Vaginal microbiota can be partially restored in c-section babies: study

A pilot study has demonstrated that vaginal microbes can be partially restored in babies delivered by a caesarean section.

The microbes in a woman’s vagina colonises the skin, oral cavity and gut of babies as they’re born, contributing to their future immune system. Some research says the lack of exposure to vaginal microbiota in babies born via C-section can lead to health problems later on.

Maria Dominguez-Bello, Jose Clemente and colleagues set up a vaginal microbial transfer, where four C-section delivered babies were swabbed with gauze that had been incubating in their mother’s vagina for an hour prior to the birth.

The small study then compared the babies’ microbiota with seven c-section infants not exposed to vaginal fluids and seven babies born vaginally.

They found that after 30 days c-section infants exposed to vaginal fluids had microbiota more similar to vaginally born infants than to c-section born infants not exposed to vaginal fluids. However they also noted that only some of microbes transferred.

“Although the long-term health consequences of restoring the microbiota of C-section–delivered infants remain unclear, our results demonstrate that vaginal microbes can be partially restored at birth in C-section–delivered babies,” they wrote in Nature Medicine.

Bookshop: Caesarean Section: a Manual for Doctors

However Associate Professor Andrew Holmes from the Discipline of Microbiology in the School of Molecular Bioscience and the Charles Perkins Centre at the University of Sydney says the paper has been “essentially meaningless in terms of scientific insight or clinical application”.

He said that there isn’t enough data collected to make a meaningful comment and that the authors are testing a solution to an idea that few in the industry feel is likely to be a significant issue.

“All this article does is raise doubts in women’s minds about the implications of a C-section birth and leave them prone to considering an intervention that did not appear to work,” he said.

In an accompanying News & Views article, Alexander Khoruts wrote: “Going forward, large randomized trials with long-term clinical outcomes will be needed to learn whether any benefits can be derived from supplementing C-section delivery with some restorative microbiota treatments.”

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Chronic Ayurvedic medicine use associated with major and fatal congenital abnormalities

Although there are potential associations between lead exposure during pregnancy and adverse pregnancy outcomes, there are limited data on whether in-utero lead exposure is associated with major congenital abnormalities. We describe a case of a major congenital renal abnormality, which resulted in severe pulmonary hypoplasia and neonatal death, that was potentially associated with maternal chronic lead ingestion via an Ayurvedic medicine throughout pregnancy.

Clinical record

A 28-year-old primigravida was referred to a maternal–fetal specialist because a fetal ultrasound at 20 weeks showed oligohydramnios, absence of the right kidney and a small echogenic left kidney with poor corticomedullary differentiation, and intrauterine growth restriction. She had a history of lethargy throughout her pregnancy and a normocytic anaemia with a haemoglobin level of 95 g/L (reference interval [RI], 97–148 g/L) at 24 weeks’ gestation and 88 g/L (RI, 95–150 g/L) at 30 weeks’ gestation. Her white cell count and platelet count were normal at 24 weeks’ and 30 weeks’ gestation. Liver and renal function test results, and serum vitamin B₁₂, folate and ferritin levels were also within normal limits at both 24 weeks’ and 30 weeks’ gestation. Chorionic venous sampling performed at 24 weeks did not detect any significant genomic abnormalities. At 30 weeks’ gestation, the maternal blood film showed basophilic stippling and her blood lead level (BLL) was high at 3.2 μmol/L (RI, < 0.48 μmol/L) or 67 μg/dL (RI, < 10 μg/dL). The toxicology unit was consulted and chelation was commenced, including oral dimercaptosuccinic acid (DMSA) at a dose of 10 mg/kg three times a day for 5 days followed by 10 mg/kg twice daily for 14 days. Three weeks after chelation, her BLL was 0.7 μmol/L (14.4 μg/dL).

For the previous 6 months, the patient had been taking two tablets per day of an Ayurvedic medicine, prescribed by a practitioner in India, that she was self-importing to Australia. Analysis of these tablets (performed by DTS Food Laboratories, a National Association of Testing Authorities-accredited laboratory) using inductively coupled plasma mass spectrometry, a process used to detect metals and non-metals, showed a lead content of 47%, small amounts of mercury (1.7%), and arsenic (< 0.01%). Urine arsenic and mercury levels were within normal limits. No other sources of lead exposure or ingestion were found.

Fetal growth improved after chelation therapy commenced; however, further ultrasound scans of the fetus showed diminished left renal tissue with progression to anhydramnios by 30 weeks’ gestation. By 34 weeks’ + 5 days’ gestation, there was no fetal renal tissue visible on ultrasound. The family received extensive counselling from the neonatal and renal specialists and the paediatric toxicologist, with consideration as to whether to dialyse the baby if chelation was needed and if the expected related respiratory failure was considered survivable postnatally.

