Letters

To the Editor: A 77-year-old woman with a history of idiopathic long-QT syndrome (presumed genetic) presented to hospital with a storm of defibrillator shocks from her implantable cardioverter defibrillator (ICD). She had a single-chamber Guidant Ventak Prizm VR, model 1850, and a Guidant ventricular lead, model 0148 (Guidant Corporation, Indianapolis, Ind, USA) implanted 12 months earlier after an episode of syncope. The lead had been implanted by left subclavian venous access. The patient’s postoperative course and responses to routine questioning indicated that the device was functioning normally. After presenting with device discharges, a 12-lead electrocardiogram showed oversensing suggestive of lead dysfunction. Stored electrograms from the defibrillator showed artifactual signals that were typical of lead disruption. These signals had triggered inappropriate detection of ventricular arrhythmia and subsequent device shocks (Box 1). The pacing threshold and lead impedance were normal. On close examination of the patient’s chest x-ray, a line of radiolucency was detected within the lead between the first rib and clavicle. At reoperation, the lead was extracted with minimum difficulty and the site of the insulation break was detected (Box 2). A new lead was implanted and the patient was discharged home well. Subsequent follow-up was uneventful. Lead failure can occur any time after implantation of an ICD, and should be suspected when patients present with inappropriate ICD discharges.1 This case illustrates oversensing as a result of the lead’s insulation being disrupted by crush compression between the first rib and clavicle. Alternative implantation techniques, such as cephalic vein cut-down or extrathoracic axillary vein puncture, have been suggested for venous access to avoid this complication.2 1 Stored electrograms from the patient’s implantable cardioverter defibrillator showed artifactual signals had triggered inappropriate detection of ventricular arrhythmia and subsequent device shocks (arrow) 2 Implantable cardioverter defibrillator lead after extraction showing the break in the insulation (arrow)

Chin V Hiew · James W Leitch

To the Editor: Accidental ingestion of foreign bodies is common in children. Most pass through the gastrointestinal tract spontaneously,1 but some, such as magnets and batteries, can cause serious problems. We treated three children, aged 4–11 years, who ingested magnets that caused multiple bowel perforations. All three children presented with abdominal pain and vomiting, and were initially treated for gastroenteritis as the history of ingestion was not available. Plain abdominal films were subsequently used to make the diagnosis of foreign body ingestion. The ingested objects were later found to be pieces from magnetic construction toy sets. The first patient was an 11-year-old child with autism. An initial laparoscopy revealed marked dilatation of the small bowel and interloop adhesions. Subsequent laparotomy revealed several magnets (rods, rings and balls) in adjacent loops of the small bowel (Box, A), as well as necrosis and 13 perforations of the small bowel. Segmental resection was performed with a defunctioning ileostomy. During surgery, radiography was performed to ensure that all foreign bodies were removed before closure of the abdomen. The child made a good recovery, and the ileostomy was closed 3 weeks later. The second patient was 4 years of age. An abdominal x-ray revealed a cluster of foreign bodies in the right lower quadrant of the abdomen, with a small gap between the fourth and fifth foreign bodies. A laparoscopy revealed a cluster of magnetic rings (Box, B) perforating the small bowel and the caecum. Two of the rings were on the caecal side and four were on the small bowel side, with an intervening fold of mesentery — the gap on the x-ray. The magnets were retrieved through a minilaparotomy, and the caecal perforation was oversewn. The third patient was a 5-year-old who presented with similar symptoms and x-ray findings. Laparotomy revealed an area of pressure necrosis underlying the magnet and causing perforation of the jejunum, which was repaired by segmental resection and primary anastomosis. As ingestion of foreign bodies is usually not witnessed, a high index of suspicion is required for correct diagnosis.2 Of confirmed cases, 50% of patients remain asymptomatic.3 Fewer than 10% of cases require intervention, and about 1% require surgery.4,5 Ingestion of multiple magnetic objects in children is particularly serious, because of their tendency to aggregate in the bowel and compress intervening tissue, and should be treated aggressively. These cases demonstrate the harmful consequences of magnets in toys. More stringent regulations on the use of magnets in toys — especially in toys for children younger than 5 years — and measures to increase public awareness of this issue are needed. Clusters of ingested magnets in children A: Magnets in loops of the small bowel. B: Magnetic rings perforating the small bowel and caecum, showing intervening fold of mesentery and bowel wall (arrow).

Manjunath B Siddaiah-Subramanya · Peter Borzi

To the Editor: The recent case report by Chow and colleagues raises questions about the causal link between black cohosh use and hepatotoxicity.1 The authors state that the patient had no history of “significant alcohol consumption”, but a presumably related adverse drug reaction report available from the Therapeutic Goods Administration reveals her alcohol use was “3–4 units [of] alcohol per day, [with] 1–2 alcohol-free days per week”.2 Alcohol misuse is a known risk factor for severe liver disease, as is gastric bypass surgery for obesity,3 also in the patient’s history. Unfortunately, because histological examination of the liver 6 weeks after first presentation found no recognisable residual hepatocytes, the diagnoses of alcoholic steatohepatitis, non-alcoholic fatty liver disease and non-alcoholic steatohepatitis cannot be excluded. Without this, the specific conclusion of the liver biopsy that the “Massive hepatocellular necrosis [was] associated with herbal medication”2 cannot be substantiated. The patient “was not taking any other medications, including other herbal preparations”, but the use of multivitamins was disclosed,2 without further information on ingredients, indication, dosage and duration of use. Notably, an overdose of vitamin A can cause severe liver disease. Finally, discontinuation of black cohosh failed to reduce the patient’s bilirubin levels, suggesting ongoing liver cell destruction by the as-yet unknown agent. Chow et al state “Extensive investigations to exclude other causes of acute liver failure gave negative results”.1 It is unclear whether rare liver diseases were excluded, notably herpes infection, which has been reported to cause severe herpetic hepatitis. Nor was polymerase chain reaction testing performed for hepatitis viruses. The authors mentioned other published case reports of hepatotoxicity potentially linked with black cohosh.1 A recent assessment of 42 cases by the European Medicines Agency (EMEA) concluded that most were insufficiently documented, or were otherwise inappropriate for analysis.4 A case in the United States initially described as “probable” (> 1000% of the recommended dosage of black cohosh), based on the report that the patient “did not drink alcohol or use illicit drugs and was not taking any medications”, was later corrected.5 The patient testified under oath that she drank wine regularly and used other drugs, and a US court judged there was no evidence to establish that black cohosh had caused her liver disease.6 There is no apparent credible evidence that black cohosh caused liver failure in the patient described by Chow et al.1 A daily alcohol consumption of 30–40 g should be considered principally in any causality assessment. In addition, idiopathic reasons, rare or unclear liver diseases, and other medications should be considered as possible causes. Even in patients with liver disease who consume little or no alcohol and have no exposure to other toxic agents, the cause of the disease remains unclear in up to 30%. In view of this, reliable and sufficient reporting of adverse drug reactions is a necessary precondition to any reliable assessment of causality.7

