Child health

Re: “Respiratory syncytial virus infections in children in Alice Springs Hospital”, the letter to the Editor by Apakasimaka Dede, David Isaacs, Paul J Torzillo, John Wakerman, Rob Roseby, Rose Fahy, George Clothier, Andrew White and Paula Kitto, in the 18 February issue of the Journal (Med J Aust 2008; 188: 261). A processing error caused the ninth and final author, Paula Kitto, BSc, BM BS, General Practice Registrar at the Centre for Remote Health, Alice Springs, NT, to be omitted from the authors’ byline. The web version of the article was corrected on 10 March 2008.

Apakasimaka Dede · David Isaacs · Paul J Torzillo · John Wakerman · Rob Roseby · Rose Fahy · George Clothier · Andrew White · Paula Kitto

Objective: To examine the relationship between child weight and vehicle booster seat usage in the context of current Australasian booster seat standards.Design, setting and participants: Questionnaire survey conducted between February and April 2005. A convenience sample of parents with children aged 4–11 years in New South Wales and Victoria completed a questionnaire, reporting on the height and weight of their children and the nature of restraint devices used in the family vehicle.Main outcome measures: Proportion of children meeting standard-specified weight and height criteria who are not restrained in booster seats; proportion of children who meet the specified height criteria but whose weight exceeds the specified weight.Results: 699 of 3959 questionnaires were returned (response rate, 18%), of which seven lacked essential details. The remaining 692 responses provided information on 1500 children. Of these children, 633 aged 4–11 years fell within the recommended height range for using booster seats, but only 29% were typically restrained in booster seats, the majority (70%) being restrained in normal seatbelts. A key finding was that 37% of the children who met the recommended height criteria exceeded the maximum weight for booster seats stipulated by the current Australasian safety standard.Conclusion: In view of increasing rates of overweight and obesity in children, it is important to reassess current Australasian standards for child restraints in vehicles. A concerted parental education campaign is also needed to raise awareness of which restraint types are appropriate for children of various heights and weights.

Michael P Fitzharris BA, BSc(Hons), PhD · Judith Charlton BEd, MSc, PhD · Megan Bohensky BA, MPH · Sjaanie Koppel BAppSc(Hons), PhD · Brian Fildes BSc(Hons), PhD

In 2007, the National Health and Medical Research Council (NHMRC) released a revised National statement on ethical conduct in human research. Public submissions in the review process leading to the 2007 statement highlighted four main areas of concern: children’s competence to consent, mature minors and the requirement for parental consent, whether children can refuse to participate, and the provision of information to children. A useful addition to the statement is the concept of levels of maturity, which help determine whether a child or young person’s consent is necessary and/or sufficient for participation in research. Changes in terminology (“capacity” instead of “competence” and introduction of the term “vulnerability”) have the potential to create confusion, as the new terms are not clearly defined, and capacity is used in several senses.

Merle P Spriggs PhD · Lynn H Gillam PhD

To the Editor: The concerns expressed by Byard and colleagues about “safe-sleeping messages”1 are based on the assumption that bed-sharing (mother and baby sleeping on the same bed surface) is intrinsically dangerous. While some case–control studies have shown increased mortality for young (but not older) bed-sharing babies of non-smoking mothers, more detailed studies have found excess risk only among parents affected by alcohol, extreme overtiredness, overcrowded housing, or where the sleeping environment was unsuitable, including prone or side sleeping, heavy bedding, waterbeds and sofas.2 Epidemiological studies support the safety of bed-sharing. For example, in Hong Kong and mainland China, bed-sharing is very common, but rates of unexpected infant death are extremely low. This implicates aspects of Western lifestyle and sleeping practices — including the V-shaped pillows (tri-pillows) highlighted by Byard et al, other suffocation and entrapment hazards, and maternal smoking — rather than bed-sharing per se. Bed-sharing is also the evolutionary norm, providing many opportunities for “mutual regulation” of maternal–infant physiology, including body temperature, sleep cycle and breastfeeding.3 Modern bed-sharing mothers may appreciate the more restful sleep and easier breastfeeding. Overnight sleep laboratory studies of bed-sharing and solitary-sleeping mother–baby pairs show that bed-sharing mothers are very aware of their baby’s presence, even in deep sleep, and move to avoid overlaying. Bed-sharing babies breastfeed more frequently, but with equivalent total sleep for mother and baby.3 Researchers note the rarity of unsafe prone positions among breastfeeding, bed-sharing infants.3 Other studies have shown increased rates and duration of breastfeeding among bed-sharing mothers and infants.4 For these reasons, bed-sharing has become more popular in Western cultures, with an Australian survey in 2000 finding around 40% of young babies bed-sharing for at least part of the night.5 As with other aspects of care, it is our duty as health professionals to discuss the risks, benefits and practicalities of bed-sharing so that parents can make an informed and safe choice. The Royal Australasian College of Physicians comments, “Co-sleeping or bed-sharing is common and associated with increased breastfeeding rates, longer and more restful sleep, and a protective posture and synchrony of mother with baby . . . All parents should be informed about how to safely co-sleep with their infants”.6 Safe bed-sharing recommendations are available from websites such as the UNICEF UK Baby Friendly Initiative.7

Sarah J Buckley

In reply: Our position on bed-sharing was not based on the assumption that it is intrinsically dangerous, but that there is an increased risk of mortality for bed-sharing babies of “parents affected by alcohol, extreme overtiredness, overcrowded housing, or where the sleeping environment was unsuitable” (to quote Buckley). These risk factors were not mentioned by the telephone health advice line quoted in our letter,1 which rather commented that mortality in bed-sharing babies was such a rare event that the caller should not worry about it — little consolation if a fatality occurred. We agree completely that parents need to be able to “make an informed and safe choice”, but this also requires informing them of potential dangers — which did not happen. Also, we do not agree that mothers are always aware of the presence of their babies, as reports of accidental suffocation during breastfeeding in bed clearly demonstrate.2,3 An informed decision is made when all the information has been provided, not just information that supports a particular point of view. Curiously, Buckley’s final point is to recommend a website for safe bed-sharing advice4 that states quite clearly (with italics): “the safest place for a baby to sleep is in a cot by your bed”. We concur.

