicines do not undergo the same stringent evaluation process as registered medicines, or indeed, that there is a difference between the two. Consumers are not sufficiently protected by regulation in this case. It is difficult to reconcile the therapeutic claims made for many CAMs with the objects of the Act: “to provide for . . . a national system of controls relating to the quality, safety, efficacy and timely availability of therapeutic goods...” (s. 4, our italics). In an attempt to explain the difference, the TGA produced a pamphlet in 1995 called Buying medicines — what’s on the label for me? It was available in pharmacies and health food shops and is now on the Internet.19 While the content reflects the legal situation, the omission that AUST L listed medicines are not evaluated for efficacy diminishes the utility of the pamphlet for the very people to whom it is directed. This has financial as well as health implications for consumers. Brian Grogan, national president of the Pharmaceutical Society of Australia, has noted: While those products that lack evidence for effectiveness may not actively harm the physical health of those who take them, they may well be harming patients’ financial health, some of whom may have to forgo other more beneficial evidence-based treatments or other necessities.20 In addition, any herb has many different chemical constituents, the presence and concentration of which vary, depending on the source of the herb, and the extraction and standardisation methods used. Marked variations of chemical constituents have been found in different commercial products that purported to contain the same amount of a particular herb.21 Currently, the TGA accepts crude assays that do not necessarily confirm that one herbal product has the same chemical constituents as another that has been proven to be clinically effective. In addition, the TGA does not require stability data on listed products. Finally, the large number of repeated breaches of the Advertising Code by certain companies, together with an increasing backlog of complaints, shows that complaint procedures are no substitute for adequate regulation at the time of market entry. Consumers (and health professionals) cannot exercise informed choice about CAMs if they are denied information about the quality and efficacy of these products. SolutionsHow could the present situation be improved? We propose the following actions: AUST L medicines (and homoeopathic medicines) should include on their labels a statement, such as “This medicine has not been evaluated by Australian health authorities for efficacy”. A campaign to educate the public about such matters is needed. This would best be done by the National Prescribing Service, which is currently conducting a survey of educational needs in relation to CAMs. Ethical codes of conduct and complaint procedures for CAMs, over-the-counter and prescription drugs should be streamlined, harmonised and brought under one adequately resourced authority. Consistent (and meaningful) sanctions should be imposed on companies that repeatedly breach codes (for example, corrective advertising orders and fines linked to company turnover, with the money used to support the complaint system). The ARTG database should be updated with respect to listed products. Sponsors should be required to add key evidence supporting each indication on the ARTG and entries should be checked by staff of the regulatory body and coded with respect to therapeutic indication. This information should be publicly available on the Internet. The TGA should check the analysis of herbal products more thoroughly and allow sponsors to use clinical trial evidence relating to other products only where their own product has been shown to have an identical herbal preparation, extraction and standardisation process. Finally, we believe that, in the longer term, the listing system should be scrapped, and CAMs (including homoeopathic medicines) should be assessed for efficacy and delisted if evidence is lacking. Public money should be used for this, not listing fees. There is a current perception that 100% cost-recovery by the TGA (as with the Food and Drug Administration in the United States) has led to commercial considerations outweighing the need for consumer protection.22,23 Listed weight-loss products would be a good place to start the regulatory reform, given the increasing problem of obesity in Australia. 1 Contrasting requirements of the Therapeutic Goods Administration (TGA) for different categories of goods Requirement Registered goods (pharmaceutical products) Listed goods (complementary medicines) Exempt goods Label designation AUST R AUST L na Compliance with Code of Good Manufacturing Practice Yes Yes No Manufacturers licensed by TGA Yes Yes No Efficacy evaluated by TGA Yes No No Stability (shelf-life) evaluated by TGA Yes No No Individual ingredients evaluated for safety by TGA Yes Yes Some (eg, those in antiperspirants, fluoride toothpastes) Examples All medicines included in a poisons schedule, all PBS medicines, all other medicines not listed or not exempt goods Most herbal preparations, vitamins, minerals, glucosamine, some homoeopathic medicines (if the sponsors so choose), export goods Homoeopathic medicines, extemporaneously dispensed medicines, dandruff shampoos, antiperspirants, fluoride toothpastes na = not applicable. PBS = Pharmaceutical Benefits Scheme. 2 Main criteria used by the Therapeutic Goods Administration for listed complementary medicines (with the exception of homoeopathic products) They may contain only ingredients approved for use in listed medicines (those with well established quality and safety profiles); They must be labelled and advertised only for indications consistent with low risk (eg, symptomatic relief of non-serious diseases, disorders and conditions) and must not be indicated for the treatment of a serious form of a disease, condition, ailment or defect as specified in the Therapeutic Goods Advertising Code; There must be evidence (which can be either traditional or scientific), held by the sponsor of the product, to support any claim that the sponsor makes relating to the medicine; and They do not contain substances that are scheduled in the Standard for the Uniform Scheduling of Drugs and Poisons or otherwise restricted (eg, included in Part 4 of Schedule 4 of the Therapeutic Goods Regulations 1990). 3 Bodies handling complaints about listed products and registered over-the-counter products Complaint Regulation About product quality or claims made on the pack or pack insert Therapeutic Goods Administration’s Office of Complementary Medicines About promotional claims made in specified media (television, radio, Internet, newspapers, magazines, outdoor signs and cinema) Complaints Resolution Panel assesses concerns against the Therapeutic Goods Advertising Code About other advertising, such as pharmacy window displays, brochures, leaflets and catalogues Complaints Resolution Committee of the Complementary Healthcare Council of Australia or Australian Self-Medication Industry’s Complaints Panel 4 Xantrax (Hershel-Beck Laboratories), an example of a listed weight-loss product Ingredients Each Xantrax tablet contains: Camellia sinensis (green tea) Citrus aurantium fruit (bitter orange) Paullinia cupana (guarana) Panax ginseng (Korean ginseng) Ilex paraguariensis (yerba mate) 11 additional vitamins and minerals Therapeutic claims Xantrax helps by: delaying gastric emptying thus prolonging a sense of fullness suppressing appetite maintaining healthy energy levels improving exercise performance enhancing the body’s ability to cope with stress supporting healthy metabolism Pharmacy poster for Xantrax.

Ken J Harvey FRCPA · Viola S Korczak BEc(SocSc), MIPH · Loretta J Marron BSc, AssocDipBus · David B Newgreen BPharm, MBA

The United Kingdom, Australia and New Zealand use different criteria for public funding of pharmaceuticals, but all include estimates of clinical effectiveness and cost-effectiveness. Drug appraisal is done through the National Institute for Health and Clinical Excellence (NICE) in the UK, the Pharmaceutical Benefits Advisory Committee (PBAC) in Australia, and the Pharmaceutical Management Agency (PHARMAC) in NZ. Of the 10 drugs deemed least cost-effective by NICE between 1996 and 2005, all were approved for funding in the UK, six were approved in Australia and five were approved in NZ. Australia and NZ refused funding for drugs for obesity, influenza and growth deficiency. All three countries made exceptions in order to fund drugs of poor cost-effectiveness for some “dread” diseases, but some drugs for less alarming conditions were either not funded or heavily restricted.

James P Raftery MA, PhD

One aim of Medicare’s Enhanced Primary Care (EPC) initiative is to encourage multidisciplinary care of patients with chronic disease by funding five allied health treatment sessions per patient per year. In many cases, the number of funded treatments is far less than standard clinical practice indicates, particularly when the five visits are shared between service providers. We believe clinical outcomes may be compromised by adhering to the funded hours, and inequity of outcome may arise based on socioeconomic status and the ability of patients to pay. Research that determines how patients and allied health practitioners are responding to this initiative is required. Research is also required to evaluate whether EPC enhances clinical outcomes compared with no allied health intervention and standard allied health practice.