Belal Naser · Eckehard Liske

To the Editor: The case reported by Chow and colleagues of liver failure associated with the use of black cohosh1 requires comment regarding causality. The case has also been the subject of an adverse drug reaction report by the Therapeutic Goods Administration (TGA), and a possible causality has been proposed.2 At presentation on 23 May 2006, the patient was aged 50 years (TGA),2 not 51 as stated by Chow et al.1 Her bodyweight was 88 kg (TGA)2 after gastric bypass for obesity.1 She had been taking black cohosh (20 mg daily) intermittently for 3 years. The subsequent temporal course is essential for assessing causality. According to the TGA report,2 the patient increased the dose of black cohosh to 40 mg daily on 31 March 2006 and stopped taking it on 31 May 2006. The case report describes a 2-month history of lethargy, nausea and arthralgia,1 obviously reported at first presentation. Back calculation shows symptom onset around 23 March 2006. Thus, symptoms emerged 1 week before the dose increase, suggesting a lack of temporal, and hence causal, association. The patient had several risk factors for severe liver disease.1 Risky use of alcohol for women is defined as more than seven standard drinks per week or more than three drinks on a single occasion.3 The patient had a daily intake of 3–4 units of alcohol, with 1–2 alcohol free days per week (reported by the TGA),2 rendering her at some risk of alcoholic liver disease. Moreover, gastric bypass with partial resection reduces gastric mucosal alcohol dehydrogenase and consequent gastric ethanol metabolism. In combination with rapid gastric passage of alcohol into the jejunum, this leads to high blood ethanol concentrations, another risk factor for liver disease. Risk factors for possible non-alcoholic steatohepatitis and cirrhosis are obesity and gastric bypass. Other causes were not excluded, including Wilson’s disease (by 24 h urinary copper measurement), hepatitis E, herpetic liver disease and infection by varicella zoster virus, parvovirus B19, parainfluenza virus, adenovirus and cytomegalovirus (by assessing for a change in IgG titre after disappearance of IgM). The marked hepatic mononuclear infiltrate is compatible with some viral infections. Certainly, various herbal products may cause liver disease. A good example is kava,4 but not black cohosh.5,6 The European Medicines Agency examined 42 cases of liver disease with a suspected association with black cohosh, and found that only four patients had some grades of causality.5 Reassessment showed that two of these patients had herpetic hepatitis, one had autoimmune hepatitis, and the fourth was not assessable.6 Further studies are necessary to show clearly whether black cohosh is potentially hepatotoxic.

Rolf Teschke

In reply: Teschke questions the temporal sequence in our reported case1 by raising an ambiguity in dates. We wish to clarify: when the patient first presented on 23 May 2006, lethargy, arthralgia and nausea had been present for only about 3 weeks. This was well after the dose increase in black cohosh in March 2006. As such, the dose escalation definitely preceded the patient’s symptoms and liver failure. To further explore causality would require rechallenge with black cohosh, which we consider dangerous and unethical. Other unlikely causes of liver failure raised by Teschke, although theoretically possible, were not evident. The clinical course and histological findings in the pretransplant biopsy and explanted liver categorically excluded alcoholic cirrhosis and non-alcoholic steatohepatitis as causes of the liver failure. We also reiterate that there was no previous history of liver disease or other medication use. Increasing numbers of case reports are being published showing evidence of hepatotoxicity in patients taking black cohosh. Two well documented cases of seriously deranged liver function in patients taking black cohosh, which resolved on ceasing its use, have just been reported.2 Teschke concedes that four other cases have been reported where some causality between black cohosh and hepatotoxicity was evident.3 Neither Teschke nor Naser and Liske offer any reassurance on the long-term safety or lack of toxicity of black cohosh by referencing any properly conducted safety study. Certainly, there is recent in-vitro and in-vivo evidence in a rat model that black cohosh is toxic to hepatocyte mitochondria and impairs oxidative phosphorylation, resulting in apoptotic hepatocyte death.4 It is notable that, based on available evidence, the Australian Therapeutic Goods Administration requires preparations containing black cohosh to carry a warning of potential liver toxicity, stating that “there appears to be an association between the use of black cohosh and liver damage, but that it is very rare”.5 Furthermore, in the United Kingdom, the Medicines and Healthcare Products Regulatory Agency stated, “Warnings regarding rare adverse reactions in the liver should be added to the product information for black cohosh for both licensed and unlicensed products”.6 Government authorities in Europe3 and Canada7 have raised similar concerns. Long-term studies as well as further animal studies would be welcome in this area.

Elizabeth C-Y Chow · Marcus Teo · John A Ring · John W Chen

To the Editor: The article by Eley and colleagues clearly articulates challenges and solutions for providing quality undergraduate medical education in rural locations.1 Simulation-based education (SBE) also helps meet the challenge of providing quality rural medical education. Simulation is an ethical means of supporting the development of technical and non-technical skills relevant for safe and competent clinical practice. SBE can be used creatively to prepare, supplement and enhance rural clinical placements. Simulation is often used to support learning of clinical events that occur infrequently, such as medical emergencies. These simulations are immersive, placing the clinician in a scenario that reflects the physical, psychological and social fidelity of a real work environment. Similarly, immersive simulations can be used to acquire competence in common examination and procedural skills. Hybrid simulations include combinations of simulators (eg, benchtop models) and actors (simulated patients) in quasi-clinical environments.2 Simulation facilities are increasingly available in rural locations. In Victoria, Gippsland Medical School has a simulation centre with a range of clinical environments including reception, consulting rooms, a fully equipped ward and an emergency room. We provide graduate-entry medical students with an opportunity to develop clinical skills in simulation, aligning scenario complexity, content and context with their learning in real clinical settings. Scenarios are often based on real patients’ experiences, exploring more than just the technical skills the student is learning. Preliminary evaluation suggests this sequencing of skills development, authentic scenario creation and immersive simulations for commonly occurring clinical encounters maximises learning in real clinical settings. We have had strong local community engagement, evidenced by the easy recruitment of simulated patients and support from medical practitioners who teach our students in clinical settings. We are exploring a range of simulated rural clinical placement activities for the remaining years of the curriculum. We believe this approach will relieve some pressure on clinical placements, as students are well prepared to learn in such settings. Additionally, clinical nurse educators have taken on teaching roles in the simulation centre, relieving pressure on medical practitioners. There are limitations to SBE. Specialist facilities are required, teachers and actors need to be trained, and curricula need to be developed and evaluated. However, our experience locally, and the rapid growth of SBE internationally, suggest that this approach to delivering high-quality medical education has relevance in all settings.