Roger W Byard · Glenda Cains · Helen Noblet · Maxine Weber

To the Editor: Little is known about the epidemiology of respiratory syncytial virus (RSV) in arid, desert regions generally, and in central Australia in particular. We performed a 5-year retrospective study from 2000 to 2004, inclusive, of children aged less than 2 years who were admitted to Alice Springs Hospital and identified as having RSV infection. RSV was detected using direct immunofluorescence (Light Diagnostics SimulFluor; Millipore, Billerica, Mass, USA) on nasopharyngeal secretions. The test has a reported sensitivity of 92%.1 We extracted demographic data from case notes and obtained population data from the Northern Territory Department of Health2 and the Australian Bureau of Statistics.3 From case notes over the 5 years, we identified 173 eligible children with RSV infection. The annual incidence rate was 21.4 per 1000 children under 2 years old. The rate in Aboriginal children was 30.9 per 1000, and the rate in non-Aboriginal children 11.6 per 1000 (P < 0.0001). The monthly distribution of cases is shown in the Box. Cases occurred throughout the year, and in every month, but there was a peak in admissions from March to August, which covers the Australian winter. Because Alice Springs Hospital is the only large hospital in the region, and almost all children needing hospital admission for RSV infection will be admitted there, our incidence rates of hospitalisation for RSV infection closely approximate population rates. However, we may have under-estimated the incidence because we only included children in hospital with proven infection, so we may have missed children who were not tested, or whose immunofluorescence test results were falsely negative. There may have been selection bias regarding admissions. Nevertheless, we found that Aboriginal children were more likely than non-Aboriginal children to be hospitalised with RSV infection, a finding in keeping with the known high incidence of pneumonia and bronchiectasis in Aboriginal children.4,5 While the incidence of RSV infection peaked in winter in central Australia, infections occurred throughout the year, and the winter predominance was less marked than is the case in temperate Australia.6 These data provide valuable information about RSV infection in an arid, desert region and can inform decisions about active or passive immunisation against RSV infection in central Australia. Monthly distribution of admissions to Alice Springs Hospital of children aged less than 2 years with respiratory syncytial virus, 2000–2004* * Inclusive.

Apakasimaka Dede · David Isaacs · Paul J Torzillo · John Wakerman · Rob Roseby · Rose Fahy · George Clothier · Andrew White · Paula Kitto

The need for stimulant treatment must be assessed regularly In a United States legal action in 2000 about educational neglect, Albany County judge G E Maney ordered the parents to resume administering methylphenidate to 7-year-old Kyle Carroll.1 At the time, this controversial ruling was understandable, because controlled trials of stimulant treatment (dexamphetamine and methylphenidate) for attention deficit hyperactivity disorder (ADHD) had consistently shown that stimulants reduce ADHD symptoms. The catch is that trials have examined short-term effectiveness (usually over less than 6 months), while ADHD is a chronic condition. In 1992, the US National Institute of Mental Health funded the Multimodal Treatment Study of Children with ADHD (MTA) to examine the long-term effects of routine community management versus carefully delivered treatments. Children with ADHD, combined type (that is, showing symptoms of inattention, impulsivity and hyperactivity), were randomly allocated to medication, psychosocial treatment, a combination of both, or standard community care. The medication group received treatment with methylphenidate in which an optimal dose was titrated, with blinding, to achieve maximum benefit. The psychosocial group received a variety of interventions that consisted of parent training, a summer treatment camp and classroom management. Those in the routine care group were given information about services and left to their own devices. In total, 579 children with a mean age of 8.5 years were randomly allocated to the four groups, about 145 in each. After 14 months, children in both the medication groups showed greater improvement than those in the behavioural treatment and community care groups, leading the authors to conclude that “carefully crafted medication management was superior to the behavioral treatment and to routine clinical care that included medication”.2 The results were influential in treatment guidelines3 and clinical practice. Participants were naturalistically followed up 1 and 2 years after the end of the trial. The results of the last follow-up (3 years from the onset of treatment), of 84% of the original sample of children (then aged 10–13 years), showed that none of the treatment groups differed on any of the five clinical and functional outcomes (parent- and teacher-rated ADHD and oppositional symptoms, reading achievement scores, social skills, and functional impairment).4 Also, there were no differences in substance use or delinquency, with the exception of a slightly lower rate of substance use among those in the psychosocial treatment group.5 While improvement had been steepest during the first 14 months (mostly in the methylphenidate group), this levelled off, and at 3 years, all groups showed a similar improvement; the methylphenidate group had not deteriorated but the other groups had caught up.4 Speculation is bound to follow these results, which have many ambiguities and nuances. For example, this follow-up was not part of the controlled trial and, as happens in practice, children switched on and off their medication over time in the various groups, with consequent difficulties for analysis and interpretation. The results highlight several issues. First, it suggests the Rolls-Royce model (medication plus psychosocial treatment involving the child, family, and school) is not more effective in the long run than any of the other treatments, including the often maligned community care. The combined treatment is seen as the ideal, but is rarely delivered in practice, because of high cost and the burden for parents and schools.6 Second, there seems to be a “growing out of” or developmental factor at work. Epidemiological7 and follow-up8 data have consistently reported a reduction in ADHD symptoms with increasing age — although some individuals continue to show problems. This is also consistent with findings that brains of children with ADHD, rather than developing abnormally (as in autism), mature later.9 The MTA did not include a placebo group, which might have led to the conclusion that regression to the mean or maturation itself were the reasons for improvement. If that was the case, it is possible that helping families and schools contain children’s ADHD behaviour during the middle and late primary school years with minimal interventions (eg, parent management training) may be enough for a proportion — but not all — of these children to get better, or for medication to be required mostly during this developmental period. Finally, the MTA confirmed that medication can cause retardation of growth, including weight, particularly during the first year of treatment.10 While results of one study rarely justify drastic changes of practice, the findings underscore the complexity of ADHD, show that stimulant drugs are far from being a silver bullet, and that there is much that we do not yet know. This does not mean that stimulants no longer have a place in the treatment of ADHD. However, that place has shrunk, and clinicians should be circumspect when assessing the need for ongoing treatment (eg, through medication breaks). Much needs to be done to clarify who benefits the most from medication, at what developmental point stimulants are most useful, and for how long they should be taken. It is also not known whether these results apply to the slow-release formulations (which may enhance adherence) and to atomoxetine (a non-stimulant drug with antidepressant activity, which is thought to act by inhibition of the presynaptic noradrenalin transporter). Parents, often caught in the bind of concerns about their children taking medication and fear of the consequences of not treating them, might be comforted by these findings. One wonders whether Judge Maney would have issued the same order to Kyle Carroll’s parents had he been aware of this information.