Michele M Foster PhD · Geoffrey Mitchell FRACGP, PhD · Terry Haines BPhysiother(Hons), GCertHealthEcon, PhD · Sean Tweedy BHMS, MHMS, PhD · Petrea Cornwell BSpPath, PhD · Jennifer Fleming BOccThy(Hons), PhD

With new funding for the National Health and Medical Research Council (NHMRC) to provide an evidence base for policy and practice reform, it is timely to revisit Australia’s recent experiences with health services research and policy development. We provide a broad review of the contribution of Australian health services research to the development of health policy over the past 20 years. We conclude that three preconditions are necessary to influence policy: political will; sustained funding to encourage methodological rigour and build decisionmakers’ confidence; and the development of sufficient capacity and skills.

Jane P Hall BA, PhD · Rosalie C Viney BEc(Hons), MEc, PhD

Objective: To describe the magnitude and distribution of health problems in Australia, in order to identify key opportunities for health gain.Design: Descriptive epidemiological models for a comprehensive set of diseases and injuries of public health importance in Australia were developed using a range of data sources, methods and assumptions. Health loss associated with each condition was derived using normative techniques and quantified for various subpopulations, risks to health, and points in time. The baseline year for comparisons was 2003.Main outcome measures: Health loss expressed as disability-adjusted life years (DALYs) and presented as proportions of total DALYs and DALY rates (crude and age-standardised) per 1000 population.Results: A third of total health loss in 2003 was explained by 14 selected health risks. DALY rates were 31.7% higher in the lowest socioeconomic quintile than in the highest, and 26.5% higher in remote areas than in major cities. Total DALY rates were estimated to decline for most conditions over the 20 years from 2003 to 2023, but for some causes, most notably diabetes, they were projected to increase.Conclusion: Despite steady improvements in Australia’s health over the past decade, there are still opportunities for further progress. Significant gains can be made through achievable changes in exposure to a limited number of well established health risks.

Stephen J Begg MPH, GradDipPopHlth, BA(Hons) · Theo Vos PhD, MSc · Bridget Barker BSoc(Hons), BBus · Lucy Stanley BHlthSci, GradCertAppEpi · Alan D Lopez PhD

We report eight recent cases of Chikungunya virus infection in travellers to Australia. Patients presented with fevers, rigors, headaches, arthralgia, and rash. The current Indian Ocean epidemic and Italian outbreak have featured prominently on Internet infectious disease bulletins, and Chikungunya virus infection had been anticipated in travellers from the outbreak areas. Diagnosis was by a generic alphavirus reverse transcriptase polymerase chain reaction with confirmatory sequencing. Prompt diagnosis of Chikungunya virus infections is of public health significance as the mosquito vectors for transmission exist in Australia. There is potential for this infection to spread in the largely naïve Australian population.

Douglas F Johnson MB BS(Hons) · Julian D Druce BSc, MSc · Scott Chapman MB BS, FRACP · Ashwin Swaminathan MB BS · Josh Wolf MB BS · Jack S Richards MB BS, FRACP · Tony Korman MB BS, FRACP, FRCPA · Chris Birch BSc, MSc, PhD · Michael J Richards MB BS, MD, FRACP

In Australia, 2.9 million people continue to smoke daily, and tobacco still accounts for 8% of disease burden. Tobacco harm-reduction strategies, such as the use of Swedish snus, have been suggested as a way to further reduce this disease burden. In Australia, the most dangerous tobacco products (cigarettes) are the least regulated, while oral tobacco products, including snus, cannot be sold legally. Recent epidemiological modelling indicates that there are only small differences in life expectancy between smokers who quit and those who switch to snus. There is a case on public health and ethical grounds for allowing inveterate smokers who want to reduce their health risks to access snus. At a minimum, the recent increase in tax on smokeless tobacco should be reversed, and the ban on the commercial importation and supply of low nitrosamine smokeless tobacco should be reconsidered in light of the epidemiological evidence on its potential to reduce tobacco-related disease in smokers.