Three days before an elective caesarean section at 39 weeks, the mother received intravenous calcium disodium edetate 40 mg/kg twice daily to decrease her lead concentrations before delivery. She gave birth to a 3.14 kg baby who had severe hypoxic and hypercapnic respiratory failure and a small right pneumothorax as a result of pulmonary hypoplasia, and severe contractures with bilateral dislocated hips, each resultant of the antenatal anhydramnios. The baby did not have typical facies of Potter sequences or other congenital abnormalities associated with Potter syndrome. Renal ultrasound showed no left renal tissue and a severely dysplastic right kidney of 1 cm diameter. The cord BLL at delivery was low at 0.37 μmol/L (8.0 μg/dL). Given the low BLL, chelation was not initiated. The baby died 2 days later from severe respiratory failure owing to poor antenatal pulmonary development, a result of the severe renal dysgenesis. At autopsy, the BLL was 0.55 μmol/L (11.5 μg/dL) and there was severely hypoplastic and multicystic renal tissue bilaterally (right kidney, 15 g; left kidney, 16 g), with normal ureters and bladder. Three weeks’ postpartum, the mother’s BLL was 0.8 μmol/L (17.3 μg/dL).

Discussion

Anaemia during pregnancy is common and iron deficiency is a common cause. However, normocytic anaemia in the absence of other causative factors requires further investigation using blood film analysis. Basophilic stippling on blood film is associated with lead toxicity, arsenic toxicity, thalassaemia, sideroblastic anaemia, thrombotic thrombocytopenic purpura and hereditary pyrimidine 5′-nucleotidase deficiency.1 The combination of basophilic stippling with unexplained anaemia needs further investigation, and questions regarding potential sources of lead or arsenic exposure need to be asked. Other common sources of lead include occupational exposure, fishing sinkers, old paint (before 1960), retained bullets and pottery.

During pregnancy, chronic lead toxicity can present with anaemia and lethargy, peripheral neuropathy, hypertension, liver and renal dysfunction, abdominal pain and, in severe cases, encephalopathy.2 Long-term effects on maternal and fetal IQ are also a concern.

Lead crosses the placenta at as early as 12–14 weeks’ gestation and is mobilised from maternal bone during the formation of the fetal skeleton. Studies have shown that 85% of cord BLLs come from maternal bone stores.2 Although there are potential associations between lead exposure during pregnancy and adverse pregnancy outcomes, including spontaneous abortion, pregnancy-related hypertension, low birth weight and neurobehavioural development, the literature is less clear on whether there is an association between major congenital abnormalities and lead toxicity during pregnancy.2,3

One case report describes an asymptomatic female worker with occupational lead exposure who had a BLL of 62 μg/dL at 8 weeks’ gestation and was removed from exposure with a reduction of BLL to 5 μg/dL at 14 weeks’ gestation. The infant developed VACTERL association (vertebral anomalies, anal atresia, cardiac defects, tracheo-esophageal fistula and/or esophageal atresia, renal and radial anomalies, and limb defects); it was not possible to determine whether this was caused by the lead toxicity.4 Another case involved a mother with a BLL of 31 μg/dL at 21 weeks’ gestation from a retained bullet. There were neurological, cardiovascular and pulmonary abnormalities at birth but no functional abnormalities at 10 years of age.5

In our case, the mother had been taking Ayurvedic medication for 6 months spanning the period before pregnancy and during the first trimester during organogenesis. The baby had renal abnormalities (agenesis of one and absence of the other kidney), along with pulmonary hypoplasia and anhydramnios. The risk of nephrotoxicity increases proportionally with increasing BLL, and effects on glomerular filtration have been reported at a BLL < 20 μg/dL.6 Although it is not possible to be certain that these abnormalities were caused by the lead toxicity, a high BLL was present on investigation.

Evidence for chelation therapy for lead toxicity during pregnancy is limited to animal data and case studies.2 Removal from ongoing exposure is key to the treatment of any patient with heavy metal toxicity. DMSA was administered in this case and there have been conflicting animal studies on whether DMSA increases the risk of fetal toxicity secondary to lead or whether it significantly reduces the lead concentration without harm. Chelation during the first trimester is controversial because this is the period of organogenesis; therefore, the potential benefit of chelation has to be balanced against the unknown risks of the chelation agents on fetal outcome. Generally, unless the mother is encephalopathic or has other markers of severe lead toxicity, chelation would be deferred until at least the second trimester.7 In our case, consideration was given as to which chelating agent, if needed, could be used for the baby. Given the fetus and baby had minimal kidney tissue, an intravenous chelating agent may have caused nephrotoxicity through deposits of chelation complexes. Oral succimer via a nasogastric tube was to be the chelating agent of choice, as it would not have those same concerns of nephrotoxicity.

The popularity of traditional medicines has been increasing in Asia, North America and Australasia.8 Ayurveda is the most widely practiced traditional medicine system on the Indian subcontinent. The addition of heavy metals into Ayurvedic preparations may either be purposeful or a result of contamination. During pregnancy, there is an increased recommended iron intake of 50% compared with that for women of childbearing age. The number of women substituting Ayurvedic medicine for iron supplementation during pregnancy and to what extent is unknown. In a study from the United States, an analysis of 70 Ayurvedic products showed that 14 (20%) contained enough heavy metals to be over the recommended maximum amounts.9 There is existing legislation to help regulate the provision of Ayurvedic and herbal medicines in the United Kingdom and the US. In Australia, the Therapeutic Goods Administration (TGA) allows listing of complementary medicines if the names of the ingredients are provided to the TGA; however, testing of content (eg, for safety) is not required for such listing.10 In addition, the purchase of these medications for personal use from overseas and their availability over the internet can prove challenging to monitor.