Joseph M Rey MB BS, PhD, FRANZCP

To the Editor: The growing problem of tuberculosis in resource-rich countries has been recently highlighted,1 with immigration thought to be an important contributor. To assess a possible increase in incidence, we performed a retrospective case record review of all children who had tuberculin skin tests or who were diagnosed with tuberculosis at The Children’s Hospital at Westmead for 3 years from 2004 to 2006. This period included the establishment of a refugee clinic in May 2005, which routinely tests refugees by tuberculin skin testing. We compared our findings with published data from 1982 to 1991.2 Latent tuberculosis infection was defined as tuberculin skin test induration of ≥ 10 mm (regardless of prior BCG vaccination) and a decision by the treating physician to start isoniazid monotherapy. Proven active tuberculosis disease was defined as a child with a positive isolate of Mycobacterium tuberculosis from culture or positive polymerase chain reaction for tuberculosis or positive tuberculin skin test in association with a clinical picture strongly suggestive of active tuberculosis disease. The number of tuberculin skin tests performed increased through the study period (Box 1), largely because the refugee clinic saw 90 new patients in 2005 and 150 in 2006. The proportion of children with an increased induration response increased over the study period (Box 1 and Box 2). We observed an increase in latent tuberculosis infection, both in absolute numbers and in the proportion of the total caseload. The absolute number, but not the proportion, of cases of active tuberculosis disease increased during the study period. Over the same period, hospital admissions remained static at about 26 000 per year. Extrapulmonary tuberculosis was present in 12 of 23 patients (52%) with active tuberculosis, compared with 34% in the earlier study.2 There was no increase in tuberculosis meningitis. The active tuberculosis cohort ethnicity was consistent with the earlier study, with 22 of 23 patients of non-European origin, and 18 born outside Australia. The predominant ethnic groups were from Africa (eight, all born outside Australia) and the Indian subcontinent (four, two born outside Australia). Our finding of an increase in the proportion of patients with latent tuberculosis infection but not active tuberculosis disease is largely due to increased testing of refugees. It is reassuring that we did not find active tuberculosis. The United Kingdom has reported an increased incidence of tuberculosis in African immigrants.1,3 Australian immigration trends have shown a demographic shift, with increasing numbers of refugees from Africa.4 Although our study is likely to suffer from referral bias, it is the largest review of paediatric tuberculosis from a tertiary centre in Australia. Children very rarely transmit tuberculosis, but it is important to identify and treat latent tuberculosis to prevent progression to active disease.5 We believe our results are encouraging in showing a low incidence of active tuberculosis and indicate the need to screen refugees for latent tuberculosis to direct chemoprophylaxis. 1 Comparison data on tuberculosis among children, 2004–2006 Year Total TSTs performed Results available > 10 mm > 15 mm No. of patients commenced on isoniazid No. with active TB disease No Yes No Yes 2004 116 111 104 7 108 3 5 4 2005 257 247 202 45* 221 26* 25 8 2006 278 263 193 70* 215 48* 36 11 TST = tuberculin skin test. TB = tuberculosis. * P < 0.01 compared with previous year. The discrepancy between the total numbers performed and the cumulative numbers in the categorisation of response is due to patients not returning to have the TST read. 2 Results categorised by size of tuberculin skin test induration

Paul D Robinson · Dianne Dalton · Terri Cripps · Nicholas J Wood · Alison M Kesson · David Isaacs

Three types of infant formula (soy, extensively hydrolysed and amino acid) may be appropriate for treating cows milk protein allergy. Selection of a formula depends on the allergy syndrome to be treated. Extensively hydrolysed formula is recommended as first choice for infants under 6 months of age for treating immediate cows milk allergy (non-anaphylactic), food protein-induced enterocolitis syndrome, atopic eczema, gastrointestinal symptoms and food protein-induced proctocolitis. Soy formula is recommended as first choice for infants over 6 months of age with immediate food reactions, and for those with gastrointestinal symptoms or atopic dermatitis in the absence of failure to thrive. Amino acid formula is recommended as first choice in anaphylaxis and eosinophilic oesophagitis. If treatment with the initial formula is not successful, use of an alternative formula is recommended.

Andrew S Kemp PhD, FRACP · David J Hill FRACP · Katrina J Allen FRACP, PhD · Kym Anderson FRACP · Geoffrey P Davidson FRACP · Andrew S Day MD, FRACP · Ralph G Heine MB ChB · Jane E Peake FRACP, DTM · Susan L Prescott BMedSc, PhD, FRACP · Albert W Shugg DCH, FRACGP, FRACP · John K Sinn MMed(ClinEpi), FRACP

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

A number of recent studies have allayed fears about antidepressants precipitating suicidal behaviour in young people. Indeed, antidepressants appear to be conspicuous by their absence of use in young people who die by suicide. Furthermore, there is concern that the reduced prescribing of antidepressants to young people may be associated with an increase in youth suicide in the United States. Although not first-line treatment, antidepressants should not be denied young people if psychosocial and cognitive behavioural therapies are not effective for major depression.

Robert D Goldney MD, FRANZCP, FRCPsych

Re: “Overweight and obesity from childhood to adulthood: a follow-up of participants in the 1985 Australian Schools Health and Fitness Survey”, the letter by Alison J Venn, Russell J Thomson, Michael D Schmidt, Verity J Cleland, Beverley A Curry, Hanni C Gennat and Terence Dwyer, in the 3 September issue of the Journal (Med J Aust 2007; 187: 314-315). The Box showing the distribution of body mass index values for men and women in three different age groups showed two identical graphs of the data for men. The graphs were clearly different in the original submission, but the data supplied were incorrect. The correct graphs are shown here. Distribution of body mass index values for men and women in three different age groups* * 24–27 years, 757 men and 854 women; 28–30 years, 767 men and 807 women; and 31–34 years, 673 men and 691 women in the 20-year follow-up of the 1985 Australian School Health and Fitness Survey.

Alison J Venn · Russell J Thomson · Michael D Schmidt · Verity J Cleland · Beverley A Curry · Hanni C Gennat · Terence Dwyer

To the Editor: In recent years, there has been an increase in the use of highly mobile three-wheel strollers that facilitate parental activities such as jogging. Unfortunately, the very design feature that enables fast transit over uneven ground also makes it possible for unsupervised strollers to move rapidly into situations that may be highly dangerous. Within the past year in South Australia there have been two separate incidents where infants, one aged 5 months and the other aged 10 months, died after being immersed in the Torrens River. They had both been strapped into three-wheel strollers. In both instances, carers, who had been walking or jogging in the park along the banks of the river, were momentarily distracted — one by a mobile phone call and the other while attempting to use a plastic bag dispenser. The strollers had not had their front wheels locked or their brakes engaged, or been attached to the carers by wrist straps and so were unrestrained, enabling them to roll rapidly forwards into the water. Police re-enactments confirmed the scenarios described by the carers. While three-wheel strollers have safety features, such as brakes and sometimes wrist straps, these are not always used. Although consumer organisations have listed a series of recommendations for users of these strollers, this advice is not always being followed. The recommendations include never leaving a child unattended in one of these strollers, always using a wrist safety strap, always engaging the brake when stationary, and locking the front wheel when jogging to prevent swivelling. In addition, specific warnings are issued about stopping on slopes, being distracted by mobile phone calls, and being particularly careful near water, roads and railway lines.1 Drowning of infants and toddlers in rivers is an uncommon event, with only two cases documented of a total 32 drowning deaths of children under the age of 2 years in South Australia over the 35 years from 1963 to 1998 (rate, 6.25%).2 Thus, the occurrence of two drowning deaths within 4 months associated with three-wheel stroller use in parks next to a river is of concern. While mandatory requirements for safety devices such as parking brakes and tether straps will take effect on 1 July 2008,3 this legislation will have little effect if the devices are not used. Parents and carers must be made aware that infants or toddlers in three-wheel strollers near water are at risk of immersion and drowning. Such warnings should be clearly specified on these products.