Coral E Gartner BHlthSci(Hons), PhD · Wayne D Hall BSc, PhD

We need to be sure any introduction of smokeless tobacco will actually reduce overall harm In the mid 1980s, I assisted in South Australia becoming the first Australian state to ban the sale of smokeless tobacco products.1 In 1991, the ban went national, effectively restricting access to small quantities imported for personal use. New Zealand and the European Union imposed similar bans, although in almost all other nations smokeless tobacco products are sold openly, with many also allowing advertising. The bans sought to prevent the tobacco industry from building demand for an uncommon form of tobacco use known to increase the risk of oral cancers.2 Since that time, growing understanding of differences in the risk profiles of different smokeless tobacco products has generated often volatile debate on whether such bans had the unintended consequence of preventing genuinely less harmful products being available to smokers who might be interested in switching from cigarettes. The emergence of low nitrosamine smokeless tobacco (LNST) products such as Swedish snus, which pose far less risk than smoking,3 and the emerging, compelling epidemiological evidence of an association between rising LNST use in Swedish men and their low rates of tobacco-caused disease,4 has led to widespread debate on whether this form of tobacco should be made more accessible. Gartner and Hall have articulated a strong case for the affirmative (→ Should Australia lift its ban on low nitrosamine smokeless tobacco products?).5 They and others6 have correctly excoriated those who continue to mislead the public by obfuscating the reduced risks associated with LNST use, and have raised important ethical concerns of denying reasonable access to less harmful forms for adults who wish to continue to use tobacco products. Nonetheless, several broad concerns demand that any liberalisation should be subject to strict access controls and that the tobacco industry be prevented from using the issue as a wedge to subvert advertising bans and undermine the important benefits of reduced smoking caused by smoking restrictions. Much is made of the example of Sweden. However, in nations where no bans exist, demand for smokeless products has not mirrored the Swedish experience, with use remaining marginal. In 2002 in the United States, where there is a long tradition of use and the products are aggressively advertised, only 1.5% of men and 0.16% of women used smokeless tobacco.7 In Canada, use is similarly marginal.8 There has been little reflection on why, outside Sweden, LNST use remains apparently unacceptable to most consumers despite the best efforts of transnational tobacco companies. Sweden has a 200-year history of smokeless tobacco use, which may explain a great deal about why an intuitively strange form of tobacco use, typically involving holding the product in the mouth for up to 15 hours a day, holds little attraction for today’s consumers elsewhere. Advocates for the liberalisation of access in nations that ban sale of LNST products are thus almost certainly over-hyping their potential for widespread adoption. The core of Gartner and Hall’s argument is the objective of assisting “inveterate” smokers to access smokeless tobacco products. The term is shorthand for smokers who either do not wish to stop smoking, or whose repeated failed attempts at quitting have resigned them to be reluctant, continuing smokers. The size, characteristics and stability of this group merit close consideration. In recent years, daily smoking prevalence in Australia has been falling faster than at any time (Box). In 2006, daily smoking prevalence in New South Wales fell to 13.9%,10 following unprecedented but still relatively modest campaign expenditure by the Cancer Institute NSW. If national effort could match this commitment and, conservatively, we halved the most recent relative annual rate of decline experienced in NSW (ie, − 10.06% to − 5.03%) and applied it nationally, we would see smoking prevalence fall below 10% by 2013. Some claim that today’s remaining smokers are “hardening” and that those still smoking are mostly inveterate, with poor prospects of ever stopping. A US review of the evidence for hardening found “little evidence that the population of smokers as a whole” was hardening.11 Twenty-nine per cent of Australian smokers now describe themselves as only occasional smokers,12 and daily consumption is reducing — facts incompatible with hardening. Moreover, around 70% of smokers are planning to quit and making attempts to do so,13 meaning that only about 4.2% of adults say they want to continue using tobacco. Nonetheless, many of these will subsequently quit without previously planning to do so.14 So, it is an unknown but plausibly small fraction of this “smoking committed” group that harm-reduction advocates believe might be interested in using LNST. The potential for LNST to reduce health risks for this group needs balancing against any collateral negative effects of re-introducing smokeless tobacco. Few analysts of the tobacco industry doubt that its ambitions for LNST products lie well beyond servicing nascent demand from the small proportion of smokers likely to be interested in switching to these products. With youth smoking prevalence at an all-time low in Australia, the industry would be vitally interested in the potential of LNST to rekindle tobacco use in the group which is its future customer base. By naming smokeless products with cigarette brand names (Marlboro, Lucky Strike, etc) the industry hopes to heighten brand name prominence, with spin-off benefits in promoting cigarettes. Most obviously though, LNST provides would-be quitters with a reassuring product to use “for those times when you can’t light up”. Nowhere is there any evidence of companies seriously urging smokers to abandon smoking. The investment advisors Citigroup are very clear on the potential for dual use: “The [retail] trade believes that snus will be consumed in addition to cigarettes. Given the increased bans on smoking, snus products seem like an obvious substitution.”15 These sentiments are echoed in the US retail trade newsletter Brandweek: “There’s money to be made from municipal smoking bans as another cigarette maker chases after smokers who get their nicotine fix between their cheek and gum during those many moments when they can’t light up.”16 Smoking bans have depressed daily consumption17 and stimulated cessation.18 If widespread dual smokeless/cigarette use were to occur to the delight of the industry, the net population effect of this would be to increase harm if the cessation effect was reduced and the numbers switching to snus marginal, as has occurred outside of Sweden. Some argue that the dual use concern is over-stated because in Sweden the phenomenon is typically a transitionary phase as smokers wean themselves on to snus. But, as argued, the Swedish experience has not been replicated elsewhere, so it is prudent to be cautious. Overt tobacco advertising is banned in Australia, so some argue that tobacco companies will be unable to promote dual use. However, with the demise of overt advertising and promotion, the global industry is now harnessing “below-the-line” strategies like viral, buzz and stealth marketing,19-21 where covert efforts are made to spread interest in products. The Internet provides unparalleled opportunities here,22 with major sites heavily dominated by youth traffic already showing fingerprints of tobacco industry involvement.23 On 16 September 2007, for example, on the massively popular Facebook website, there were 242 “friendship” networks incorporating the word “snus” and 105 with “smokeless tobacco”. Many of these are overt promotional sites. Although the rationale is compelling for allowing what is likely to be a small proportion of smokers to access LNST, precautionary health policy should tread warily. Optimists can point to Swedish-style outcomes of widespread smoking substitution, or at the very least to the small-scale uptake seen in the US, where choice is at least available to inveterate smokers wanting to switch. But other scenarios are plausible. The tobacco industry has shown itself to be resourceful, rapacious and duplicitous in the service of sales maximisation, and any notion that they would be disinterested in the youth market, in providing nicotine substitutes for smoking “downtime”, and in preventing smokers from abandoning tobacco use altogether is naïve. Thus, the challenge remains of how to provide choice to smokers without repeating the catastrophic legacy that the history of allowing cigarettes to be sold from every conceivable retail outlet, packed and advertised beguilingly, has brought. Tobacco retailers have repeatedly been shown to ignore the law prohibiting sales to minors, and so inspire little confidence in being trusted to confine distribution of smokeless products to adults, should the ban on smokeless tobacco sales be partly repealed. Trials of allowing LNST products to be scheduled S3 and made available under the counter from pharmacies offer a model of highly controlled access that could be investigated. These should investigate whether dual use with smoking is occurring so that the net public health benefit of permanently allowing such access could be assessed. LNST brand names using cigarette names, symbols or colours should be banned. Public awareness of the products’ reduced harm status could be generated via health authorities, with parallel investigation and prosecution of tobacco industry efforts to promote the products via below-the-line strategies. Pharmacists who might baulk at the thought of dispensing a tobacco product24 can reflect on the many precedents already embraced in medical practice, where lower risk agents and procedures are prescribed or implemented in the hope of achieving more important health benefits than the risks being posed by treatments and (for example) diagnostic radiation. In the meantime, the recent tax increase on the importation of smokeless tobacco products should be reviewed, so that it discriminates between LNST and the very much more harmful varieties of smokeless products, such as those now openly sold illegally from most South Asian groceries.25 Changes in daily smoking prevalence, Australia, 1985–2006, for people aged 14 years and older9 Year Daily smoking Absolute percentage change per year Relative percentage change per year 1985 29.0% − 0.78 − 2.70 1991 24.3% +0.35 +1.44 1993 25.0% − 0.60 − 2.40 1995 23.8% − 0.67 − 2.80 1998 21.8% − 0.73 − 3.36 2004 17.4% − 1.75 − 10.06 2006* 13.9% Total 1985–2006 − 0.72 − 2.48 * 2006 figure is for New South Wales only, for people aged 16 years and older10 (national data unavailable).

Simon Chapman PhD

Periarticular shoulder disorders are common in clinical practice, and diagnosis is often difficult. Medicare statistics indicate that between 2001 and 2006 the use of diagnostic shoulder ultrasonography increased significantly. Rotator cuff disease, shoulder impingement syndrome and subacromial bursitis are among the most common diagnoses reported on shoulder ultrasonography. Shoulder ultrasonography is useful in the diagnosis of full thickness tears, but its utility for other rotator cuff disorders, shoulder impingement syndrome and subacromial bursitis is less well established.