Health care practitioners and consumers need to be aware of the potential for heavy metal toxicity to be associated with the use of Ayurvedic medications. A focused drug history including traditional remedies should be undertaken in all patients. Pregnant patients need to know the side effects of medications prescribed throughout pregnancy and the risks associated with taking complementary medicine, especially given the “loopholes” in content testing by regulatory agencies not only in some countries overseas but also in Australia.

New treatment to overcome peanut allergies in children

By Jane Trembath, Southern Health News / 4th of November, 2015

This story was first published by The Lead, South Australia.

A new study is successfully helping children to overcome peanut allergies by exposing them to peanuts and desensitising them to their allergy.

For the past four years, paediatric allergist Dr Billy Tao has been developing a novel two-step desensitisation process at Flinders Medical Centre (FMC) in South Australia.

The first step involves boiling peanuts for an extended length of time to make them less allergenic.

The boiled peanuts are given to patients to partially desensitise them, and then once the patient shows no signs of allergic reaction, roasted peanuts are given to the children to increase their tolerance in the second step of the process.

Dr Tao said the low-cost and effective two-step process resulted in less adverse events than previously used single-step desensitisation methods – also known as oral immunotherapy.

“With traditional methods, a lot of people ingesting increasing amounts of roasted peanut flour or similar products start to react – so much so that many have to drop out and can’t finish the treatment,” Dr Tao said.

The FMC trial is carried out over a year or longer and includes patients aged between 10 and 15 years.

Of the 14 participants, 10 have already completed the first step and are now eating varying amounts of roasted peanuts, while four continue to eat boiled peanuts and are progressing well.

“One patient who had to be administered three adrenaline injections after consuming peanuts is now eating several roasted peanuts every day without problems,” Dr Tao said.

Studies show the number of children living with peanut allergy appears to have tripled between 1997 and 2008, and as many as one in every 200 children will have severe allergy to nuts.

Allergy symptoms can vary from very mild (including tingling mouth, puffy lips and welts around the mouth) to moderate symptoms (facial swelling, body rash, runny nose and red eyes, abdominal pains and vomiting); while severe reactions include trouble breathing, looking pale and unwell, and anaphylaxis. Very occasionally death may result from a most severe reaction.

Dr Tao’s idea for hypo-allergenic (less allergenic) nuts to be consumed first was based on an observation by German researcher Professor Kirsten Beyer, who in 2001 noted that peanut allergies were less prevalent in China than the western world because the Chinese ate boiled peanuts rather than peanut butter or roasted peanuts. She found that boiling peanuts for 20 minutes made them less allergenic than roasted peanuts.

Dr Tao said that a partnership with Dr Tim Chataway, Head of the Flinders Proteomics Facility, and Professor Kevin Forsyth from the FMC Paediatrics Department, proved that peanuts boiled for at least two hours were less allergenic and the pair designed a study using this immunotherapy approach.

Dr Tao hopes his research could one day be carried out in a doctor’s clinic and then at home and avoid the need for hospital-based treatment.

However he strongly warned people against ‘do-it-yourself’ desensitisation at home and stressed that patients should be seen by an allergist and individual care plans developed.

Among those who have already undergone Dr Tao’s new desensitisation method is 16-year-old Shehan Nanayakkara, who was diagnosed with a severe peanut allergy at the age of three.

“We first realised Shehan had an allergy when friends gave him a peanut butter sandwich and he had to be rushed to hospital…there have been many accidents since then,” father Asanka said.

“During one round of allergy testing he ended up in the Intensive Care Unit – that time I thought I’d lost him.

“I approached Dr Tao to help and at first Shehan ate boiled peanuts, working his way up to consuming 13 a day, and now he eats five normal roasted peanuts daily, mixed in with his meals.

“It’s been a big relief because children and teenagers don’t care too much about what they eat and just eat whatever, and there has always been that worry that something might happen – now we can relax a bit because Shehan has some tolerance.”

[Correspondence] Standing up for refugees

The Lancet is wrong to suggest that the Royal College of Paediatrics and Child Health (RCPCH) has not advocated on behalf of children caught up in the refugee crisis (Editorial, Sept 12).1 We have welcomed the UK Government’s commitment to accept more refugees, but have also urged the leadership not to play politics with the world’s most vulnerable infants, children, and young people.

How cancer doctors use personalised medicine to target variations unique to each tumour

The Children’s Cancer Institute in Sydney recently launched an ambitious program. From early next year, scientists will analyse the unique cancer cells of 12 children diagnosed with the most aggressive forms of the disease to find the best treatment for each child.

By 2020, they aim to have these individualised treatment options available to all children diagnosed with cancers that have a less than 30% survival rate. This way of tailoring treatment to each person is known as personalised medicine, and advances in DNA sequencing have paved the way for a new era in cancer management.