Roger W Byard · Neil Matthews

Objective: To analyse changes in the incidence of injuries requiring hospitalisation for child passengers in motor vehicle crashes.Design, setting and participants: Population-based study of children (aged 0 –15 years) residing in New South Wales and admitted to hospital for injuries resulting from a traffic crash in the period 1 July 1998 – 30 June 2005, identified from the NSW Inpatient Statistics Collection.Main outcome measures: Age-standardised rates of hospitalisation for injuries, and trends by inpatient demographics, severity of injuries, and injury sites and types.Results: 2297 children were hospitalised for injuries sustained in a motor vehicle crash over the study period. The overall hospitalisation rate for injuries was relatively constant, with a non-significant decline of − 0.4% (95% CI, − 3.1% to 2.3%). The rate of hospitalisation for serious injuries also declined non-significantly (− 5.5% [95% CI, −11.8% to 1.1%]). Only hospitalisation rates for traumatic brain injuries declined significantly (−11.1% [95% CI, −19.0% to − 2.8%]) over the study period.Conclusion: The rate of hospitalisation for injuries to NSW-resident child motor vehicle passengers due to traffic crashes has not significantly decreased. High hospitalisation rates and the subsequent burden to the community and public health system make further injury prevention efforts for child motor vehicle passengers a priority.

Wei Du MPH · Caroline F Finch PhD · Andrew Hayen PhD · Julie Hatfield PhD

To the Editor: The recent editorial by Ring and Wenitong1 about interventions to prevent child abuse in the Northern Territory highlights the importance of treating the causes as well as the symptoms. This is true not only for children in remote Aboriginal communities, but for all children across Australia. Child abuse and neglect is not a “new” national emergency. In 1966, Bialestock2 wrote in the Journal: This situation should be considered as a national emergency as lethal to the lives of potential Australians as is a war. Immediate allocations of revenue to prevent this situation should be made if the[se children] . . . are to be allowed to grow into adults able to live in dignity and to work to contribute to our economy. We must not sentence these children to a lifelong need for State support. There are no reliable prevalence data, but Australian Institute of Health and Welfare data indicate that there were 266 745 notifications of suspected child abuse and neglect in Australia last year, double the number 6 years ago. About one in five of these notifications were “substantiated”. Over 25 000 children are in state care at any one time, an 82% increase in the past decade.3 Our child protection systems are at risk of imploding under the strain. These systems are also potentially dangerous, with high levels of multiple placements contributing to the very high prevalence of mental health problems among children in care.4 The contributory factors are well known. Children with disabilities, chronic health problems, difficult temperaments and externalising behaviours, families where there is domestic violence and parental mental health or substance misuse, and communities characterised by poverty, unemployment, higher residential mobility, and a low adult to child ratio are at much greater risk. We must close the gap between what we know and what we do. A public health approach is needed to reduce the risk factors, using population-based measures of child abuse and neglect, and tapping the potential of universal health, welfare and education services as platforms for primary and secondary prevention. In relation to health services, the adequate provision of universal maternal and child health services, including sustained nurse home-visiting programs, is vital. General practitioners and mental health and drug treatment services using child-sensitive and family-centred approaches also have a major role to play. These interventions have also been shown to improve overall outcomes for children in education, health, and social and economic participation. Hence, economists have suggested that they are the most cost-effective intervention for a nation.5 Now is the time to ask whether governments are really serious about preventing child abuse and neglect.

Fiona J Stanley · Dorothy A Scott · Melissa O’Donnell

To the Editor: A recent editorial in the Journal suggested that blood could be sent overseas for genetic testing for maturity onset diabetes of the young (MODY).1 We are pleased to be able to point out that genetic testing, including clinical and laboratory support with full gene sequencing for both MODY1 and MODY3 and for neonatal diabetes (mutations in SUR1 and Kir6.2), is available in Australia. Testing for MODY2 and for a number of other disorders of the pituitary–adrenal and pituitary–gonadal axis in children is also available. We are happy to receive specimens and referrals from clinicians who would prefer to use an Australian clinical laboratory accredited by the National Association of Testing Authorities. More information is available via: http://www.mater.org.au/Home/Services/Pathology.aspx.