Mark S Awerbuch MB ChB, FRCP, FFPMANZCA

A 2-year-old boy and a 10-year-old girl presented to the emergency department with a decreased level of consciousness. The girl had had persistent vomiting and a seizure. Urine metabolic screening tests were positive for γ-hydroxybutyrate (GHB). Samples from toy beads ingested by both children contained 1,4-butanediol, which is metabolised to GHB in humans. Regulatory authorities were notified, leading to an international recall of the toy beads. Clinical recordsPatient 1 A 2-year-old boy presented to the emergency department (ED) with a decreased level of consciousness. Earlier, he had been playing with his siblings in the backyard. He had been unsteady on his feet an hour before and then became difficult to rouse. There was no history of trauma, ingestion of medicines or plants or intercurrent illness. He had been well previously and was the youngest of 10 siblings. On arrival at the ED, his Glasgow Coma Score (GCS) fluctuated between 7 and 12, with no focal neurological deficit. Pupils were 2 mm, equal and reactive. A pustular vesicle on his right cheek was the only other significant finding. He was afebrile and had no neck stiffness. An electrocardiogram showed sinus bradycardia at 60 beats/min. He was hypotensive, with blood pressure of 59/39 mmHg. Blood glucose level was 5.2 mmol/L. Without a history of ingestion, we initially considered a postictal state or encephalitis. Laboratory investigations, including full blood count, electrolytes, and renal and liver function tests, were all within normal limits. Computed tomography of the brain showed no intracranial abnormality. Lumbar puncture was not attempted because of the child’s fluctuating level of consciousness. He was investigated and treated with cefotaxime and acyclovir for suspected intracranial infection. Urine was sent for toxicology and metabolic screening. Seven hours after presentation, remarkable clinical improvement was noted, and he became fully alert and cooperative. At this point he vomited and also passed a substantial number of coloured beads in his stool. The family were further questioned about a history of ingestion; the boy’s mother divulged that he had been playing with Bindeez brand toy beads (Moose Enterprise, Melbourne, Vic) (Box). With no obvious diagnosis, he was admitted to hospital for observation and further investigation. An electroencephalogram showed no abnormalities. The urine toxicology screen returned with a negative result for illicit drugs. The urine metabolic screen became available on Day 5 and was positive for γ-hydroxybutyrate (GHB). The source of GHB in this patient was thought to be either exogenous (that is, poisoning) or an inborn error of metabolism. The latter was excluded when a repeat metabolic screen from urine taken on Day 3 returned with a negative result for GHB. In searching for an exogenous source of GHB, toy beads from the boy’s home, similar to those ingested, were sent for analysis and subsequently found to contain 1,4-butanediol (1,4-BD). The patient recovered completely and was discharged on Day 7 with no residual sequelae of his poisoning. Patient 2A 10-year-old girl presented to the ED after a 4-minute generalised seizure. She had been unrousable by family an hour earlier. She had then vomited up to 100 Bindeez beads and then had the seizure. She had been well earlier in the day, and there was no history of intercurrent illness or trauma. The patient had a further seven episodes of vomiting and was persistently drowsy. She had a background of Asperger’s syndrome and attention deficit hyperactivity disorder, for which she took extended-release methylphenidate. On arrival at the ED, she was drowsy, with a GCS of 14 and no focal neurological signs. Her heart rate was 70 beats/min, she was normotensive and physical examination was otherwise normal. On advice from the New South Wales Poisons Information Centre, a urine sample was collected, and beads from the patient’s home, similar to those ingested, were sent for analysis. Five hours after ingestion, she became alert and communicated appropriately. She was admitted to hospital for overnight observation and discharged the following day with no further complications. The urine metabolic screen was positive for GHB, and the beads were found to contain 1,4-BD. Public health responseAfter confirmation of GHB poisoning in Patient 1 from 1,4-BD detected in Bindeez toy beads, the NSW Poisons Information Centre was notified. The Centre and the NSW Biochemical Genetics Service alerted the NSW Office of Fair Trading about the product. They in turn contacted the company marketing the product to investigate the formulation of the toy beads. When the manufacturer in Hong Kong was contacted, it supplied a list of ingredients in the production of the toy beads; this list did not include 1,4-BD, but did mention the agent 1,5-pentanediol. Meanwhile, two further samples of Bindeez toy beads were tested at our institution. Both samples tested positive for 1,4-BD. None of the beads tested contained 1,5-pentanediol. With confirmation of similar biochemical analyses from the beads in the second case, the NSW Department of Health and the NSW Office of Fair Trading were further alerted about banning the product. The following day, the NSW Minister for Fair Trading issued an interim ban on the sale of Bindeez products in NSW; other Australian states rapidly followed suit. Further cases of GHB poisoning in Australia came to light during the ensuing days. Staff of the Poisons Information Centre also alerted toxicologists and poisons control centres worldwide where similar products are marketed (eg, Bindeez in the United Kingdom and Aqua Dots in North America) and the potential for GHB poisoning may have existed. With worldwide media coverage and similar cases in North America, an international recall soon followed. DiscussionGHB is an endogenously occurring neurotransmitter derived from γ-amino butyric acid (GABA).1 Its known metabolic precursors are 1,4-BD and γ-butyrolactone. A potent sedative and anaesthetic agent, it was initially synthesised in the 1960s.2 GHB and its precursors have recently found notoriety as recreational and club drugs. In 2000, GHB became a banned substance by the United States Drug Enforcement Agency and classified as Schedule 1 by the US Food and Drug Administration.2,3 1,4-BD is a widely available industrial chemical used as a solvent and in the manufacture of some types of plastics and fibres. When ingested, it is metabolised rapidly by alcohol and aldehyde dehydrogenases to GHB.4,5 Hence, the toxicity and clinical features of 1,4-BD poisoning are similar to those of GHB. While 1,4-BD is not a scheduled drug in Australia, it is a category 1 precursor under the Drug Misuse and Trafficking Regulations 2006, which restrict the supply of 1,4-BD (Pharmaceutical Services, NSW Department of Health, personal communication, 12 Nov 2007). GHB is an agonist at inhibitory GABAB receptors and is excitatory at specific GHB receptors. There is a dose–response relationship in GHB toxicity. Low doses result in vomiting, drowsiness, visual disturbance and disinhibition, while higher-dose effects include confusion, coma, bradycardia and myoclonic (seizure-like) movements.3 Routine urine toxicology screens do not detect GHB in their profile. Specific analysis with gas chromatography–mass spectrometry (GC–MS) or as part of a urine metabolic screen is required. The urine sample from Patient 1 was investigated for possible inherited metabolic diseases, including urinary organic acid analysis by GC–MS.6 This showed a marked increase in GHB (a metabolite seen in succinic semialdehyde dehydrogenase deficiency) but without any increase in 4,5-dihydroxyhexanoate lactone, as would be expected in the inborn error. This pattern strongly suggested an exogenous source of GHB, which was confirmed by the compound being undetectable in a second urine sample taken 3 days later. Treatment of GHB poisoning is primarily supportive and may involve airway and ventilatory intervention, and atropine for symptomatic bradycardia7 Gastrointestinal decontamination with activated charcoal is not indicated, owing to the rapid absorption of this liquid poison. Additionally, there are no specific antidotes that reliably reverse GHB toxicity.7 Where patients are suspected of ingesting Bindeez toy beads (containing 1,4-BD), they should be observed in the ED for depressed level of consciousness. Patients who remain asymptomatic after 4 hours are unlikely to have ingested enough beads to cause toxicity and can be safely discharged from hospital. Patients developing symptoms should be managed in a similar way to those with GHB intoxication. Moderately intoxicated patients may be managed and observed in the coma position until awake, while patients with airway compromise or respiratory failure may require intubation and mechanical ventilation until toxicity resolves. The identification of these cases highlights the important role of poisons centres in toxicovigilance and monitoring of potential clusters of poisoning related to new pharmaceuticals and chemical agents. Rapid electronic communication of these cases to worldwide toxicological networks enables health authorities to make a risk assessment of similar toy products overseas. So far, this has resulted in identification of similar suspected cases of GHB poisoning in children and an international withdrawal of the product. Chinese authorities confirmed that toy beads from the Hong Kong manufacturer contained a substance which metabolised to GHB.8 Bindeez bead set “Make, spray and they stay! Bindeez are magic beads that you use to create colourful and fun designs. Just lay out your design in the special Bindeez tray, then spray them with water and your artwork will magically set in place!” (from an advertisement for the toy).

Naren Gunja MB BS, FACEM · Evelyn Doyle MB BCh, BAO, MRCPCH · Kevin Carpenter PhD, FHGSA · Olivia T Chan BSc, MB BS · Simon Gilmore BPharm, MRPSGB · Gary Browne MD, FRACP, FACEM · Andis Graudins PhD, FACEM, FACMT