Tailoring treatments

The modern use of the term “personalised medicine” is based on the idea that by understanding the specific molecular code of a person’s disease, and particularly its genetic makeup, we can more accurately tailor treatment to them. This approach is also referred to as precision medicine.

Cancer is fundamentally a disease of altered genomics – genetic material making up the structure of cells. Because these alterations are different in each person, every tumour is programmed differently with genes made up of varying sequences of DNA.

How cancer doctors use personalised medicine to target variations unique to each tumour - Featured Image

Cancer cells are programmed with a unique code. From shutterstock.com

This is why not everyone will respond the same way to a given treatment. Determining the DNA sequence that makes up the genome of each tumour (genomic sequencing) helps doctors understand how the tumour may be effectively targeted.

Traditionally, identifying effective cancer treatments relied on large clinical trials involving thousands of patients. This approach successfully identifies drugs effective for general cancer features, but these may miss the unique Achilles heel in some people’s cancers.

Because personalised medicine is customised treatment for individuals, clinical trial designs are moving from population-based to one-person trials. Here, a person with a specific genomic makeup is given targeted therapies and the responses are tracked over time.

Genomic framework

While the Sydney children’s program has been described as the first of its kind in Australia, the concept of personalised medicine is not new. Cancer doctors have always managed each person’s cancer by using all the available information about the tumour and other pre-existing medical conditions.

But there are important differences in the development of personalised medicine today.

Breast cancer treatment is one example. For the last 40 years, a large factor dictating the clinician’s choice for breast cancer therapy was the presence or absence of oestrogen receptors in the tumour. Oestrogen receptors receive signals from the hormone oestrogen, which then generates a reaction. Without them, oestrogen wouldn’t have any affect.

If a woman’s tumour didn’t have these receptors, then doctors wouldn’t give them drugs that affected oestrogen as there would be no point.

But now it has become apparent that having oestrogen receptors is not the only criteria for the use of these drugs, as not all women who have oestrogen receptors will benefit from them.

A personalised approach to treatment can prevent having to undergo a therapy that isn’t working. From shutterstock.com

So researchers have gone deeper to see that this is due to the different way oestrogen receptors function in cancer cells.

Understanding the genomic framework of the tumour can determine this function and thus predict the types of women who, despite having the receptor, would likely not benefit from such hormonal therapy.

Different classifications

This understanding of a tumour’s genomic makeup has also led scientists to expand the way cancer is classified. Where previously we categorised cancers by their organ of origin (breast, pancreas etc), findings like the above mean we can now also use a genomic definition.

This has positive implications for optimising cancer treatment.

For instance, one of the most aggressive forms of breast cancer is HER2-positive cancer (human epidermal growth factor receptor 2). The subtype accounts for about 15% of breast cancers, and occurs when the tumour has extra copies of the HER2 receptor gene that promotes cancer cell growth.

Drugs targeting the HER2 protein have shown dramatic success in improving outcomes for people with this subtype. They have become standard treatment.

But it has recently been discovered that excessive HER2 is also present in about 8% of gastric cancers and 3% of pancreatic cancers. This means a therapy successful in one location has the potential to work in another, because the tumour types are similar.

Clinical trials are currently assessing whether HER2-targeted drugs can then also be effective against these pancreatic tumour types.

Cost and benefit

Most major cancer hospitals in Australia have trials investigating personalised medicine at some level. But genomic analyses aren’t widely performed on an individual patient basis.

It is likely examining each tumour in this way will become routine treatment in the near future. There are already international providers who will (for a fee) sequence tumours and suggest treatments based on this information.

For instance, the Foundation Medicine test profiles some 400 known cancer driver genes and can be purchased for $US5,800 (approximately $A8,000). This type of test is not routine in Australia, but internet-savvy patients who have the financial means can arrange to have their tumour analysed with the help of their doctor.

Further to that cost of sequencing is the actual treatment, which may sometimes be an expensive drug not listed on the Australian Pharmaceutical Benefits Scheme for this particular use.

But there are advantages to the personalised approach that transcend cost.

Besides the potential of finding the right treatment, it can lead to stopping a therapy that isn’t working. Or result in a therapy not being undertaken at all; therapies that in many cases are themselves expensive and often have the added burden of side effects.

Elizabeth Williams, Associate Professor, School of Biomedical Sciences, Queensland University of Technology and Rik Thompson, Professor of Breast Cancer Research, Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology. If you work in healthcare and have a blog topic you would like to write for doctorportal, please get in touch.

This article was originally published on The Conversation. Read the original article.

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Upstream or downstream?

The river analogy helps describe the health continuum from prevention to treatment

Winner — Medical student category

When I first looked at a map of Alice Springs, the ephemeral Todd River was marked as a deceptive blue snake, winding its way through the centre of town. For the local Arrernte people, the river is known as Lhere Mparntwe. In my head, I pictured a desert oasis, brown-skinned children gleaming with sun and water, screaming with glee as they plunged from rope swings into the cool river water. During my first week in Alice, somebody told me that it’s only after you have seen the river flow three times that you can be considered a local. The rest of the time it is just a dusty creek bed, filled with the soft rusty sand that has now found its way into almost every item that I own.