Mark F Harris · Ivan N McGown · David M Cowley

Significant similarities between the challenges of lung transplantation in patients of all ages should lead to better access to this life-saving surgery for children and adolescents Lung transplantation (LTx) is firmly established as a therapy for end-stage lung and pulmonary vascular diseases in patients aged over 18 years and into the seventh decade of life.1,2 However, for those under the age of 18, be they child or adolescent, the role of LTx is less clear.3,4 In Australia, this has contributed to a perception that the risk of undertaking LTx in children and adolescents does not warrant the reward. Indeed, presently in this country, there is no major paediatric hospital offering a lung transplant program, likely recognising the complexity of treating such patients coupled with the potential risk of achieving poor results with a low case load — the reality is that the projected case numbers will only be of the order of four to eight per year across Australia and New Zealand. Thus, by focusing on successful LTx outcomes for an adolescent population, the article by Morton and colleagues in this issue of the Journal5 highlights a number of the key issues regarding the efficacy and utility of LTx for younger Australians (→ Successful lung transplantation for adolescents at a hospital for adults). Although adolescence refers to a transitional state from childhood to adulthood, patients 15 years and younger are generally excluded from adult hospitals and those 18 years and above excluded from paediatric hospitals. Two-thirds of the patients in the study by Morton et al could have been “routinely” treated in adult hospitals. Notwithstanding this limitation, the report gives important insight into the issues, experience and successful outcomes that can be achieved in younger lung transplant recipients. From this article, it is apparent that in Australia, a well developed, large adult LTx unit is able to use its highly specialised services to overcome some of the problems and deficiencies that can limit a stand-alone service for such a small population as children and adolescents requiring LTx. However, the age of any potential Australian lung transplant recipient is critically important — at this time, this technology is not being routinely offered to younger children. Indeed, at present, Australia’s youngest ever lung transplant recipient was aged 9 years at the time of LTx.6 The improved outcomes for LTx now described in adolescents5 should provide an impetus to provide access for younger potential LTx recipients. In looking to achieve this advance, we need to keep in mind that the transplant recipient’s age can matter in several different ways. Fortunately, severe lung disease warranting consideration of LTx in children and adolescents is relatively rare, although interestingly, it does have a bimodal distribution. The International Society for Heart and Lung Transplant (ISHLT) Registry 2005 paediatric report notes about 65 procedures performed worldwide each year.7 In older paediatric patients, typically over 12 years of age, about 70% will have cystic fibrosis as the primary indication for LTx, whereas in infants aged less than 3 years, the indication in about 60% is congenital heart disease or pulmonary hypertension. Despite the perception that transplant recipients fare worse if they are younger, the recent ISHLT Registry reports a half-life of around 5 years after LTx, and no significant survival difference between adults, adolescents and the very young.7 Rates of early graft dysfunction and late graft dysfunction (ie, bronchiolitis obliterans syndrome [BOS]) are also similar. However, causes of death are quite different, with adults and adolescents dying from respiratory failure related to BOS, and younger children dying from infection. The functional status of survivors is excellent, with over 80% reporting no activity limitations at 5 years,7 although morbidity related to the obligatory immunosuppressant drugs is very common across all age groups. Further, there are some specific issues (medical, psychosocial and legal) associated with LTx in adolescents and children compared with adults. Post-transplant lymphoproliferative disorders, growth retardation, respiratory tract infections and medical non-adherence appear much more commonly in children.8 As discussed by Morton and colleagues, facilitating compliance with therapies and medication are particularly challenging areas when working with adolescents.5 As an example, immunosuppressive protocols need to reflect potential concerns about physical appearance. Also, a particular “at risk” period arises when paediatric LTx recipients transition from paediatric to adult care.9 Performing major surgery with substantial short-term and long-term mortality risks in a patient unable to give consent presents ethical and legal dilemmas. For paediatric patients with severe lung disease, recent technological advances provide the potential to build on the excellent results of LTx in adolescents presented by Morton et al.5 Minimal waiting list mortality is a critical component of any assessment of the efficacy and utility of organ transplantation. Thus, the management of severe lung disease by experienced teams, with appropriate use of newer therapies such as bi-level positive airway pressure (BiPAP), dornase alfa and azithromycin in patients with cystic fibrosis, may lead to a successful “bridge to transplant”. Similarly, intravenous epoprostenol, oral bosentan and sildenafil may provide a bridge to transplant for patients of all ages with severe pulmonary hypertension. The study by Morton et al included several terminally ill individuals transplanted after support with mechanical ventilation or extra-corporeal membrane oxygenation.5 Morton and colleagues are to be commended for their successful endeavour, but we contend that further detailed discussion about excessive early mortality10 and resource use is needed before bridging in this fashion is routine in any age group. Such bridging has become increasingly used in the United States (11% of all LTx in 200611) and we believe that many, including ourselves, would argue that Australia does not have the intensive care facilities and staff to routinely bridge in this manner. There are also other developments that should increase transplant opportunities and access to LTx for children and adolescents, hopefully shortening waiting times, thereby further decreasing waiting list mortality, and potentially allowing at least the possibility of retransplantation in the event of late graft dysfunction. One possibility is that large-volume LTx transplant centres (typically not small-volume paediatric-only centres, as yet) might increase organ availability by using extended donor lungs (eg, where there are secretions or an abnormal chest x-ray, etc),12 or cadaveric or living-related lobar transplants (eg, so-called “cut-down lungs”).13 The use of cut-down lungs typically involves transplanting one lobe from each of two adults to make a bilobar transplant for a child or smaller adolescent. Although this resource-intensive and challenging operation is possible, some question the philosophy of undertaking the only known procedure to have a “potential 300% mortality”.13 Donation-after-cardiac-death (DCD) retrieval of lungs for transplantation (as distinct from the usual donation-after-brain-death retrieval) is also now a viable prospect being used to acquire adult lungs for LTx,14 and will soon be extended to paediatric DCD lung donation.15 Thus, evidently, expanding the complexity and extent of LTx offered to children and adolescents might consume significant resources, so LTx results must be carefully considered and evaluated to ensure continued successful outcomes. In this regard, we note with great interest the recent institution of a complex mathematical lung allocation score model by the American United Network for Organ Sharing (UNOS).16 This model uses disease-relevant clinical and physiological variables to predict who will get the most significant improvement in survival with LTx and, therefore, who should be preferentially transplanted. Although historically based, the model will evolve with ongoing clinical experience and should be able to provide new evidence to guide future practice. Interestingly, because of differences in diagnostic categories and post-LTx outcomes in younger lung transplant recipients, the UNOS lung allocation score is only to be applied to those aged over 12 years.16 So, although there are important differences to consider when evaluating the efficacy and utility of LTx across the wide age-spectrum of disease and physiology in the very young, adolescents and adults with terminal lung disease, there is also significant overlap. Medical and allied health experts in paediatric and adolescent medicine have much to offer adult LTx programs venturing into adolescent transplantation; their involvement should be routine. Similarly, units experienced in adult LTx bring knowledge and technology to paediatric and adolescent LTx that can only benefit the small number of critically ill young Australians previously without local access to LTx expertise.

Gregory I Snell MB BS, FRACP, MD · Glen P Westall MB BS, FRACP · Trevor J Williams MB BS, FRACP, MD

To the Editor: The recent article by Venn et al reported that childhood overweight carries through into adult overweight and obesity, but that most obese young adults in their study were “healthy” weight as children in 1985.1 As demonstrated by National Health Surveys, age is one of the strongest predictors of overweight,2 with body mass index (BMI) increasing as we grow older. However, there are two additional time-related components influencing obesity. Since 1985 (when Venn et al reported the prevalence of overweight and obesity in children was less than 10%), the environment appears to have become more obesogenic — a 2004 survey in New South Wales showed that 26% of children were overweight or obese.3 It is not only children who are vulnerable — the percentage of overweight adult Australians increased for almost all age groups from 1990 through 2001, and the mean BMI at which Australians enter adulthood has increased with each subsequent survey. For example, for women aged 20–24 years, mean BMI increased from 22.1 kg/m2 (1990) to 22.5 kg/m2 (1995) to 23.2 kg/m2 (2001) to 23.3 kg/m2 (2004). As the heights and weights were self-reported in these surveys, true BMI values may be even higher. We recently reported that year of birth (birth cohort) also predicts prevalence of overweight and obesity, independent of age and survey period; the prevalence of overweight and obesity in adults increased progressively with birth cohorts born since 1960.4 This birth span includes the cohort in the study by Venn et al.1 While obesity begins in childhood for only a small proportion of adults, the so-called healthy weight children now have a higher mean BMI, giving little margin for the seemingly inevitable increases in weight with ageing, before the population mean BMI reaches the cutpoint for overweight and later obesity. The 2004–2005 National Health Survey showed that men reached the overweight cutpoint at 25–29 years and women reached it at 30–34 years.5 Given increasing child and adult obesity, the need for allocation of public health resources to improve dietary and physical activity habits is undisputed. However, these data1,4 indicate that efforts should be directed to the hard-to-reach group, young adults, to prevent weight gain at this point. This will pose considerable challenges, because this group has minimal contact with health services, and perceives the threat of chronic illness as irrelevant. However, swift intervention is required, not only for their own health and that of their children as they become parents, but also because they will become overconsumers of health care for chronic diseases within a generation.