Debra F Nestel · Robyn A Hill · George T Somers · Christopher A Browne

To the Editor: We read with interest the article by Griffin and colleagues,1 which provides valuable insight into the practice effects of coaching on medical school selection tests. As senior clinical students, we have watched with more than a passing interest the introduction and growing popularity of coaching courses in recent years. What was once regarded as a costly, unnecessary and potentially disadvantageous exercise has, in recent years, given rise to a flourishing industry. As the authors point out, alternative selection tests such as the Undergraduate Medicine and Health Sciences Admission Test (UMAT) and entry interviews were devised in part to overcome the socioeconomic bias associated with using matriculation results alone.2,3 Ironically, these overpriced coaching courses are often available only to those from higher socioeconomic backgrounds, jeopardising the equity of access that the tests aimed to improve. At many independent high schools, in fact, attendance at coaching courses is now often the norm, in contrast to schools from lower socioeconomic backgrounds. Many students now opt to undertake coaching for fear of “missing out” on what may potentially be an edge obtained by other prospective students. It is the psychological comfort provided to students that they have done some preparation that marketers of coaching courses have been exploiting, as evidenced by the finding from the Australian Medical Students’ Association Medical Education Survey in 2006 that 70% of students felt better prepared for the UMAT as a result of coaching.4 In light of this, data provided by Griffin and colleagues thus provides welcome reassurance that expensive coaching courses may provide little or no benefit in relation to UMAT or interview outcomes. Although their study reported a slight increase in interview scores on the second attempt at entry to medical school, what was not discussed by the authors was the students who undertake coaching before resitting either an interview or the UMAT. While they mention that a proportion of students resit the UMAT, there was also no discussion on the effect of simply repeating the UMAT. Further analysis of the effects of repetition and coaching on candidates who resit the UMAT or interview would circumvent the limitation of directly comparing coached and non-coached groups that are unlikely to be equivalent, given that coaching is voluntary and may be linked with personality, ability and socioeconomic factors. It would be interesting to observe what effect, if any, coaching might have had on these candidates’ results. This might provide further evidence in support of the authors’ findings.

Christopher X J Wong · Ross L Roberts-Thomson

To the Editor: In addition to its well established link with rickets and osteoporosis, vitamin D deficiency has been associated with increased risk of autoimmune, malignant and cardiovascular disease.1 Marginal deficiency occurs at serum 25-hydroxyvitamin D [25(OH)D] levels of 25–50 nmol/L and frank deficiency at levels < 25 nmol/L,2 but there is some evidence that levels < 80 nmol/L3 or even < 110 nmol/L2 could be suboptimal. In Australia, vitamin D deficiency is most frequent in nursing home residents, dark-skinned veiled women, and residents of southern latitudes.2 However, those who are instructed to habitually minimise sun exposure following a diagnosis of skin cancer may also be at particular risk. We recruited patients with a history of non-melanoma skin cancer, who were not taking vitamin D or calcium supplements, from outpatient dermatology clinics at Royal Prince Alfred Hospital, Sydney (latitude, 33° south). Ethics approval was obtained from the Sydney South West Area Health Service and University of Sydney ethics committees, and all participants provided written informed consent. Serum 25(OH)D levels were measured by radioimmunoassay (DiaSorin, Saluggia, Italy)4 in both late summer (February 2006 or 2007) and late winter (August 2006), with participants completing a 2-week diary detailing daily sun exposure and sunscreen application before each measurement. Twenty-five participants (12 men, 13 women; mean age, 64 years; range, 44–78 years) completed both assessments. We found a significant reduction in mean 25(OH)D levels in winter (summer, 69 ± 3.4 nmol/L; winter, 59 ± 6.2 nmol/L; P < 0.05). In summer, all but one participant had 25(OH)D levels > 50 nmol/L, and eight had levels > 80 nmol/L. In winter, 12 participants had 25(OH)D levels < 50 nmol/L, two had levels < 25 nmol/L, and only three had levels > 80 nmol/L (Box). Hence, using the accepted target value of 50 nmol/L,2 12 participants (48%) were vitamin D-deficient at the end of winter, compared with one (4%) at the end of summer. In summer, the mean reported daily sun exposure was 1 hour (range, 10 min–2.5 h), comprising 40 minutes of off-peak (before 11 am or after 3 pm) and 20 minutes of peak exposure. In winter, the mean daily exposure was also 1 hour (range, 20 min–1.5 h), comprising 30 minutes each of both peak and off-peak sunlight. Volunteers reported wearing sunscreen during about 50% of their summer sun exposure and 27% of their winter sun exposure. Despite mean reported daily sun exposure falling within recommended guidelines, half of our participants were vitamin D-deficient at the end of winter, with almost all demonstrating reductions in winter 25(OH)D levels. Our findings suggest that vitamin D deficiency may be much more prevalent than expected in these patients, and that vitamin D supplementation might be indicated for this group, at least during winter. Vitamin D levels in summer and winter 25(OH)D = 25-hydroxyvitamin D.

Anna-Marie McCombie · Rebecca S Mason · Diona L Damian

To the Editor: I read with interest the article by Hardie and Critchley, in which the authors attempted to measure attitudes towards both Australia’s current health care system, and shifts to greater public or private funding of health care.1 The article’s finding that pro-public funding attitudes were greatly favoured over pro-private funding attitudes may in fact be more of a reflection of the leading nature of the authors’ pro-private statements than of the true attitudes of the 800 study participants. Most Australians, regardless of their views on public versus private funding of health care, would be unlikely to support the statements “Australia should adopt a private, user-pays system like they have in the [United States]” and “The very best health care should be available only to those who can afford it”.1 The results are certainly not consistent with the findings from the 2007 Ipsos Health Care and Insurance study2 — a survey with more than 5300 participants and a solid 20-year history, which is supported by governments (Commonwealth and state/territory), private providers and industry associations. This study found that just over half of respondents (52%) supported full government funding of Australia’s health care system, while 42% opposed such a funding approach. In fact, more than 20% of respondents “disagreed a lot” with the proposal that “All hospital and medical costs should be met out of government revenue — the taxes we all pay — people should not have to pay anything directly”.2 The Ipsos results suggest there is still significant diversity of views on how Australia’s health care system should be funded and, importantly, these results do not support the conclusion of Hardie and Critchley that Australians “overwhelmingly favour a more socially responsive public health system, funded by the public purse”.