In public health, there is the concept of “upstream” and “downstream” factors. The analogy of the river is used to describe how pre-existing social, cultural, financial, environmental and historical factors ultimately go on to influence health outcomes in a profound way.1

The children’s ward at Alice Springs Hospital is busy. The nurses exasperatedly chase a young boy down the corridor. This pint-sized patient is surprisingly speedy as he makes his naked bid for freedom. A happy little boy and exceptionally cute, this child has quickly become a favourite of mine. It’s close to a month since he was first admitted for ongoing weight loss on a background of acute gastroenteritis. He has had chronic diarrhoea since he’s been here, his stool best described as a microbiological zoo. His small body has been bombarded with every antibacterial, antifungal and antiparasitic agent we have. His poor gut is so damaged from his numerous recurrent infections that it’s essentially no more than a slippery dip. It’s difficult for him to absorb any nutrients from his food, and we desperately need him to gain weight so his body and brain can grow.

In the treatment room Bananas in Pyjamas is playing. The room is crowded. In between the paediatrician, two nurses, the surgical registrar, mum and a writhing, screaming patient, there are bubbles. So many bubbles. The young surgical trainee gingerly examines the numerous boils that cover the little girl’s legs and groin. They will require an operation to drain them. She too has been with us for a week already. Her kidneys are struggling, after her body mounted an autoimmune reaction to the streptococcal infection from the boils. We closely monitor her weight and blood pressure until her kidneys are out of the woods.

The diabetes educator and paediatrician discuss a 13-year-old girl, who has just been diagnosed with type 2 diabetes mellitus. Already she weighs over 100 kg. Her case being outside the realm of conventional paediatric practice, the paediatrician is seeking advice on the best management plan for this patient. The girl’s mother, in her 30s, already suffers from retinopathy from her diabetes. One of the challenges of managing type 2 diabetes in an adolescent is the general lack of evidence to inform practice. It’s simply too new a phenomenon. The evidence to inform the management of type 2 diabetes in an Indigenous child is virtually non-existent.

At the hospital, we are so far downstream that we are practically out to sea. Essentially, we patch the kids up, keep them from dying, and make an attempt at educating the child’s parents about what has happened and why. It is grossly inadequate when almost everything that we see is preventable.

How is it then, in a wealthy nation like Australia which boasts a universal health system that is arguably one of the best in the world, that the life expectancy of Indigenous Australians is still (at a conservative estimate) 10–17 years less than their non-Indigenous counterparts? Why do the babies of Aboriginal mothers die at more than twice the rate of non-Aboriginal mothers? Why are so many remote communities still plagued by poor hygiene, overcrowding and dysfunctional living conditions, condemning their inhabitants to lifelong chronic disease? To me, it’s incomprehensible.

The instinct of many is to blame the individual. I know that I am often tempted to do so, especially when you see children who are suffering. However, blaming or inducing guilt is counterproductive. It does not help anyone. If anything, it alienates and denigrates. It is simply not correct to suggest that a person engages in certain behaviours by “choice”, and choice alone. It is too simplistic. To do so ignores the fact that every individual is a member of a community and is shaped by that community, his or her environment, education, and a personal and collective history.

To date, many health promotion programs have made a grossly inaccurate assumption that health education will automatically translate to behaviour change. It’s the same flawed logic that tells me I should floss daily and do at least 30 minutes of moderate-to-vigorous physical activity each day. Does knowledge alone empower me to change my behaviour? Sometimes it can, but only when the environment allows. Can I prevent my children from getting scabies when 15 people live in my home, multiple people share mattresses and I don’t have running water in the house, let alone a washing machine? Unlikely.

There is no strategic plan or coordination between services to promote hygiene improvement in remote communities.2 The social determinants of health have been ignored or, at the very least, addressed in a piecemeal manner. Public servants in air-conditioned offices write hygiene promotion strategies that fail to address the functional state of housing infrastructure and the unique environmental conditions of remote communities. Obesity and micronutrient deficiency in remote communities is a direct result of food insecurity caused by low incomes and the high price of fresh, nutritious food. This is unlikely to ever be overcome as long as local stores (often the sole providers of food in remote communities) continue to be viewed as a small business, rather than an essential service such as health or education.3 The past and continuing erosion of Indigenous culture and language serves only to perpetuate the vicious cycle of poverty and poor health.4

Government departments are often only as far apart as a different floor in the same building, yet the level of communication and collaboration between departments would suggest there is in fact a chasm between them. Multisector collaboration and high-level engagement and partnership with Indigenous peoples are the only hope we have to “close the gap”.

Good health is not made in hospitals. Good health is made by the food we eat, the water we drink, by feeling safe, secure, loved and connected. It is the roof over our heads, our sense of purpose in the world. Education is not just power, but health too. It is health, not illness that I am passionate about. I need to be further upstream. Maybe I need to see the Todd River flow.

–

The Todd River, Alice Springs. Photo taken in March 2015.