Margaret A Allman-Farinelli · Lesley King · Adrian E Bauman

In reply: Allman-Farinelli et al make an important point about the influence of age, survey period and cohort effects on the prevalence of overweight and obesity. While age and cohort effects could not be clearly separated in the 1985 Australian Schools Health and Fitness Survey, the prevalence of overweight and obesity increased with age in 7–15-year-olds.1 Our data collected from 4571 of the individuals in that survey at follow-up about 20 years later also showed an increase in the prevalence of overweight and obesity with age, although these findings were not presented in our report.2 In the Box, we show the distribution of body mass index (BMI) values for men and women in three age groups (24–27 years, 28–30 years and 31–34 years). Mean BMI values across the age groups were 25.2 kg/m2, 25.6 kg/m2, and 26.5 kg/m2 in men and 23.5 kg/m2, 24.2 kg/m2, and 24.6 kg/m2 in women. The prevalence of obesity (BMI ≥ 30 kg/m2) increased with increasing age as follows: age 24–27 years — men 12.2%, women 9.9%; age 28–30 years — men 12.3%, women 12.0%; and age 31–34 years — men 15.6%, women 14.6%. Distribution of body mass index values for men and women in three different age groups* * 24–27 years, 757 men and 854 women; 28–30 years, 767 men and 807 women; and 31–34 years, 673 men and 691 women in the 20-year follow-up of the 1985 Australian Schools Health and Fitness Survey.

Alison J Venn · Russell J Thomson · Michael D Schmidt · Verity J Cleland · Beverley A Curry · Hanni C Gennat · Terence Dwyer

To the Editor: Kawasaki disease (KD) is an acute vasculitis of unknown aetiology occurring mostly in infants and young children. KD is characterised by fever of more than 4 days’ duration; conjunctivitis; rash; cervical lymphadenopathy; erythema of the lips, oral mucosa, palms and soles; and oedema of the hands and feet.1 Coronary artery aneurysms develop in 15%–25% of untreated children,2 with attendant risk of ischaemic heart disease, myocardial infarction and sudden death.3,4 Treatment with intravenous immunoglobulin (IVIG) within the first 10 days reduces the incidence of aneurysm to less than 5%.4 A KD diagnosis is clinical, based on the recognition of a characteristic set of signs and symptoms.4 The 10%–45% of children who meet only some of the classical criteria are said to have “atypical” or “incomplete” KD. These children have a higher risk of coronary artery aneurysm than children with typical KD.4 Abdominal symptoms, including acute appendicitis and appendicular vasculitis, can occur before the development of classical features of KD.4,5 A 50% coronary artery aneurysm rate has been reported in children with KD and acute abdomen. It is still unclear whether this reflects a delay in diagnosis and treatment or is a marker of a more severe vasculitis involving the intestinal tract. A 3-year-old boy presented with a 2-week history of remittent, high-spiking fever (37.5–39.0° C; 2–3 spikes/day), right lower quadrant abdominal pain, and McBurney’s sign with rebound tenderness. Abdominal ultrasonography suggested a diagnosis of acute appendicitis with peritonitis. The postoperative diagnosis was appendicular vasculitis with peritoneal inflammation and serous secretion. Fever persisted despite treatment with intravenous cephalosporin. Several days later, the boy developed conjunctivitis, cracked lips, a raised erythrocyte sedimentation rate and C-reactive protein level, and thrombocytosis (715 × 109 platelets/L). KD was suspected, and an echocardiogram revealed two sacciform coronary artery aneurysms (diameters, 3.1 mm and 2.9 mm) in the proximal part of the common trunk. The child was given IVIG (2 g/kg) and oral acetylsalicylic acid (100 mg/kg per day in four divided doses). As the fever failed to resolve, the patient was given a second dose of IVIG,4 this time leading to a dramatic clinical improvement. Five days later, he developed oedema of the hands and periungual peeling of the fingers. His aspirin dose was reduced to 5 mg/kg/day. Follow-up echocardiograms at 3 months and 6 months demonstrated persistent coronary artery dilatation. Persistent fever with conjunctivitis and cracked lips should alert clinicians to the possibility of KD. At our patient’s age, acute appendicitis is rare, and other causes of abdominal pain must be excluded. In this case, the unusual postoperative course, with persistent fever even after antibiotic treatment, was another clue to establishing the correct diagnosis.

Maria Cristina Maggio · Andrea Liotta · Salvino M Vitaliti · Giovanni Corsello

To the Editor: With the ski season in Australia drawing to a close for another year, it is a good time to reflect on the injury prevention benefits of wearing helmets when skiing or snowboarding. Skiing falls can be fatal. Two people have died from head injuries on Australian skifields in recent years: a skier died after colliding with a tree branch on an intermediate run at Mt Buller, Victoria, in 2003; and in 2006, a novice snowboarder died after falls sustained while snowboarding at Thredbo, New South Wales.1 Neither person was wearing a helmet. In Australia in 2002–03, 3.5% of skiing-related hospital admissions and 6.2% of snowboarding-related admissions were due to intracranial injuries.2 During the 2004 and 2005 ski seasons we collected data on the use of helmets in snowboarders presenting to the Mt Buller Medical Centre. Of 494 snowboarders, 17.6% had been wearing helmets, and none had sustained a head injury. Of the nine patients with head injuries, none had been wearing helmets. These figures are similar to those reported in overseas studies, which have shown that wearing a helmet can reduce the snow-sport head injury rate by up to 60%.3,4 The use of helmets for snow sports makes intuitive and biological sense, as it does for cyclists, but, unfortunately, Australia is yet to issue a snow-sport helmet performance standard, as it does for bicycle helmets. Helmet use should be strongly recommended for all snowboarders and skiers. In particular, helmets should be made compulsory for children, who are more susceptible to head injury4 and who are often present at ski resorts in large organised school groups that could readily be made to comply. At present in Australia, helmet use is not compulsory for children attending skiing or snowboarding lessons, as it is in North America. This is in spite of the fact that helmet use is compulsory in Australia for school skiing and snowboarding competition events. Some skiers and snowboarders are gradually getting the message about helmets, and a recent informal survey at Mt Buller (Buller Ski Lifts personnel, personal communication) estimated the rate of helmet use to be 20% among adults and 68% among children — but this still leaves over 30% of children vulnerable. Snow-sports helmets now come in many colours, shapes and sizes, and are increasingly acceptable to young people. A helmet is probably the cheapest individual item of clothing for a ski holiday. And it may save your life.