Over a 6-month period, two patients presented to a community hospital emergency department with perforated gastric ulcers as the result of recreational misuse of over-the-counter ibuprofen–codeine preparations. Misuse of these medications appears to be an emerging cause of significant morbidity in patients with codeine addiction. Clinical recordsPatient 1A 39-year-old woman was referred by her general practitioner to the emergency department (ED) of our community hospital with a 24-hour history of acute epigastric pain. She had a past history of alcohol misuse, codeine misuse and pancreatitis. While in the ED, she described recreationally taking 16–24 Nurofen Plus tablets (Reckitt Benckiser, Sydney, NSW) (containing ibuprofen and codeine) per day for the previous 3 weeks. Clinical examination revealed pallor, mild diaphoresis, a heart rate of 130 beats/min and blood pressure of 92/60 mmHg. The patient’s abdomen was grossly distended and maximally tender on palpation in the epigastrium. Bowel sounds were absent. Intravenous access was established and infusion of 2 L crystalloid fluid was commenced. An erect chest x-ray confirmed the presence of gas under the diaphragm (Box 1). An urgent laparotomy revealed a perforated anterior gastric antrum ulcer and 2.6 L of green turbid fluid in the peritoneal cavity. The patient was given an additional four units of packed red cells intraoperatively, and her ulcer was oversewn. Postoperatively, she was transferred to an intensive care unit at another hospital. Patient 2A 41-year-old man presented to our ED with a 12-hour history of progressively worsening severe abdominal pain. The patient had been recreationally taking “a packet” of Nurofen Plus each day for the past year. To ease the abdominal pain, he had already tried a liquid paraffin-based laxative (Parachoc [Paedpharm, Sydney, NSW]) and an osmotic laxative (Microlax [Johnson & Johnson Pacific, Sydney, NSW] at home, with no relief of his discomfort. Clinical examination revealed generalised abdominal tenderness, with no guarding, and the presence of bowel sounds. He had a heart rate of 93 beats/min and blood pressure of 143/93 mmHg. The pain initially settled in the ED after the patient had received a total of 10 mg intravenous morphine over a 2-hour period. After admission for observation, he developed a slight fever (37.8°C), his heart rate increased to 120 beats/min, and his abdomen became increasingly distended. Pain recurred on the ward, and was not responsive to 20 mg intravenous morphine given over a 2-hour period. Intravenous contrast computed tomography revealed the presence of free fluid and gas in the peritoneal cavity (Box 2). An urgent laparotomy revealed a 1.5 cm gastric antrum ulcer with gross peritoneal contamination. Postoperatively, the patient was offered care at an inpatient drug and alcohol service, but absconded before transfer could be arranged. DiscussionIbuprofen–codeine preparations first entered the Australian over-the-counter (OTC) market in October 2002. The leading product in the market, Nurofen Plus, contains 200 mg ibuprofen and 12.8 mg codeine phosphate in each tablet,1 making it the strongest codeine tablet available in Australia without prescription. Codeine phosphate is a known drug of misuse. Ibuprofen–codeine products are particularly vulnerable to misuse because of the relatively high amount of codeine contained in each preparation and the absence of toxicity in overdose that is associated with paracetamol preparations. Several cases of severe hypokalaemia secondary to ibuprofen-induced renal tubule acidosis after Nurofen Plus misuse have been reported in the literature.2-4 One study showed that patients with acute upper gastrointestinal presentations were 5.2 times more likely to have consumed high-dose OTC non-aspirin non-steroidal anti-inflammatory drugs within the previous week, and the increased risk was dose-dependent.5 To our knowledge, the two cases described here are the first reports of perforated gastric ulcers associated with recreational Nurofen Plus misuse. The database of Australia’s Adverse Drug Reactions Advisory Committee (ADRAC) relies on voluntary reporting, and a drug’s adverse reaction profile becomes better defined as the market gains experience with it. As at July 2007, there had been 26 cases reported to ADRAC of adverse events in patients taking Nurofen Plus (Dr Patrick Purcell, Medical Officer, Adverse Drug Reactions Unit, Therapeutic Goods Administration, personal communication). ADRAC records show that Nurofen Plus was the sole suspected agent associated with two duodenal ulcer perforations. The first case involved a 28-year-old woman who took eight tablets a day “for a period of months” for back pain, and the second involved a 24-year-old woman for which there was no further clinical information. ADRAC has received no reports of perforated gastric ulcers associated with Nurofen Plus, and only one report of this condition in a patient taking an ibuprofen-only preparation. With only two patients presenting to our community hospital with perforated gastric ulcer in the past 6 months, the presentation is unusual. Misuse of ibuprofen–codeine analgesics, associated with both cases, appears to be a new and important aetiology for this condition. Vigilant reporting of adverse drug reactions to ADRAC, tighter enforcement of legislative requirements for the dispensing of pharmacy-only medicines, or reformulation of this product (as has occurred with OTC pseudoephedrine products) may help to minimise the health sequelae of ibuprofen–codeine misuse. 1 Erect portable chest x-ray of a 39-year-old woman with acute abdominal pain A = free air under the diaphragm. 2 Computed tomography image of the abdomen of a 41-year-old man with acute abdominal pain A = free air within the peritoneal cavity. F = free fluid within the peritoneal cavity. L = liver.

Martin J Dutch MB BS(Hons), BMedSci(Hons)

To the Editor: We report elevated mercury levels in three infants, each the only child of Chinese parents living in Sydney. All three children had eaten fish congee (a rice and fish porridge) as a weaning food and ate fish regularly as toddlers. Their parents had sought medical advice for either developmental delay or neurological symptoms in the children. A 2-year-old boy had demonstrated increasingly aggressive behaviour for the past 6 months. A general practitioner had diagnosed mercury poisoning in the boy’s father 2 months earlier, following investigation for complaints of allergies, rashes, abdominal pain and diarrhoea. The family ate fish (usually salmon, barramundi or snapper) at least five times a week, and had used unspecified herbal medicines in the past. The child had eaten fish regularly since weaning. The boy’s blood mercury level was 158 nmol/L (normal range [NR], < 50 nmol/L), a random urine mercury/creatinine (Hg/Cr) ratio was 9 nmol/mmol (NR, < 6 nmol/mmol*), and his hair mercury level was 1.42 mg% (NR, < 0.18 mg%). The boy’s father and mother (who was pregnant) also had elevated hair mercury levels, of 4.3 mg% and 6.0 mg%, respectively. The father and child were treated with chelation therapy elsewhere. * The two laboratories reported different normal ranges for the urine Hg/Cr ratio. A boy aged 2 years and 10 months presented with delayed speech and some autistic features. Since weaning, he had eaten fish (barramundi, sea perch, salmon and rock cod) up to eight times a week. He had no history of herbal medicine use, and his thyroid function, blood lead level, and a DNA screen for fragile X syndrome were normal. The child’s blood mercury level was 350 nmol/L and urine Hg/Cr ratio was 14 nmol/mmol (NR, < 10 nmol/mmol*). The boy’s father did not eat fish, and his blood mercury level was 19 nmol/L. The child’s mother did eat fish, and had a blood mercury level of 27 nmol/L. Two weeks after removing fish from the diet, the child’s blood mercury level had fallen to 99 nmol/L and his urine Hg/Cr ratio to 7 nmol/mmol. However, his behaviour did not improve, and he was subsequently diagnosed with classical autism. A 15-month-old boy presented with delayed development since birth. Fish had been introduced to his diet at 8 months of age, and he had since continued to consume fish four to five times a week. He had recently eaten either ling or salmon. The boy’s mother had consumed ling three to four times a week after the fifth month of her pregnancy. The child’s thyroid function, DNA screen for fragile X syndrome, chromosome karyotype, and urinary metabolic screen were normal. His blood mercury level was 143 nmol/L, but fell to 19 nmol/L over a period of 1 year after ceasing fish intake. His longer-term developmental status is unknown. Fish congee, made with either freshwater species or locally caught fish, is a common weaning food in coastal regions of southern China and South-East Asia.1 Adding fish to the weaning diet has health benefits,1,2 such as reducing anaemia, and is actively promoted. However, fish, particularly the large pelagic (open ocean) species more likely to be bought in Australia, may also contain mercury. Excessive consumption of mercury has been associated with neurological impairment.3-5 The Box shows that the consumption by infants of fish congee made from portions of large fish species may exceed the provisional tolerable weekly intake (PTWI)7 for methylmercury of 1.6 μg/kg bodyweight/week (the limit considered sufficient to protect a developing fetus). Food Standards Australia New Zealand’s most recent risk assessment concluded that median-level consumers of fish are unlikely to exceed the PTWI for methylmercury,6 but frequent consumers might if all their consumption is of predatory or long-lived fish species, which tend to acccumulate higher concentrations of mercury. It has been previously noted in the Journal that public health policy regarding fish consumption needs to balance the health benefits for cardiovascular disease and anaemia with the possible ill effects of mercury on neurological development in infants.8 We recommend that multilingual information about fish and mercury be made available to pregnant women and mothers, especially targeting groups who are likely to be frequent consumers of fish and who use fish in weaning and infant foods. Regulatory and health promotion activities could also be informed by surveillance of blood or hair mercury levels in infants from ethnic groups at high risk of mercury intoxication, and of the frequency of fish consumption in this age group (by type of fish). Estimated weekly mercury intake in infants consuming fish congee Mean mercury concentrations in fish tissue* (μg/kg fish) Child’s estimated weekly mercury intake† (μg/kg bodyweight/week) Fish fillets‡ Maximum 50 1.25 Median 16 0.40 Minimum 5 0.13 Barramundi Maximum 310 7.75 Minimum 40 1.00 Snapper Maximum 520 13.00 Minimum 52 1.05 * For species consumed in Australia.6 † For a 12-month-old child weighing 10 kg; weekly fish consumption is estimated to be 0.25 kg, assuming 50 g servings five times per week. Provisional tolerable weekly intake for methylmercury = 1.6 μg/kg bodyweight/week.7 ‡ Average concentrations of all fillets purchased.