Breastmilk banking and the Mercy Health experience

Breastmilk banking provides an alternative to infant formula, not a substitute for mother’s own milk

Breastmilk banks collect, process, store and distribute donated human milk for hospitalised premature and growth-restricted infants. Pasteurised donor human milk (PDHM) as an alternative to artificial formula when mother’s own milk is unavailable is not a new concept. Before infant formula became widely available, milk sharing and wet nursing were common practices in Australian maternity wards in the 1940s. Concerns regarding transmission of infectious diseases in the 1980s saw breastmilk banks fall out of favour. With improved screening, storage and handling procedures, and evidence surrounding the importance of breastmilk in human development, breastmilk banking has re-emerged as a viable option when the supply of mother’s own breastmilk is insufficient. Insufficient supply may occur because of maternal illness, medications or difficulties in establishing or maintaining lactation. Some 450 breastmilk banks exist internationally and the numbers are rising.

Infant feeding guidelines from the World Health Organization1 and the National Health and Medical Research Council2 recommend exclusive breastfeeding for the first 6 months of life. When this is not possible, the alternatives are either expressed donor breastmilk or formula milk. Given that artificial formula cannot provide many benefits beyond basic nutrition, the American Academy of Pediatrics states that PDHM should be first choice for preterm infants when there is insufficient mothers’ own milk.3 Evidence shows that compared with formula, donor human milk is associated with a lower incidence of necrotising enterocolitis and other infections during initial hospitalisation.1

In Australia, five recognised facilities currently exist, led by the establishment of the Perron Rotary Express Milk Bank in 2006, at the King Edward Memorial Hospital in Western Australia. Although there are no universal Australian guidelines governing practice, most centres adhere to the 2010 United Kingdom National Institute for Health and Care Excellence (NICE) guidelines for the operation of donor breastmilk banks,4 which include donor screening recommendations. In 2014, the Australian government published an examination of donor human milk banking in Australia,5 comprehensively reviewing the evidence, quality assurance and regulatory issues surrounding risk management and quality control. The report concluded that voluntary regulation guided by existing legal frameworks is sufficient and appropriate.

Current international guidelines recommend pasteurisation of donor human milk to minimise the risk of disease transmission by inactivating most viral and bacterial contaminants. Additionally, screening is recommended for donors, similar to that for routine blood donation. Minimum serological standards include testing for HIV-1, HIV-2, hepatitis B and C virus, human T-lymphotropic virus types 1 and 2, and syphilis, as recommended by the Australasian Tissue Banking Forum.6

2015 marks the fifth year of operation for the Mercy Health Breastmilk Bank (MHBMB). As Victoria’s first breastmilk bank, founded in 2011, and the second largest of its type in Australia, this service continues to grow, providing for extremely sick and premature babies born at Mercy Hospital for Women in Melbourne.

Since conception in 2011, the MHBMB has collected over 1551 litres of PDHM, received from 162 mothers, supplying 276 babies. Following international criteria, neonates born before 34 weeks’ gestation or weighing less than 1500 g at birth are eligible for PDHM. Last year alone, over 254 litres of donor milk was consumed by babies cared for at Mercy Hospital for Women.

The MHBMB collects, screens, pasteurises and stores donor milk according to NICE guidelines. With parental consent, PDHM is available to babies in the special care nursery and intensive care unit, usually as a bridging supply until mothers’ own milk becomes sufficient. This donated milk provides preterm neonates with essential nutritional requirements for growth and neurological development, and human specific proteins and immunoglobulins for protection against infectious disease and immunity against other disorders.5,6

The MHBMB currently relies on donated breastmilk from mothers who have recently given birth at Mercy Hospital for Women. Our future hope is to include new mothers around Victoria and provide PDHM to eligible infants in other Victorian tertiary nurseries.

Oxytocin may benefit some children with autism, but it’s not the next wonder drug

A synthetic version of the “trust” hormone oxytocin, delivered as a nasal spray, has been shown to improve social responsiveness among some children with autism, researchers from the University of Sydney have found.

Published today in the journal Molecular Psychiatry, the trial is the first to rigorously examine the effects of oxytocin over a long time period in young children with autism spectrum conditions (ASC). ASC affect many aspects of a child’s development, including social and communication development.

But while it’s an important step forward, the effects observed in the study are simply too small and too inconsistent – and the stakes are simply too high – for anyone to herald a new autism wonder drug.

Current treatments

Behavioural therapies are considered the first line of therapies for ASC, and on many fronts these have proven to be effective. The drawbacks, which are not discussed as often as they should, are the considerable costs.

Consider for a moment that one recommended regimen of behavioural therapy is upwards of 20 hours per week. Highly trained therapists cost approximately A$150 for every one hour session, and so the financial burden adds up very quickly. Only a small number of families have the capacity to allocate the necessary resources to these kind of programs. This leaves the majority of families seeking therapy alternatives.

The search for effective pharmaceutical therapies is not just due to the financial and time costs associated with behavioural interventions, but also because these behavioural therapies are not highly effective for all children with ASC.

Autism has had a faddish relationship with pharmaceuticals. Numerous drugs over the past half a century have shown promise for benefiting individuals with ASC, and almost instantaneously achieve world-wide fame. But without fail, after further rigorous research, each of these drugs have been found to be no more effective than a placebo.