Graham M Slaney · Judith Finn · Angus Cook · Philip Weinstein

Objectives: To determine (i) the relationship between asthma management and socioeconomic status; (ii) whether recent estimates from the International Study of Asthma and Allergies in Childhood (ISAAC) conducted in Melbourne apply to a broader cross-section of Victorian children; and (iii) age-related trends in asthma prevalence.Design: A questionnaire survey, based on the ISAAC protocol.Participants and setting: Subjects were children aged 4–13 years from a random sample of primary schools in the Barwon region of Victoria. The survey was conducted between March and September 2005.Main outcome measures: Parent-reported wheeze and wheeze-related use of health resources during the preceding 12 months.Results: Questionnaires were returned by 7813/9258 students (84%). Lower socioeconomic status was associated with increased frequency of regular asthma reviews (P < 0.01 for trend), but not of emergency department visits (P = 0.19). The prevalence of wheeze among 6- and 7-year-old children in the Barwon region was similar to that in Melbourne children (20.2% v 20.0%, respectively).There was an age-related increase in the proportion of children with ≥ 12 episodes of wheeze (P = 0.01); but an age-related decrease in emergency department visits (P = 0.02).Conclusions: Disadvantaged children have good access to regular asthma reviews and are no more likely to attend an emergency department with an episode of acute wheeze. Asthma prevalence in 6- and 7-year-old children in the Barwon region is similar to that in Melbourne. The prevalence of children with very frequent wheeze increases with age, but their use of health resources decreases.

Peter J Vuillermin FRACP · Mike South MD · John B Carlin PhD · Maree I Biscan Mstrs · Sharon L Brennan Mstrs · Colin F Robertson MD

To the Editor: Childhood overweight and obesity have become a major public health concern in Australia. Between July 2003 and December 2004, we conducted the Australian National Iodine Nutrition Study (NINS) among schoolchildren.1 While visiting primary schools across Australia, we observed that many children were overweight or obese. The NINS data allowed us to estimate the prevalence of overweight and obesity among 8–10-year-old Australian schoolchildren, and to determine whether the prevalence was associated with socioeconomic background. The study population comprised a one-stage random-cluster sample from all Year 4 school classes in 92 government and non-government schools.1 Children were aged 8–10 years (mean, 9.3 years). Height and weight were measured by standard techniques and were used to calculate body mass index. Overweight and obesity were identified using international standard definitions.2 Socioeconomic status was defined by the Index of Relative Socio-Economic Advantage/Disadvantage of the Census of Population and Housing’s Socio-Economic Indexes for Areas (postal areas).3 This index is a continuum of advantage to disadvantage. A higher score indicates that an area has a relatively higher proportion of people with higher incomes or a skilled workforce. The prevalence of overweight and obesity in 8–10-year-old schoolchildren was 18.5% and 6.5%, respectively. There was no significant sex difference in prevalence and no significant evidence of an association between socioeconomic status and overweight or obesity (Box). The prevalence of overweight and obesity combined and of obesity alone was similar to previously reported prevalence,4,5 although the age range of the participants was more limited than in other studies. We minimised measurement error bias by using the same equipment throughout, in the same setting. Furthermore, most measurements were taken by the same person. We could not demonstrate an association between socioeconomic status and the prevalence of overweight and obesity combined, or of obesity alone. This suggests that childhood overweight and obesity is common to all Australian communities, irrespective of socioeconomic background. Preventing overweight and obesity in children may reduce the risk of adult overweight and obesity and related diseases. Regular monitoring and surveillance of the situation is needed. Australia is one of the first countries in the world to develop a national strategy for overweight and obesity.6 However, the strategy needs to be communicated to the wider community and turned into action to combat this public health problem. Proportion (number) of boys and girls categorised as overweight or obese by index of advantage/disadvantage* SEIFA percentile Not overweight or obese Overweight Obese n Overall Boys Girls Overall Boys Girls Overall Boys Girls Lowest 10 130 79% (102) 77% (56) 82% (46) 12% (16) 12% (9) 13% (7) 9% (11) 11% (8) 5% (3) 10–25 286 72% (207) 72% (103) 73% (103) 22% (64) 22% (31) 23% (33) 5% (15) 6% (9) 4% (6) 25–50 210 74% (156) 72% (72) 76% (84) 17% (35) 18% (18) 16% (17) 9% (19) 10% (10) 8% (9) 50–75 505 75% (379) 72% (183) 79% (195) 19% (98) 21% (53) 18% (45) 6% (28) 8% (20) 3% (8) 75–90 427 75% (319) 78% (179) 71% (140) 18% (78) 17% (39) 20% (39) 7% (30) 6% (13) 9% (17) Highest 10 225 77% (174) 79% (84) 76% (89) 17% (39) 16% (17) 19% (22) 5% (12) 6% (6) 5% (6) Total 1782 75.0% (1337) 74.4% (677) 75.6% (657) 18.5% (330) 18.4% (167) 18.8% (163) 6.5% (115) 7.3% (66) 5.6% (49) * Overall χ2 = 11.42, P = 0.33; Boys χ2 = 8.73, P = 0.56; Girls χ2 = 12.36, P = 0.26. SEIFA = Socio-Economic Indexes for Areas (a higher score corresponds to higher socioeconomic status).