Michael H Armitage

In reply: We are intrigued by the discrepancy between our findings1 and the 2007 Ipsos study results2 noted by Armitage. We took a psychometrically rigorous approach to measuring the public’s preference for health care systems. If our pro-private statements seem “leading”, then the pro-public statements (“Australia should adopt a collective social health system supported by higher taxes as is done in some Scandinavian countries”, “I would be willing to pay higher taxes to improve Australia’s health care services”) could be similarly construed. Armitage reports that 52% of the Ipsos sample supported (and 42% opposed) full public funding of health care. If we apply this support–oppose dichotomy (ie, per cent above and below the scale mid-point) to our own data, a striking 70% of our sample support (and 30% oppose) greater public funding, while just 7% support (and 93% oppose) more private funding. This is consistent with other Australian studies showing a preference for health and medical research being conducted in public, as opposed to private, settings.3-5 We cannot directly compare our methods and results with the Ipsos survey because, ironically, when we tried to access this research supported by “governments ... private providers and industry associations”, we were advised by Ipsos that the report is not publicly available.

Elizabeth A Hardie · Christine R Critchley

To the Editor: Arnold is correct to question whether the New South Wales reportable misconduct legislation will be effective,1 because it relies on doctors making a judgement about whether a colleague has flagrantly departed from accepted standards of professional practice. Doctors have a high threshold for referring to medical boards, in part because they perceive the system to be adversarial rather than recognising that individual and system factors can combine to create poor professional performance. Also, medical boards have no direct ability to modify the workplace circumstances to make them more supportive of a poorly performing doctor. Poor performance has multiple causes, including mental and physical illness, cognitive impairment, substance misuse, professional isolation, and personality disorders.2 Flagrantly poor performance is rare, but research shows that the prevalence of poor performance is about one in a hundred doctors per annum.2 Many of these doctors are amenable to local remediation, provided there are properly promulgated procedures. The United Kingdom and some states in the United States have developed systems for assessing poorly performing doctors that require directors of medical services to manage complaints locally. In the UK, the National Clinical Assessment Service is available to support medical directors in more complicated cases. Consequently, the number of referrals to the General Medical Council has decreased, but the number of doctors being reviewed has increased to the number that would be expected from research.3 Doctors reviewed by medical boards in Australia do not reach the predicted prevalence levels, and boards’ processes seem slow by comparison with what can be done locally. It is a moot point whether Dr Jayant Patel would have been reported under the new NSW legislation, because some of his colleagues appeared not to have thought that he flagrantly departed from accepted standards. The real problems in Bundaberg were that there were no local mechanisms for health professionals to raise their concerns. For almost 2 years, the director of medical services at the hospital took no direct action.4 Queensland Health is developing local processes that will be administered by directors of medical services supported by a clinical performance support service.5 The evidence against relying solely on medical boards and in favour of local procedures for managing poorly performing doctors is now incontrovertible. Currently, many poorly performing doctors are not being identified and offered remediation, and patients are being left at risk. These are important issues for the National Health and Hospitals Reform Commission.

James A Dunbar · Prasuna Reddy

In reply: The opinion expressed by Dunbar and Reddy that: “The real problems in Bundaberg were that there were no local mechanisms for health professionals to raise their concerns” ignores the many real difficulties (canvassed in my editorial)1 confronting any member of staff who tried to raise their concerns within that institution. Local mechanisms cannot play their part if the institution’s senior staff do not wish to implement them. The ability of and, indeed, encouragement for all staff, regardless of seniority, to report their concerns directly to the medical board, bypasses all local deterrents. Our medical boards have the experience needed to sort out the major from the trivial, the genuine from the frivolous, incompetence from impairment. Dunbar and Reddy continue: “The evidence against relying solely on medical boards and in favour of local procedures for managing poorly performing doctors is now incontrovertible.” This is a straw man. No one, to my knowledge, has made any such suggestion. What I support is: (i) a direct avenue for someone local to report to the medical board; (ii) diligent and sensitive enquiry by the medical board; and (iii) if needed, the cooperative implementation of remediation by the local entity and the medical board.

Peter C Arnold

To the Editor: A number of commentaries and articles have been published recently about the ability of doctors working in primary care skin cancer clinics to diagnose and manage skin cancer.1-3 However, limited information has been published comparing the patient populations that attend the different service providers (ie, “traditional” general practitioners versus doctors at skin cancer clinics). In 2005, we conducted a large population-based survey of Queensland residents aged 20–75 years to examine the prevalence of behavioural risk factors for cancer and current cancer screening practices.4 Using data from our study, we examined the prevalence of clinical skin examination and identified factors associated with choice of service provider. A total of 9419 respondents completed the interviews (response rate, 45.6%). Complete data for this analysis were available for 5499 of the respondents, of whom 48.2% were men. Thirty per cent of respondents reported they had had a general check of all or nearly all of their body in the previous 12 months. Factors associated with an increased likelihood of having a whole-body skin examination in the previous 12 months included being male (odds ratio [OR], 1.15 [95% CI, 1.00–1.31]), being 60–75 years of age (reference group, 20–39 years) (OR, 1.73 [95% CI, 1.45–2.07]) and having an annual gross income of ≥ $60 000 (reference group, < $20 000 annual gross income) (OR, 1.42 [95% CI, 1.18–1.71]). The strongest predictors were a self-reported history of melanoma (OR, 2.68 [95% CI, 2.01–3.57]) or non-melanoma skin cancer (OR, 2.01 [95% CI, 1.65–2.45]). No associations were seen between choice of service provider and any sociodemographic variables, including sex and age group. Additionally, skin cancer risk factors (such as having highly sensitive skin or a history of melanoma) did not make respondents any more or less likely to attend either a GP or a skin cancer clinic doctor. Various reasons were given by respondents for their choice of service provider (Box). Skin cancer clinics appeared to be chosen primarily because they offered bulk-billing or because respondents just wanted a general skin check. Traditional GPs were more likely to be chosen for convenience or because of concern about a specific spot or mole. Skin cancer is a major public health issue, and the provision of adequate and appropriate clinical services is a continuing and growing challenge. We found that a significant proportion of the Queensland population had undergone a whole-body skin examination by a doctor within the previous 12 months, and that those attending appeared to be the group most at risk of developing skin cancer. We did not find any significant differences in the profiles of those who chose a skin cancer clinic or a general practice for their skin examination. Reasons given for choice of service provider* by 2895 respondents who had had some type of skin check in the previous 12 months† * General practitioner or skin cancer clinic doctor. † Percentages do not total 100 due to multiple responses.