Other drugs have been found to be ineffective in reducing core ASC behaviours, such as social and repetitive behaviours, but may provide benefits for associated difficulties, such as sleep or anxiety.

Fads come and go. Hope gets raised and inevitably dashed. It was into this landscape that oxytocin began being tested as a potential pharmaceutical for ASC.

What is oxytocin?

Oxytocin is a hormone that affects social cognition and behaviour, and has been the “molecule of the moment” for close to a decade. The human brain produces oxytocin naturally, and is involved in promoting childbirth and lactation reflexes.

Research in ASC has focused on the possible effects of providing the brain with a dose of synthetic oxytocin. In studies of adults, the administration of oxytocin as a nasal spray has been found to improve trust as well as several aspects of social ability, including eye gaze and emotion recognition. These latter abilities are characteristic difficulties of individuals with ASC, and so oxytocin was very quickly examined as a potential pharmaceutical therapy for ASC.

Until this point, studies examining the effects of oxytocin on individuals with ASC have produced contradictory findings. Several research groups have identified small improvements in social behaviours in adults with ASC, while others have identified little to no benefits (in studies of adults children, and adolescents).

The new study

The study included 31 children with an ASC aged between three and eight years of age.

The study used what is called a “cross-over” design, which involves two phases of drug administration. In the first phase, each child is allocated into receiving either oxytocin or the placebo. After five weeks of taking the drug, the groups then switch, so that the group that received the oxytocin in the first phase now receives the placebo, and vice versa for the group that initially received the placebo.

This is a neat design because it means that participants act as their own “control”. This enables scientists to directly compare each child’s abilities after taking oxytocin with their abilities after taking the placebo.

The children received the oxytocin or a placebo through a nasal spray bottle. The placebo looked and smelled exactly like the oxytocin spray, but contained none of this active ingredient. Children received one spray of the relevant bottle in each nostril, morning and night.

Importantly, the study was “double blind”, which meant that neither the family nor the investigators knew what was in the spray bottle during each phase until the conclusion of the trial. After the trial finished, the researchers were “unblinded” to the content of the spray bottles.

The key finding was that the children with ASC showed significant improvements in “social responsiveness” after a period receiving oxytocin, but no improvements after a period receiving the placebo. Social responsiveness refers to abilities such as social awareness, reciprocal social interaction and social anxiety avoidance. In this study, social responsiveness was assessed by the parent using a widely used questionnaire.

However, oxytocin was found to be no more effective than the placebo in its effect on measures of repetitive behaviours and emotional difficulties.

What does this mean?

This was a rigorously conducted trial, and the results indicate that oxytocin may provide small benefits to some children with ASC.

There are limitations to this study that must be acknowledged. While the number of children included in this trial is among the largest of any previous study – particularly given the “cross-over” design, which increases the statistical power – the sample size is too small to make any sweeping conclusions about the importance of oxytocin in ASC intervention.

But the study does provide a strong platform upon which further science can be conducted.

Larger studies of oxytocin as a potential therapeutic for ASC are currently underway in both the United States and Australia, and will provide a greater evidence base in this area, as will studies examining the effect of oxytocin in conjunction with more traditional behavioural therapies.

However, despite these preliminary positive findings, it is important to remain keen observers of the complicated history between ASC and the limited progress into new pharmaceuticals.

And in that context, the decade of research on oxytocin that has preceded this study is highly instructive. Oxytocin may provide benefit to some children with ASC, but it is not a panacea and it cannot yet be recommended for children until further studies are conducted.

Andrew Whitehouse, Winthrop Professor, Telethon Kids Institute, University of Western Australia and Gail Alvares, Postdoctoral Research Fellow, Telethon Kids Institute

This article was originally published on The Conversation. Read the original article.

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Signs workforce planning getting back on track

It’s been a chequered time for medical workforce planning in recent years.

Health Workforce Australia (HWA) was a Commonwealth statutory authority established in 2009 to deliver a national and co-ordinated approach to health workforce planning, and had started to make substantial progress toward improving medical workforce planning and coordination. It had delivered two national medical workforce reports and formed the National Medical Training Advisory Network (NMTAN) to enable a nationally coordinated medical training system.

Regrettably, before it could realise its full potential, the Government axed HWA in the 2014-15 Budget, and its functions were moved to the Health Department. This was a short-sighted decision, and it is taking time to rebuild the workforce planning capacity that was lost.

NMTAN is now the Commonwealth’s main medical workforce training advisory body, and is focusing on planning and coordination.

It includes representatives from the main stakeholder groups in medical education, training and employment. Dr Danika Thiemt, Chair of the AMA Council of Doctors in Training, sits with me as the AMA representatives on the network.

Our most recent meeting was late last month, and the discussions there make us hopeful that NMTAN is finally in a position where it can significantly lift its output, contribution and value to medical workforce planning.

In its final report, Australia’s Future Health Workforce, HWA confirmed that Australia has enough medical school places.