Stephen J Corbett · Christopher C S Poon

To the Editor: Prostate cancer screening remains controversial. There is currently a lack of evidence that treating prostate cancers identified by screening leads to prolonged survival,1 and the main screening test (serum prostate-specific antigen [PSA] concentration) has poor sensitivity and specificity. Patients with an elevated PSA level usually undergo a transrectal ultrasound-guided (TRUS) prostate biopsy for definitive diagnosis. TRUS biopsy is associated with risks that include bleeding, urinary tract infections, prostatitis and bacteraemia. Infective complications can occur even when prophylactic antibiotics are administered.2 Gram-negative bacteraemia is usually associated with a mortality rate of at least 5%.3 We reviewed prostate biopsy-associated bacteraemia in Australian Capital Territory residents using data collected over the 5-year period from 2002 to 2006. All patients in ACT public hospitals who have positive blood culture results are followed as part of a bloodstream infection surveillance program. Although all prostate biopsies are performed in the private sector, nearly all patients who develop major complications are cared for in public hospitals. The number of biopsies performed on ACT residents during the study period was obtained from Medicare Benefits Schedule statistics (item numbers 37215, 37218 and 37219).4 Over the 5-year period, we identified 19 episodes of bacteraemia following 1843 prostate biopsies, representing a 1.0% risk of bacteraemia (95% CI, 0.6%–1.6%) (Box). No patients died, but five required admission to the intensive care unit. A 1% bacteraemia rate associated with prostate biopsies would be an underestimate of the true rate, for a number of reasons: some patients were also admitted with severe sepsis syndromes but with negative blood cultures; some patients may have been treated in another state; and some patients may have presented to private hospitals, specialists or general practitioners and been treated empirically without blood cultures being collected. Three additional cases of bacteraemia following TRUS biopsies were excluded from our rate calculations because they involved New South Wales residents. It has been estimated that, if a million men over 50 years of age were screened, about 110 000 would have raised PSA levels.5 Of these, about 90 000 would undergo a biopsy and 20 000 would be diagnosed with prostate cancer. Our data show that TRUS biopsies carry a risk of serious infective complications and, notably, about 75% of these complications would occur in men without prostate cancer. We believe that data on the likely complication rates resulting from PSA testing and TRUS biopsies must be factored into considerations of the benefits versus risks and the cost-effectiveness of any prostate cancer screening program. Prostate biopsies and associated bacteraemia episodes, Australian Capital Territory, 2002–2006* 2002 2003 2004 2005 2006 Total Prostate biopsies performed 322 324 465 377 355 1843 Bacteraemia episodes 6 3 2 4 4 19 Proportion of biopsies resulting in bacteraemia 1.9% 0.9% 0.4% 1.1% 1.1% 1.0% * Three New South Wales residents who were diagnosed and treated for bacteraemia in the ACT were excluded (two had biopsies in Sydney and one in the ACT). Two patients had two episodes of bacteraemia (each more than 1 month apart). Fifteen episodes of bacteraemia were caused by Escherichia coli and one each by Klebsiella pneumoniae, Group C Streptococcus, Citrobacter freundii and Proteus mirabilis.

Francis J Bowden · Jan Roberts · Peter J Collignon

To the Editor: The report by Risson and colleagues of a fatal case of necrotising pneumonia caused by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA)1 appropriately highlights the emerging issue of CA-MRSA infections in Australia,2 and the possibility that severe S. aureus sepsis may follow recurrent furunculosis. We wish to draw attention to the association between severe staphylococcal pneumonia and a preceding influenza-like illness. In September 2006, a 56-year-old woman of European background with a history of chronic back pain and depression presented to the Royal Darwin Hospital after a 4-day influenza-like illness characterised by cough, fever and sore throat. She then developed dyspnoea and pleuritic chest pain, followed by an abrupt respiratory deterioration. She was intubated and admitted to the intensive care unit with severe sepsis. A chest x-ray showed widespread bilateral pneumonia. We began broad-spectrum antibiotic therapy with piperacillin–tazobactam and azithromycin as per the hospital’s dry-season protocol for severe community-acquired pneumonia. Further history from her husband revealed an episode of boils 1 month previously, which responded to antibiotic therapy. We added vancomycin to the therapy and, when sputum and blood cultures showed MRSA 48 hours after admission, we also added rifampicin and gentamicin. On Day 5 of admission, her clinical condition deteriorated further and we replaced rifampicin and gentamicin with linezolid. Complement fixation testing of serum taken on admission showed an influenza A antibody titre of 128, consistent with recent acute infection. Despite ongoing intensive supportive care, the patient died from refractory respiratory failure 10 days after admission. Typing of the S. aureus isolates from blood and sputum showed that their single nucleotide polymorphism and variable gene profile was consistent with the Queensland clone (ST93-MRSA-IV) of CA-MRSA, and that the Panton–Valentine leukocidin gene was present. S. aureus has long been a recognised cause of influenza-associated pneumonia. Of concern, two recent reports from the United States identified 25 patients with CA-MRSA associated with severe pneumonia following influenza-like illnesses.3,4 Most of these patients were young (median age of 21 years3 and 17.8 years,4 respectively) and otherwise healthy. Combined mortality in these two studies was 40%. With an increasing prevalence of CA-MRSA in areas of Australia,2 CA-MRSA pneumonia should be suspected in patients presenting with worsening respiratory status and sepsis following an influenza-like illness. We stress the importance of annual influenza vaccination for those at increased risk of influenza-related complications.5

Steven Y C Tong · Nicholas M Anstey · Gary D Lum · Rachael A Lilliebridge · Dianne P Stephens · Bart J Currie

To the Editor: The recent editorial by Collignon and colleagues emphasised the importance of infection control mechanisms in reducing patient harm from antibiotic-resistant organisms.1 It focused on disinfection of the hands of health care workers in hospitals. However, a vigorous education and surveillance program in a hospital in Victoria failed to achieve compliance among health care workers of even 50%.2 Top of the list of self-reported factors leading to poor compliance is “skin irritation and dryness associated with the use of hand hygiene agents”.3 There have been no properly controlled trials, with clinically important endpoints, of currently recommended hand-hygiene practices. With the likely poor compliance rates, such trials would likely fail. A different approach might be more effective. Reducing skin contact between health care workers, patients and their immediate environment seems logical. Data show that skin contact produces two-step transfer of material in 82% of cases.4 The Victorian study did include gloving as an alternative to disinfection in measuring hand-hygiene compliance.2 However, in what might be a backward step, a recent study concluded that physicians should be encouraged to shake hands with patients!5 Perhaps an educational campaign to avoid skin contact with environmental surfaces and other health care workers, with use of disposable gloves for patient contact, could be the basis of a successful trial to address more effectively the transmission of antibiotic-resistant organisms in hospitals.