Philippa H Youl · Peter D Coxeter · David C Whiteman · Joanne F Aitken

To the Editor: Extended-spectrum-β-lactamases (ESBLs) are enzymes capable of hydrolysing penicillins, broad-spectrum cephalosporins and monobactams. Worldwide, ESBL-producing organisms are posing an increasing challenge for empirical antibiotic use and infection control. We recently carried out a review of microbiological isolates from clinical specimens taken from 2003 to 2007 at the Alfred Hospital, Melbourne. From 15 917 gram-negative bacilli, we identified 234 ESBL-producing organisms (1.5% of isolates) using double-disk synergy testing. Over the 5-year period, we noted three apparent changes in ESBL epidemiology relating to Escherichia coli isolates. First, E. coli became the most frequent organism in which ESBL production was observed, making up 55.6% of all ESBL-producing organisms in 2007 (up from 23.5% in 2003) (P = 0.03). Second, while the total number of E. coli isolates remained essentially constant over the study period, there was an increase in the proportion of E. coli isolates found to produce ESBLs: 1.8% of E. coli isolates in 2007 compared with 0.36% in 2003 (P < 0.001). The third and perhaps most striking change was in the epidemiology of ESBL-producing E. coli. In 2003, ESBL-producing E. coli infections were largely hospital-acquired, with 87.5% of isolates acquired after 48 hours in hospital or after a hospital admission in the previous 12 months. However, by 2007, ESBL-producing E. coli infections were found to be predominantly community-acquired, making up 62.2% of ESBL-producing E. coli isolates (P = 0.01). The increased proportion of community-acquired infections occurred despite a parallel increase in the frequency of hospital-acquired ESBL-producing E. coli infections (Box). Community-onset infections with ESBL-producing organisms have become increasingly recognised as important clinical entities.1 ESBL-producing E. coli bacteraemia is associated with higher mortality than bacteraemia caused by non-ESBL-producing organisms,2 a finding that has also been specifically demonstrated in the setting of community-acquired infections.3 Although local epidemiological data for infections with ESBL-producing organisms are not readily available, it appears that rates of community-associated infection vary greatly worldwide, with some regions of China reporting rates of ESBL-producing E. coli as high as 34% of all isolates.4 Although our study was limited by being a single-centre review, our findings are consistent with the emergence of multiresistant Enterobacteriaceae noted in Australian surveillance reports.5 It is not clear whether the change in our ESBL-producing isolates is reflective of local resistance patterns, or perhaps associated with travel to regions where ESBL-producing E. coli are known to be prevalent. Corroboration of these changes in other regions will be important for assessing the magnitude of this issue and responding appropriately, particularly in considering empirical antibiotic therapy for community-acquired gram-negative infections. Hospital-acquired (HA) versus community-acquired (CA) ESBL-producing E. coli isolates, Alfred Hospital, 2003–2007 E. coli = Escherichia coli. ESBL = extended-spectrum-β-lactamase.

Justin T Denholm · Michael Huysmans · Denis Spelman

To the Editor: Reported adverse reactions to food, which are common in many developed countries, can be produced by a wide variety of mechanisms. However, a low proportion of these are true food allergies.1 Recent Australian data show an increase in hospital presentations for food-induced anaphylaxis,2,3 but there are no Australian population data on the prevalence of either food allergies or adverse reactions to foods. Waiting lists for allergy services continue to remain long, and it is not known whether this is due to an increase in the prevalence of true food allergy or simply an increase in perceived food allergy. In October 2007, we undertook an Internet-based survey to assess the prevalence of self-reported perceived food allergies in Australian households. Participants were drawn from a consumer research panel of 8385 people (solicited through Internet-based marketing) who were proportionally representative of the Australian population with respect to age, sex and state. Cohort members were invited to participate in an Internet-based “health survey”, with no mention of food allergy during recruitment. Within 24 hours we had 1386 respondents and the required quota of participants was deemed to have been reached. Of the 1386 respondents, 406 (29.3%) reported at least one household member who believed he or she had a food allergy (Box). Of these, 250 (61.6%) reported at least one doctor-diagnosed allergy and 56 (13.8%) reported that the allergy was allergist-diagnosed. In addition, 42 respondents (3.0% of all respondents) reported that the person with the allergy had an EpiPen (Dey, LP, Napa, Calif, USA). Although there will be some selection bias in our sample because people without Internet access could not be sampled, we believe this bias is likely to be low, as at least 64% of the Australian population currently has home access to the Internet.4 Our questionnaire did not attempt to distinguish between true food allergy, sensitisation to foods, food intolerance or adverse reactions to food, although the majority of allergies had been diagnosed by a doctor or allergist, and foods such as peanut are more likely to be associated with allergies than intolerances. The high rate of perceived allergy to fruit and vegetables in an Australian context was surprising, although allergic reactions to fruit and vegetables are well documented.5 This may reflect either a rising prevalence of birch-pollen syndrome, as has been reported in Europe,6 or a community poorly informed about the true nature of food allergy reactions. Our data add to the evidence that there may be an increasing, largely unmet demand for health care information for patients with adverse reactions to food, including allergies. More formal evaluation should be undertaken to assess the type and prevalence of food allergy in the Australian context in order to facilitate future workforce planning and better community education. Proportion of Australian households in which at least one member believed they had a food allergy, and the individual foods nominated* Incidence of allergy (%) Food All households surveyed Households with perceived food allergy Cows milk 8.3 28.3 Peanut 6.9 23.4 Shellfish 5.9 20.2 Wheat 5.6 19.2 Fruit 5.3 20.9 Egg 3.4 11.6 Vegetables 2.7 6.7 Fish 2.5 8.4 Tree nuts 2.2 7.4 Soy 1.7 5.7 Other 6.3 21.4 * 40% had more than one food allergy.