Instead, it recommended the focus turn to improving the capacity and distribution of the medical workforce − and encouraging future medical graduates to train in the specialties and locations where they will be needed to meet future community demands for health care.

The AMA supports this approach, but it will require robust modelling.

NMTAN is currently updating HWA modelling on the psychiatry, anaesthetic and general practice workforces. We understand that the psychiatry workforce report will be released soon. This will be an important milestone given what has gone before.

Nonetheless, it will be important to lift the number of specialties modelled significantly now that we have the basic approach in place, so that we will have timely data on imbalances across the full spectrum of specialties.

The AMA Medical Workforce Committee recently considered what NMTAN’s modelling priorities should be for 2016.

Based on its first-hand knowledge of the specialities at risk of workforce shortage and oversupply, the committee identified the following specialty areas as priorities: emergency medicine; intensive care medicine; general medicine; obstetrics and gynaecology; paediatrics; pathology and general surgery.

NMTAN is also developing some factsheets on supply and demand in each of the specialities – some of which now available from the Department of Health’s website (http://www.health.gov.au/internet/main/publishing.nsf/Content/nmtan_subc…). I encourage you to take a look.

These have the potential to give future medical graduates some of the career information they will need to choose a specialty with some assurance that there will be positions for them when they finish their training.

Australia needs to get its medical workforce planning back on track.

Let’s hope that NMTAN and the Department of Health are up to the task.

Scrapping the Healthy Kids Check: a lost opportunity

Maintaining child preventive health and developmental assessments will challenge general practice from 1 November

In May, the federal government announced in the 2015–16 Budget that the Healthy Kids Check (HKC) Medicare items will be discontinued from 1 November 2015,1 citing underperformance, cost blowouts and duplication of state and territory programs.

The HKC was introduced into general practice in 2008, policy that reflected advances in neuroscience (eg, the evolution of brain architecture, critical time points for development and the benefits of early intervention) and significant health shifts towards prevention. Uptake of the health assessment was slow (16% of eligible children in its first year2) and beset by argument about a lack of evidence for some of its mandatory components3 and by scaremongering about labelling 3-year-olds with mental health diagnoses.4 In the ensuing negative debate, it was easy to forget major barriers to preventive health care before the HKC: sick child consultations, poor remuneration, lack of time, resources and training,5 and the ever-increasing demands of chronic disease management in an ageing population. Nevertheless, over the next 7 years, uptake of the HKC climbed to 50%,2 as practice nurses were upskilled and parents were incentivised by tax benefits.6 Our research with practitioners, 3 years after its introduction, indicated that in some circumstances, the HKC had acted as a catalyst for general practitioner and practice nurse (PN) role development, and in some cases promoted an entire practice shift towards preventive health care for young children.7 The important contribution made by PNs, in particular, has been overlooked by the government in its statement that GPs can continue to provide health assessments as part of Medicare-funded general GP attendance items,8 because PNs are excluded from those services.

The government also contends that no evidence had been provided to show that HKCs deliver superior benefits to children. The findings of an evaluation of the “expanded HKC”, which underwent trialled in eight Medicare Locals in 2013, have not been made public, but one published study considered the outcomes from HKCs and found that a fifth of HKCs uncovered some sort of health or developmental problem, and between 3% and 11% of HKCs changed the health management of the children concerned.9 Despite lower than expected prevalence estimates for some childhood conditions reported in this study (eg, overweight and oral health problems), the findings still showed that significant numbers of children could benefit from an HKC.

Duplication of state-funded child and family health nurse (CFHN) services was put forward as justification for the removal of HKCs. However, CFHN service delivery varies widely between the states. Even in Victoria, where comprehensive services are provided, only two-thirds of families attend the 3.5 year health assessment.10 Our research with parents revealed that although some parents were willing to visit CFHNs with their infants, not all parents presented with their toddlers.11 For a variety of reasons, parents “get busy”, so that attendance rates drop off after the first year of a child’s life and with successive children.11 We do not know if CFHN non-attendees are the families receiving HKCs from the GP, but GPs are used to working with families and young children. Within this setting of established relationships, some parents choose to have their children vaccinated by their GP, rather than attend local council services or CFHN clinics. Providing parents with a choice of immunisation providers improves access and thus contributes to overall high coverage of child immunisation coverage.

Without a similar comprehensive approach to child developmental assessment, children will miss opportunities for early intervention. In 2012, for example, the average age of children being diagnosed with an autism spectrum disorder was 4 years 1 month despite diagnosis being possible in the second year.12 This suggests that many children are not being diagnosed before school.

The HKC also provides the context to address rates of childhood overweight that already affect more than 20% of preschoolers13 and rates of dental caries that affect one in two children aged 5 years.14 Without protected opportunities to engage parents regarding child preventive health and without the signal that the HKC gives to parents that GPs are interested in such issues, children will continue to miss out on preventive health activities routinely delivered to other sectors of the population.

By scrapping the HKC, not only are we reducing the chances of identifying problems earlier but we are effectively reducing the capacity of general practice to promote the health and development of young children, the most vulnerable in our population, who stand to gain the most over the course of their lifetime. This is a retrograde step for Australia’s future.