Keith V Woollard

To the Editor: The magnitude and distribution of the problem of health care-associated methicillin-resistant Staphylococcus aureus (MRSA) in Australia can be gauged from the report of a forum on MRSA control conducted at the Australasian Society for Infectious Diseases (ASID) in March 2007.1 This report contrasted approaches to control of health care-associated MRSA and quantified the population incidence rate of health care-associated MRSA bacteraemia across Australia from data derived from direct surveillance systems (Box). Reporting of MRSA infections is thought to be complete from all jurisdictions except Victoria and New South Wales. Figures for Victoria were extrapolated from accurate surveillance data representing 50%–60% of events. The degree of incompleteness of reporting in NSW could not be determined, and a range based on reports to NSW Health over 3 years was used. Overall morbidity of health care-associated MRSA in Australia is much higher, as only a minority of MRSA infections lead to bacteraemia. The ASID report estimated that between 699 and 924 cases of bacteraemia would be prevented if other states and territories reduced their incidence of MRSA bacteraemia to that of Western Australia through implementation of more stringent infection control measures. The mortality of MRSA bacteraemia is 8%–50% (average, 29%).2 A recent study showed that more than half (59%) of such deaths were directly attributable to MRSA3 rather than other non-infective causes. These outcome proportions provide a minimum estimate of between 120 and 158 preventable deaths per annum in Australia directly caused by health care-associated MRSA — comparable to the annual South Australian road toll. As identified recently in the Journal by Collignon and colleagues, there are significant structural barriers to achieving infection control — especially inadequate isolation resources and pressure on bed stock.4 Other dimensions of the MRSA problem include the high incidence of MRSA in many aged care facilities, the epidemic emergence of community strains of MRSA (best described in the recent report from WA on MRSA notification data up until 20025), the possibility of significant zoonotic reservoirs,6 and the role played by imprudent antibiotic use. MRSA colonisation or infection needs to be made a nationally notifiable disease, with a system in place to enable typing of isolates. As in WA, such a system would enable more effective identification of MRSA carriers before hospital admission, the detection of emerging epidemic strains, and timely investigation of MRSA outbreaks occurring in community groups, such as in aged care facilities. Most importantly, all states and territories need to adopt, and provide resources for, consistent, stringent approaches to surveillance, prevention and control of health care-associated MRSA that are in keeping with internationally recommended approaches. Given the scale of preventable injury occurring in many states, MRSA control must be made one of the highest priorities for patient safety. Relative burden of health care-associated MRSA morbidity across Australia1 Area Health care-associated MRSA bacteraemia events Year(s) of data Rate per 100 000 population Darwin 16 2006 13.3 New South Wales/ACT*† 437–602 2003–2005 6.2–8.5 Queensland* 133 2005 3.4 South Australia* 37 2006 2.4 Tasmania* 3 2006 0.6 Victoria*† 270–330 2000–2006 5.4–6.6 Western Australia* 22 2006 1.1 Total 918–1143 4.5–5.7 MRSA = methicillin-resistant Staphylococcus aureus. ACT = Australian Capital Territory. * Figures from these jurisdictions include private hospital event estimates. † Figures from NSW and Victoria are minimum estimates, because of incompleteness of current reporting in these states.

John K Ferguson · Helen Van Gessel

To the Editor: The recent editorial by Collignon and colleagues challenged Australian physicians and health care leaders to confront the rising burden of methicillin-resistant Staphylococcus aureus (MRSA).1 Compared with Australia, the United States has a bigger problem with MRSA; more than 60% of all hospital-acquired S. aureus infections are now caused by MRSA.2 Appropriately, the medical community has made an urgent call for action. For example, the Institute for Healthcare Improvement (a not-for-profit organisation based in the US that aims to improve health care throughout the world) incorporated specific MRSA prevention measures into its recent 5 Million Lives Campaign (see http://www.ihi.org/ihi). One of these prevention measures, a recommendation for active surveillance, has generated controversy. Specifically, the cost-effectiveness of this strategy is still vigorously debated in the infection control literature.3 At present, it is unclear what surveillance testing method should be used in the laboratory, and whether testing should be done for all patients or just those identified as high risk. The cry for help from community activists in the US and the United Kingdom has reached the ears of their legislative representatives. In two northern US states, lawmakers are considering bills that require universal active surveillance in their hospitals. Mandating resource-stretched health systems to implement obligatory active screening is not a prudent use of resources. The Society for Healthcare Epidemiology of America and the US Association for Professionals in Infection Control and Epidemiology recently published a joint position paper opposing this legislative activity, noting that data in support of active surveillance have been restricted to high-risk populations.4 We support this position and remind readers that active surveillance does not obviate the need for adherence to basic and consistent hand-hygiene practices. Complacency and lack of clinical leadership remain the greatest challenges in the efforts to reduce the transmission of MRSA. Why do we accept this epidemic as a fact of life as our health care workers complacently contribute to the nosocomial transmission of MRSA? By implementing simple prevention policies, feedback of data on nosocomial transmission of MRSA, and increased infection-control education, we have achieved a 22% reduction in MRSA infections in our network of community hospitals.5 Still, we acknowledge the absence of a zero-tolerance approach to failures in hand-hygiene practices. More needs to be done. We challenge our clinical leaders to demand higher standards for hand hygiene. Most cases of nosocomial MRSA transmission represent failures of basic hygiene practices. The problem is surmountable. Infection control is not a skill of a few, but the responsibility of every team member. The onus is on all of us.

Luke F Chen · Deverick J Anderson · Keith S Kaye · Daniel J Sexton

In reply: We thank Woollard for his comments on hand hygiene. While important, hand hygiene is just one component of what is needed to decrease the spread of methicillin-resistant Staphylococcus aureus (MRSA) in hospitals. Decontamination of the environment, contact precautions for colonised patients, active surveillance and screening, effective programs to prevent common infections such as intravascular catheter sepsis, good antibiotic stewardship and better hospital design are also indispensable.1 We do not accept that “There have been no properly controlled trials, with clinically important endpoints, of currently recommended hand-hygiene practices”. For instance, the recent study quoted by Woollard showed that hand hygiene reduced infections hospital-wide, using the clinically important endpoint of serious bloodstream infections (MRSA and antibiotic-resistant gram-negative bacteria).2 Thus, at least two large peer-reviewed studies show that alcohol-based hand-hygiene programs reduce hospital-acquired MRSA infections2,3 (Level III evidence4). There is nothing wrong with using disposable gloves, as suggested by Woollard, provided they are changed every time a health care worker moves between patients. Otherwise, gloves spread MRSA just as efficiently as unclean hands. Applying good-quality hand-hygiene products is less cumbersome than changing gloves and also allows direct human contact, which Woollard reminds us is important to patients. How MRSA is spread in hospitals is now well known — our problem is getting health care workers to remember to practise good hand hygiene all the time, every day, before and after every patient contact. The data shown by Ferguson and Van Gessel reaffirm how common and serious a problem we have with MRSA bacteraemia. They estimate there are about five episodes per 100 000 people annually across Australia. However, we believe that the true rate is double this. The rate of S. aureus bacteraemia (ie, MRSA and methicillin-sensitive S. aureus combined) in Australia is around 35 per 100 000 per year,5 with 27% caused by MRSA.5 This crudely translates to an MRSA rate of 9.5 per 100 000. The rates are probably much higher in the states with more health care-acquired MRSA (New South Wales and Victoria). More recent data suggest that 36% of hospital-acquired invasive S. aureus infections were caused by MRSA, with the highest percentages in NSW (41%) and Victoria (39%).6 It is also worth noting that, when MRSA bacteraemia became notifiable in England in 2001, there was a 50% increase in reported S. aureus bacteraemia episodes.1 This suggests that under-reporting is common in any voluntary reporting scheme, and is also likely for Australian data. Worryingly, Chen and colleagues point out that MRSA is an even bigger problem in the United States than in Australia. However, we are not far behind.6 Although we share their concerns about legislative impositions, some external controls and measurements can be an advantage. Western Australia, the only Australian state where MRSA is notifiable, has the lowest rates of health care-associated MRSA. While we do not want imposed “one size fits all” legislated controls, we do need change: the practice of the past 40 years has not worked. Every institution needs to have an effective MRSA control program, with components chosen according to the local situation. Institutions should measure MRSA and report centrally, especially if their rates are high and not falling continually (eg, over a year). Shop-floor quality improvement programs with empowered workers are much better than top-down management-imposed regulation (eg, from government). We need to shake our complacency and that of our health care colleagues, accept clinical leadership and take control. Otherwise, legislative controls will be imposed on us.

Peter J Collignon · M Lindsay Grayson · Paul D R Johnson

To the Editor: Xue and colleagues reported an interesting randomised, single-blind trial of acupuncture for persistent allergic rhinitis (PAR) and concluded that acupuncture is an effective treatment for this condition.1 I am not entirely sure that this is true. The authors state that “once needling sensation (known as de-qi) was obtained, the needles were manipulated . . .”. In the sham group they inserted needles at non-acupuncture points where, according to acupuncture theory, no de-qi can be elicited. Thus the intervention patients were experiencing de-qi, and the control patients were not. This means that neither the patients nor the therapist were blinded. Consequently, the difference in outcome between the two groups could be unrelated to acupuncture itself, and caused by patient expectation, therapist expectation or both. In addition, the statement of Xue et al that “no other randomised controlled trial of acupuncture in adults with PAR has been reported in the English medical literature”1 was misleading. Our review of this topic2 included no fewer than six randomised controlled trials, all either published in English or, in one case, with an English abstract. Interestingly, three of them suggested acupuncture to be effective, while three failed to do so. I fear that the study by Xue et al does little to resolve this intriguing discrepancy.