Katrina J Allen · Jennifer J Koplin · Carmen Gould · Nicholas J Osborne

To the Editor: So a large proportion of women experience pelvic pain, often over years. What’s new? Of course they do. Pitts and colleagues1 fail to mention that virtually every normal, physiological event that occurs within a woman’s pelvis is associated with pain. Clearly, such pains vary in duration and intensity and are associated with events such as ovulation, menstruation, pregnancy, labour and childbirth. We men have it easy by comparison. But to conclude by saying that “only about a third of women who experience chronic pelvic pain seek advice from a health professional” gives the impression the authors are trying to medicalise yet another essentially normal event. One can get into long, philosophical discussions as to why such normal events should be so painful, but it remains a fact. I have spent my career urging general practitioners and fellow specialists to avoid surgery and “silver bullets” in most cases of pelvic pain and follow a conservative approach.2 It would have been more helpful if the authors had gone on to discuss what type of pain is suffered by what type of woman and who is treated by what type of doctor. This truly would have assisted in determining who would benefit from the attention of a health professional and who would not.

Jules S Black

To the Editor: We read the recent article by Pitts and colleagues1 with interest, given the rising trend of diagnosed chronic pelvic pain (CPP) in Australian women. The article identified three types of CPP, but did not differentiate pain into the two major categories of nociceptive (visceral and somatic) and neuropathic. In pain management settings it is considered essential, where possible, to make this differentiation, as it significantly alters management strategies, particularly in relation to medication. While the true incidence of neuropathic pain is unknown, it is believed to be underdiagnosed and inadequately treated. A 2008 French study based on a nationwide postal survey revealed a 6.9% prevalence of neuropathic pain in the general population, with 5.1% of respondents reporting pain levels as moderate to severe.2 Neuropathic pain results from damage to the nervous system. Specifically, this can be from damage to, or pathological changes in, the axons of peripheral nerves or from damage to the central nervous system, probably as a result of deafferentation. This is the process whereby neurones in the central nervous system lose their accustomed afferent input, either from a peripheral nerve or from an ascending sensory tract. Furthermore, neuropathic pain can and does cross neuroanatomical boundaries, often presenting viscerally as referred pain and eliciting pain descriptors such as burning, shooting, stabbing, and searing. For this reason, CPP is often wrongly assumed to be visceral in origin.3 In such cases, awareness that CPP may in fact be neuropathic may avoid inappropriate surgical interventions. Moreover, an association between CPP and neuropathy has been demonstrated in studies of sacral nerve and percutaneous tibial nerve stimulation in women presenting with CPP.4,5 Differential diagnosis of pain of neuropathic origin has been shown to be pertinent for the accurate implementation of pain management strategies.6 Therefore, we suggest that future studies on the epidemiology and/or prevalence of pain include tools to determine the proportion of pain of neuropathic, nociceptive and mixed origin. There are a number of tools available, including questionnaires such as painDETECT, DN4 (Douleur Neuropathique en 4), LANSS (Leeds Assessment of Neuropathic Symptoms and Signs) and NPS (Neuropathic Pain Scale). Some of these, such as the self-assessed LANSS (S-LANSS), do not require clinical examination and thus can be worked into population-based questionnaires. The ability to identify neuropathic pain should lead to individualised treatment, resulting in improved pain control for patients with CPP.

David Vivian · Adele Barnard

In reply: We are pleased to see our article about chronic pelvic pain in Australian women has provoked interest.1 Black’s suggestion that virtually every normal physiological event that occurs within a woman’s pelvis is associated with pain is surprising, and not supported by our evidence. Of the women in our sample, 23% were totally pain free, and most of the chronic pelvic pain reported was mild. A parallel study showed that men also suffered chronic pelvic pain — a smaller proportion than women, but still significant.2 We are not medicalising normal events; rather, we are alerting general practitioners to the normal range of pelvic pain experience to help them assess its clinical significance. A GP who says to a female patient “it’s normal, love, just grin and bear it” denies the psychosocial complexity of her experience. Vivian and Barnard suggest we might have differentiated between two major types of pain, nociceptive and neuropathic. It would not be practical to collect this information in a broad survey on sexual and reproductive health. Certainly, a study of the prevalence of neuropathic pain in the Australian population that mirrors recent studies overseas would be informative. However, our study concerned pelvic pain only. The pelvis is not a common site for neuropathic pain.3

Marian K Pitts · Jason A Ferris · Anthony M Smith · Julia M Shelley · Juliet Richters

To the Editor: With ageing and population growth, the number of people with disabilities is rising. By 2010, it is projected that 1.5 million Australians will have severe or profound limitations to core activity in the areas of self-care, mobility and/or communication.1 In 1976, the United Nations proclaimed that 1981 would be the International Year of Disabled Persons, with the aim of promoting the rights of all people with disabilities to participate fully in society and to enjoy living conditions equal to those of other citizens.2 Yet today, more than 30 years later, even in a country as affluent as Australia, families struggle to care for children with disabilities, ageing parents look after adult children, and middle-aged people have their lives put on hold while caring for partners or parents with disabilities. Every aspect of life is affected, including physical and psychological health, employment prospects, and the ability to take holidays and maintain social relationships. While the physical and emotional demands can never be underestimated, an added pressure is the huge financial impact on every family affected by disability. Homes are mortgaged, endless time is spent securing funds for essential equipment, and some individuals reluctantly share their plight with the media. The time is right to reform the disability sector. We need to shift from the current crisis-driven welfare approach to a planned and fully funded national disability insurance scheme (NDIS) that will underwrite sustained, significant, long-term improvements in meeting the needs of people with disabilities. The models for an NDIS already exist, with fully funded no-fault insurance schemes for people injured in the workplace and in car accidents in several states and territories. At a forum in October 2007, National Disability Services (the national industry association for disability services) supported the extension of coverage provided by road accident insurance schemes to new groups, a proposal that was endorsed at the recent Australia 2020 Summit.3 The NDIS could be funded from a number of sources, including a supplement to the Medicare levy, third-party car insurance or workplace insurance. The costs would be modest and the benefits significant, because an NDIS would be more equitable than current arrangements (whereby a few achieve multimillion-dollar payouts and many others in similar situations receive nothing), and would enable people with disabilities and their families to be in control, make choices and plan their lives with confidence.