Mu Li · Karen Byth · Creswell J Eastman

To the Editor: Recent studies provide evidence that having a low serum vitamin D level is a risk factor for autoimmune disease, including type 1 diabetes mellitus (T1DM).1,2 Available data come from northern hemisphere countries where sunlight exposure levels and the genetic background of the population are different from those in Australia. We compared vitamin D levels in stored serum from Brisbane children and adolescents with T1DM who attended the Mater Children’s Hospital clinic with local historical control data from a previous study.3 Levels of 25-hydroxyvitamin D (25-OHD; the major circulating form of vitamin D) were lower in those with T1DM than in the control group, with no difference in levels of 1,25-dihydroxyvitamin D (1,25-[OH]2D; the biologically active form). Children and adolescents with T1DM were more than three times as likely to have vitamin D deficiency4 as those in the control group. There was a trend towards seasonal variation in 25-OHD levels, with mean levels (95% CI) being 53.8 nmol/L (47.0–60.6 nmol/L) in summer, 61.4 nmol/L (54.9–67.9 nmol/L) in autumn, 56.4 nmol/L (51.7–61.0 nmol/L) in winter and 64.7 nmol/L (58.8–70.6 nmol/L) in spring (P = 0.06), but no difference in seasonal variation between T1DM and control groups (P = 0.73). There was no difference in the ages or proportions of males and females in the two groups (Box). There were no differences in vitamin D levels between the sexes in either T1DM or control groups, nor any correlation with duration of diabetes. These observations support previous reports. One found low 25-OHD levels in 459 Swedish patients aged between 15 and 34 years who were newly diagnosed with T1DM compared with age-matched and place-matched controls.1 Another found low 25-OHD levels in 88 newly diagnosed children and adolescents.2 Understanding the nature of low vitamin D levels in people with diabetes is important because it potentially clarifies the mechanisms of autoimmune β-cell destruction, and may lead to interventions for preventing or delaying insulin dependence by using vitamin D or its analogues. Vitamin D probably acts by modifying the autoimmune response, as 1,25-(OH)2D modulates dendritic cell function to promote tolerogenic T cells. It may be relevant that we have recently found low blood dendritic cell counts in children and adolescents with T1DM.5 Vitamin D levels in our Queensland sample of children and adolescents were lower overall than those found in the subjects of the Swedish study, (mean 25-OHD levels [± SEM] were 96.7 ± 2.7 nmol/L for the control group and 82.5 ± 1.3 nmol/L for those with T1DM); this is unexpected given Brisbane’s latitude (29°S) compared with that of Sweden (about 55–65°N). These differences might be explained by differences in dietary intake, sun avoidance behaviours promoted in Queensland, or differences in the assays used, as the Swedish group used the Nichols chemiluminescence assay (Nichols Institute, San Juan Capistrano, Calif, USA) and we used the DiaSorin radioimmunoassay (DiaSorin Inc, Stillwater, Minn, USA). The observation in the Swedish study that the deficit in 25-OHD level did not resolve over time after diagnosis concurs with our finding of low levels in children and adolescents several years after diagnosis. While our pilot data cannot support causal inference, and is limited by being retrospective and our lack of information about history of sunlight exposure, dietary vitamin D intake, cultural factors such as sun avoidance or veiling, skin tone, and not having contemporaneous controls, it strongly supports the case for prospective clinical studies of vitamin D in T1DM. Comparison of clinical characteristics and vitamin D levels in healthy children and adolescents and those with type 1 diabetes mellitus Variable Control group Type 1 diabetes mellitus group P No. of children and adolescents 94 47 Age (range) 13.2 years (12.5–13.8 years) 13.6 years (12.6–14.6 years) 0.47* No. of males/females 44/50 21/26 0.81† Mean duration of diabetes (95% CI) — 4.7 years (3.9–5.5 years) Sample collection period July 2000 – December 2001 June 2001 – July 2006 Mean 25-OHD level (95%CI)‡ 64.6 nmol/L (61.3–67.9 nmol/L) 54.7 nmol/L (50.3–58.9 nmol/L) 0.0005* Mean 1,25-(OH)2D level (95% CI)‡ 126.7 pmol/L (115.8–137.6 pmol/L)§ 127.6 pmol/L (114.8–140.4 pmol/L) 0.92* Proportion 25-OHD-deficient (≤ 50 nmol/L) 18% (17/94) 43% (20/47) 0.002† (OR,¶ 3.4; 95% CI, 1.5–7.3) Proportion with 1,25-(OH)2D level below reference range (40–150 pmol/L) 0 (0/84) 4% (2/47) 0.13** (OR,¶ 9.3; 95% CI, 0.4–197.6) * t test. † χ2 test. ‡ DiaSorin radioimmunoassay double antibody assay (DiaSorin Inc, Stillwater, Minn, USA), performed by Queensland Health Pathology Services. § 84 controls; insufficient serum for analysis in 10. ¶ Odds ratio for deficiency in type 1 diabetes mellitus. ** Fisher’s exact test. 25-OHD = 25-hydroxyvitamin D. 1,25-(OH)2D = 1,25-dihydroxyvitamin D.

Ristan M Greer · Meredith A Rogers · Francis G Bowling · Helen M Buntain · Mark Harris · Gary M Leong · Andrew M Cotterill

To the Editor: V-shaped pillows (“tri-pillows”) may cause suffocation of an infant left to sleep between the two arms of the pillow when he or she slips into the crevice between the arms, or beneath the pillow. The deaths of two infants who died in this manner were reported in South Australia in 1997, and a third death was the subject of a coronial inquiry.1,2 In 1998, the SA State Coroner recommended that “a public warning be issued against the use of tri- or U-shaped pillows by infants under two years of age for sleeping”.2 This message has also been issued in subsequent safe-sleeping campaigns, with a statement in the SIDS and Kids national “Safe sleeping” brochure that “tri-pillows are too soft and can cover baby’s face”, and a statement on the SA Child and Youth Health website that “. . . babies should not be left in these pillows while they are sleeping”.4 Despite these clear messages, deaths continue to occur in SA,5 and V-shaped pillows are still being sold in the foyer of a local obstetric hospital. Although the pillows are being promoted to assist breastfeeding, infants who have been left to sleep on them will be exposed to the risk of suffocation. Deaths of infants in shared sleeping situations may also occur due to suffocation from “overlaying”. However, parents are still being advised by health advice telephone enquiry services to sleep in the same bed with their children. This was the unequivocal message given to one of the authors (G C) when she recently telephoned for advice following the birth of her first child. No mention was made of the potential danger of suffocation if parents are physically large, intoxicated, sedated, or simply exhausted, or if the infant is placed between the parents under bedcovers. It appears, despite clear evidence that certain sleeping situations are potentially dangerous for infants, as well as the widespread dissemination of this information in safe-sleeping literature, that certain organisations or individuals continue to give a contrary message. What hope do parents have of understanding these issues and making informed decisions to optimise the safety of their infant’s sleeping environment if they are exposed to such conflicting messages and advice? Perhaps another question to ask is, “What responsibility do organisations and employees bear if an infant dies as a result of parents following such advice or purchasing equipment such as a V-shaped pillow?”

Roger W Byard · Glenda Cains · Helen Noblet · Maxine Weber