Edzard Ernst

In reply: Ernst is concerned about the sham acupuncture procedure used in our trial.1 Although not universally agreed, the sham/placebo control we adopted has been described as best practice.2,3 The assumption that, without de-qi, participants would not be blinded is not supported by the literature. In fact, a sham procedure without de-qi was used in a recent trial reported by Ernst and colleagues on acupuncture for subacute stroke rehabilitation.4 In that study, as in ours, to increase the credibility of blinding, participants with previous experience of acupuncture were excluded, and those assessing the outcomes of treatment were blinded. With regard to previous randomised controlled trials of acupuncture for adults with persistent allergic rhinitis in the English medical literature, Ernst failed to distinguish between seasonal allergic rhinitis (SAR) and persistent allergic rhinitis (PAR).5 Of the six studies included in his review,5 five were on SAR, and the sixth, which was cited in our report (reference 14), was on children with PAR. These reports, therefore, are not inconsistent with our findings.

Charlie C L Xue · David F Story

Sick to death. Hedley Thomas. Sydney: Allen & Unwin, 2007 (ix + 427 pp). ISBN 978 1 74114 881 7. Typically, journalists write readable books; even journalism textbooks are easy to follow. So it is with Hedley Thomas’ story of Bundaberg Hospital’s saga with Dr Jayant Patel. The journalist credited with publicly exposing the discredited surgeon (and more importantly, the terrible deficiencies of the Queensland public health system) leads us on a trail of discovery, ineptitude, political chicanery and tragedy. The tragedy lies with the patients who put their trust in both their local hospital and Patel, then Director of Surgery, a trust that was shattered and will take a generation to repair. There is a terrible poignancy in the level of personal harm suffered and documented in the book. The ineptitude is staggering: from the local hospital administration up to the highest levels of Queensland Health. In retrospect, how easy it would have been to avoid much of the scandal by conducting a proper investigation into Patel rather than trying to cover up the truth. Instead, here is a tale which harmed almost everyone who came in contact with it. Thomas chronicles rather than analyses as he exposes how a thriving department of surgery was destroyed by an appalling administrative culture and turned into Patel’s fiefdom. Thomas is mostly, but not always, accurate. He relies a little too much on National Party gossip instead of checking facts. Gastroenterologists would no doubt be astonished to learn that they are the most qualified practitioners to perform oesophagectomies, Patel’s signature procedure. At the end of 427 pages, one has to reflect on whether there are any winners. Many Bundaberg patients are still waiting for compensation, surgical waiting lists are no better, and institutional reform of Queensland Health is still required. Burdensome legislation makes medical registration and quality assurance in Queensland inefficient and insidious. There were no political winners, except, perhaps, the incumbent state government. Plus ça change, plus c’est la même chose...

David Molloy

The patient from hell: how I worked with my doctors to get the best of modern medicine and how you can too. Stephen H Schneider, with Janica Lane. Cambridge, Mass: Da Capo Press, 2006 (xix + 300 pp). ISBN 978 0 7382 1078 0. When Doug, the father of a patient of mine, handed me this book, I should not have been so worried. I am a paediatrician and practitioner of evidence-based medicine; reading this has triggered me to reflect on my own thought processes and practice. The book is written by world-renowned climate expert, Professor Stephen Schneider. He was diagnosed with a rare lymphoma in 2002 and chronicles his course, making astute observations on the processes surrounding his tests and treatments. He questions everything, suggesting changes to just about anyone who will listen. Schneider and his wife, both intelligent academics, gather information but also take responsibility for his disease and make health care professionals part of their team, rather than the other way around. When the data are absent, they challenge doctors to make decisions using decision analysis and Bayesian thinking tools (prompting me to re-examine notes from a course I took on decision analysis and to read more about Bayes’ theorem). There is much we can learn about the health care conveyor belt by taking the patient’s perspective. Paediatricians know that children with good advocates generally get the best out of health professionals, and other patients would probably benefit from good advocacy too. Schneider overstates it by calling himself a “patient from hell” — he is simply doing what he can to get the best out of the health care team. Every patient should attempt to do so, but not many could use Schneider’s approach. I wonder what the health consumer may feel reading it — perhaps intimidated if they can’t be as dogmatic and thorough as he is. Hence, this book is perhaps more valuable for health professionals than patients. I still don’t know what Doug was trying to say by lending me this book, but I’m glad he did. I commend this book to every doctor.

Rob Roseby

Circumcision revisited An Australian review article supports and reviews the perceived role of male circumcision as a protective mechanism against certain infections and diseases in both men and women. The paper gives an overview of the circumcision procedure and the possible benefits. According to the author, the positive outcomes of circumcision include protection from urinary tract infections, penile cancer, and sexually transmitted HIV, human papilloma virus and thrush. Bioessays 2007; 29: 1147-1158 No gain for pain Patients with acute low back pain do not appear to benefit from the addition of diclofenac and/or spinal manipulative therapy to recommended first-line care, according to an Australian study. A total of 240 participants with low back pain were allocated at random into four groups receiving combinations of diclofenac 50 mg twice daily, spinal manipulation, and placebo treatments. All patients had seen a general practitioner and had been given paracetamol. The primary outcome was time taken to recover from pain. Physiotherapists administered the spinal manipulation two or three times a week for a maximum of 4 weeks. Secondary outcomes included pain, function, and disability. Neither diclofenac nor spinal manipulative therapy appeared to show a clinically positive effect on the time taken to recovery. Patients taking active diclofenac and/or having active spinal manipulative therapy did not recover more quickly than those on the placebo forms of treatment. The researchers comment that, when appropriate baseline care is given, further treatments may not provide additional benefit. Lancet 2007; 370: 1638-1643 Obesity and breast cancer Increasing body mass index (BMI) and waist : hip ratio in women appear to be associated with an increased risk of breast cancer, say United States researchers. In a large study established in 1995, data on weight gain, diet, reproductive and menstrual history, and incidence of breast cancer from almost 100 000 postmenopausal women were analysed. Current BMI and waist : hip ratio were associated with an increased risk of breast cancer, as were the same parameters at 50 and 35 years. The risk was more pronounced in women not using menopausal hormone therapy. Weight gain between 18 years and the current age was also consistently associated with an increased breast cancer risk. Arch Intern Med 2007; 167: 2091-2102 The spoils of war Soldiers returning from service in Iraq have shown an alarming incidence of mental health problems on a second screening, according to United States Army re-searchers. On rescreening several months after return from deployment, soldiers reported significantly higher rates of mental health concerns including post-traumatic stress disorder, major depression, and alcohol misuse than when initially surveyed. Concerns about interpersonal conflict, as reported by participants, increased fourfold between the two surveys, which were conducted a median of 6 months apart. The authors advise that soldiers appear more likely to report mental health problems several months after their return from a war zone. JAMA 2007; 298: 2141-2148 Urinary retention — prognosis poor Men who suffer acute urinary retention and are admitted to hospital have a high mortality rate in the first year after discharge, a British study reports. All men aged over 45 years admitted with a first episode of acute urinary retention were included in the analysis, which examined comorbidities and mortality rates in the 176 046 participants. In men with both spontaneous and precipitated acute urinary retention, the mortality rate increased with age and was significantly higher than that of the general population. Overall, nearly 15% of men with spontaneous acute urinary retention died within a year. More than a third of men with acute urinary retention also had at least one major comorbid condition, which greatly increased mortality. The authors admit the possible selection bias introduced by using only hospital admissions, but comment that, regardless of that effect, this group of patients is vulnerable and should be carefully managed. BMJ Online, 8 Nov 2007

Tanya Grassi