Dinah S Reddihough · Bruce P Bonyhady

To the Editor: Impacts of alcohol consumption on health and wellbeing in remote Indigenous communities are well documented. In response, governments have applied supply and demand reduction programs, including the “Meeting Challenges, Making Choices” program, which has lowered the rate of serious injury. Although a pattern of heavy, episodic drinking has been documented, the nature of physical dependence in relation to acute alcohol withdrawal syndrome is uncertain. We report the results of sudden, temporary removal of alcohol in a small Indigenous community. In a remote Queensland Indigenous community (population, 1021) with one licensed premises, patterns of extreme drinking (30 standard drinks per session) are commonly seen around paydays. In 2008, the Queensland Government withdrew the sole liquor trading licence with 72 hours’ notice because of a breach of licensing laws. The licence was subsequently renewed after several months. During this time, there was no significant access to alternative (illegal) sources of alcohol within the community, as the prohibition against bringing alcohol into the community (initiated in 2003) was strictly enforced by police. Health services in this community comprised a primary health care centre (PHCC) with Queensland Health resident nursing staff, Royal Flying Doctor Service medical staff on weekdays (the principal doctor was S A M), and visiting specialists provided by both organisations, including a psychiatrist (E H). When the closure was being arranged, Queensland Government authorities requested that these health providers establish a process to treat any patients who developed acute alcohol withdrawal syndrome; this was monitored by S A M. Four weeks after the sudden cessation of alcohol availability, PHCC staff did not notice any outmigration of regular drinkers, and no patients presented with acute alcohol withdrawal syndrome. These findings are consistent with the anecdotal experience of E H, who has not encountered any cases of withdrawal delirium in this community over the past 16 years. By contrast, in recent years E H has observed several cases of withdrawal symptoms from cannabis use in this community, as seen previously in remote Northern Territory Indigenous communities.5 Our results suggest that people can develop physiological or psychological tolerance for heavy episodic drinking, which may be a function of adaptation to the intermittent nature of financial resources. This finding removes a potential health-related impediment preventing governments from considering sudden cessation of legal alcohol supply in these or similar environments.

Stephen A Margolis · Valmae A Ypinazar · Alan R Clough · Ernest Hunter

To the Editor: Urinary stones are very common, with a cumulative lifetime incidence of 5%–15% and a recurrence rate of about 50%.1 Many new treatment techniques have been developed, but availability, particularly in public hospitals, is variable. The Greater Metropolitan Clinical Taskforce2 assessed patterns of treatment in patients requiring urological consultation who presented to the emergency departments (EDs) of 12 New South Wales public teaching hospitals in major centres that had a specialty urology registrar. Between February and September 2007, the urology registrar or specialist completed a survey on consecutive patients presenting with urolithiasis who agreed to participate. The survey contained questions on patient demographics, the position and size of the stone, and the preferred treatment option. One of us (J W H M) conducted a telephone interview with each patient to obtain details of treatment, and follow-up interviews at 3-monthly intervals (until treatment was completed or the study ended) to determine the outcome. Ninety-two patients entered the study: 64 men (mean age, 50.4 years) and 26 women (mean age, 47.8 years) (sex was not reported for two patients). Thirty-seven patients were subsequently treated in the public system, and the remainder in the private system, either using private health insurance or at their own expense. The preferred treatment option of the treating medical officer, usually the urology registrar, was nominated: non-operative (spontaneous stone expulsion) with or without calcium-channel blockers, 13 patients (received by 6); rigid ureteroscopy with grasper or lithoclast, 21 patients (18); rigid ureteroscopy with laser, 4 patients (4); flexible ureteroscopy with laser, 17 patients (2); percutaneous nephrolithotomy, 3 patients (3); extracorporeal shock wave lithotripsy, 6 patients (2); or “other”, 28 patients — of whom stent was specified in 24 (23). The preferred treatment option was not used for 34% of patients because it was not available at the hospital. The mean duration of treatment (defined as the period between initial ED presentation and final treatment episode) for patients with pelvi-ureteric or upper ureteric stones requiring more than one treatment episode is shown in the Box. Thirty-nine patients had stents inserted in the ED, of whom four did not reach definitive management by the end of the study. Of the remaining 35, 20 were public patients and 15 were private patients. Fourteen had stents in situ for more than 3 months and required a change of stent before initiation of definitive treatment to avoid encrustation; 12 of these patients had treatment in the public system. Despite the relatively small number of participants in this study, its findings on access to timely treatment for public patients should not be ignored. Management of kidney stones was heavily influenced by insurance status. Ureteric stents are intended to be temporary, but patients treated in the public system who had a stent inserted at initial presentation had a 60% (12/20) chance of still having it 3 months later, thus requiring a change of stent before definitive intervention — an unnecessary procedure that increases hospital re-admissions. Patients would be treated more efficiently and effectively with more timely access to appropriate resources. This is an unacceptable burden of morbidity for patients. Urgent action is required to improve the current state of care for public patients with kidney stones in NSW. Duration of treatment of public and private patients with a pelvi-ureteric junction or upper ureteric stone who required more than one treatment episode* Public patients (n = 18) Private patients (n = 18) Mean duration of treatment in weeks (95% CI) 18.3 (12.9–23.7) 6.2 (3.0–9.4) Range (weeks) 3.0–49.5 0.6–25 Difference in weeks (95% CI) 12.1 (5.5–18.7) P < 0.001 * Up to four treatment episodes.

Finlay Macneil · James W H Macneil · Kylie L Fraser · Andrew J Brooks

To the Editor: The Australian Transport Council should be commended for approving the National Transport Commission’s revised road rules for the safety of children in motor vehicles.1 A key requirement is that children aged 4–7 years are to be restrained in an approved forward-facing child restraint or booster seat. It is expected that such changes, once enacted by states and territory governments, will result in fewer children being injured and killed. In a letter in the 4 August issue of the Journal, Zurynski and colleagues argued that these changes will bring Australian rules closer to — but nevertheless fall short of — overseas jurisdictions, where children up to 12 years of age or 145 cm in height must be restrained in booster seats.2 Notably, a wider selection of booster seats is available in these jurisdictions, including seats suitable for children weighing up to 36 kg. In contrast, the Australian/New Zealand Child Restraint Standard (AS/NZ 1754) stipulates that an “approved booster seat” is one that has a maximum design weight threshold of 26 kg.3 Mandatory consumer information notes that booster seats are “to be used only with lap-sash seatbelt or with a seatbelt and child harness for a child weighing from 14–26 kg”, and that they are not to be used if the child’s eye level is above the top of the booster back, or above the top of the car seat back or headrest when restrained in the booster seat.3 The matter of children exceeding the maximum weight threshold of 26 kg while failing to meet the transition height to adult seatbelts is far from trivial. Previous research published in the Journal found that about 50% of 7-year-olds whose height fell between 100 cm (the upper recommended height for child car seats) and 145 cm (the recommended seatbelt transition height) exceeded 26 kg, with only 27% having an age- and sex-adjusted body mass index > 25 kg/m2.4 Consequently, due to the current range of approved booster seats available in Australia, children may be placed at some unquantified risk in the event of a crash, as optimal protection above this weight threshold cannot be guaranteed. Further compounding this scenario is that pursuant to r266 of the Australian Road Rules, if a child “cannot safely be restrained as required . . . because of his or her height or weight”, the use of a seatbelt may be deemed acceptable.1 To avoid this scenario, it is essential that booster seats with a higher maximum weight threshold be made available in Australia as soon as practicable.

Michael P Fitzharris · Diana M Bowman

To the Editor: Despite expert recommendation, Australian states have yet to enact legislation requiring use of child restraints beyond the age of 12 months. Our analysis of police crash records and linked hospital separation data for the period July 2000 to June 2001 in New South Wales found that a large proportion of children who were hospitalised following motor vehicle accidents were reported by police as having used adult (standard) seatbelts at the time of injury (Box). It is of particular concern that over 80% of 5–8-year-olds in this cohort were using standard seatbelts rather than child restraints (eg, booster seats). This pattern of premature “graduation” to seatbelts has also been reported in general populations of child motor vehicle passengers both overseas1 and in Australia,2 and also in presentations of child motor vehicle passengers after a crash to a NSW hospital’s emergency department.3 Child restraints are specifically designed to provide crash protection for children’s anthropometrical dimensions. Standard seatbelts are not designed to accommodate children, so they are unlikely to achieve the good fit to rigid body parts required for safety. Consequently, use of standard seatbelts by young children allows more head excursion during a crash, thereby negating their primary goal of protecting against central nervous system injury, and potentially causing Chance fractures and abdominal injuries.4 Our results provide further evidence that such seatbelt use may not protect, or may even cause injuries, during a crash. Child road trauma is largely preventable or controllable with the use of appropriate child restraints, including booster seats. A cost–benefit analysis showed that the use of booster seats produced a benefit–cost ratio for road trauma prevention of 9.4 (US$1854/US$197).5 To prevent child road trauma in Australia, all child motor vehicle passengers should use appropriate child restraints. Australian child road safety stakeholders recommend that child motor vehicle passengers use appropriate restraint systems according to their height, weight and age when travelling on road. Our findings provide further justification for proposed legislative changes that would require the compulsory use of appropriate child restraints for child motor vehicle passengers. Child restraint use among children (0–8 years) hospitalised for injury after a motor vehicle accident, compared with that of the general population, New South Wales Hospitalised children* General population† Restraint use 0–4 years 5–8 years Total 0–4 years 5–8 years Total Child restraint 9 (22%) 0 9 (10%) 295 (94%) 70 (31%) 365 (68%) Adult seatbelt 11 (27%) 42 (82%) 53 (58%) 12 (4%) 153 (67%) 165 (31%) Unknown/ no restraint 21 (51%) 9 (18%) 30 (33%) 6 (2%) 4 (2%) 10 (2%) Total 41 (100%) 51 (100%) 92 (100%) 313 (100%) 227 (100%) 540 (100%) * Linked hospital and police data from July 2000 – June 2001 were accessed from the NSW Injury Risk Management Research Centre. Case selection is based on corresponding codes in the International Classification of Diseases, 10th revision, Australian modification, 2nd edition. † Based on a telephone survey conducted in NSW during 2005–2006.

Wei Du · Caroline F Finch · Lynne E Bilston

To the Editor: Samuel and colleagues’ article on the ethics of umbilical cord blood (UCB) banking1 reflects much of the misinformation and bias that bedevil this debate. They argue against storage of autologous stem cells from UCB for a variety of contradictory, paternalistic or ideologically driven reasons. The indication for autologous UCB storage is in anticipation of developments in regenerative medicine, an exciting field that holds great promise; it is not in anticipation of transplantation for malignancy, which is unlikely to occur. Samuel et al acknowledge these points, yet base their criticism of autologous storage on the latter indication. Next, they state that autologous stem cells can be easily harvested at any time in life. Perhaps, for use in transplantation; but cells obtained later in life are likely to be of little use in regenerative medicine. Capacity for in-vitro manipulation declines with age. Third, they argue that the two alternatives of public and private UCB storage are mutually incompatible — “public good or private benefit” (my emphasis). Australia’s three public banks are close to achieving the desired number of cords (about 20 000) needed for transplantation medicine in the non-Indigenous population.2 There is no shortage, and certainly no shortage of potential donors. Why argue against autologous storage as if there is? Fourth, the authors disapprove of the for-profit motive in private-sector medicine. That may be their ideological position, but it is paternalistic to impose that view on the rest of us. Can parents not make up their own minds on the value of autologous storage? At $2000 upfront and $150 a year, storage is not so expensive that “only a small proportion of the population are able to afford [it]”. I remind readers of media reports that the Australian Government’s Baby Bonus (now $5000) was often used to purchase luxury items such as flat-screen televisions rather than being spent on the baby’s needs.3 The authors are correct in one respect: some (but not all) private UCB banks have been deliberately deceptive and misleading in their marketing, and, in so doing, have been predatory and exploitative. However, it does not then follow that parents cannot access sound and sober health advice in the marketplace. The public versus private UCB storage debate does have an ethical dimension, but not this one. This debate is really just a turf war.

David E Roberts

In reply: Roberts asserts that we are biased, paternalistic and driven by an ideological objection to private umbilical cord blood (UCB) storage. While this is impressive rhetoric, it bears little resemblance to the points made in our article.1 Contrary to Roberts’ assertion, we do not object to private UCB storage. Our primary concern is that marketing campaigns make misleading or grandiose claims about the possible application of privately stored UCB in cancer care and regenerative medicine. For, although stem cell research does have great promise, it remains clinically unproven in the management of degenerative conditions. Offering hope of cure or amelioration of illness based on scientific speculation is enormously problematic, especially when directed at vulnerable parents concerned about their unborn child. While some private UCB banks take great care to avoid deliberate deception, many do not.2,3 We agree that parents should be able to decide for themselves how and if to store their child’s UCB, but they need accurate information to do so. Finally, Roberts asserts that there is no shortage of public UCB units or donors. In reality, there is a vast shortage of UCB units available to ethnic minority and Indigenous patients.4 North Caucasian donation also needs to be maintained, particularly as the impact of double-cord transplantation becomes apparent.4

Gabrielle N Samuel · Ian H Kerridge · Tracey A O’Brien