Category: Articles

Categories
Articles Guest Articles

Genomic medicine

The last decade has seen an extraordinary revolution in the technology of DNA sequencing. This has meant that the cost of sequencing a human genome has dropped from nearly a billion dollars in 2001, when the first draft of a human sequence was completed, to less than $10,000 today (Figure 1). [1] We’re now seeing the first prototypes of sequencing machines that promise the capacity to sequence a human genome in a few hours for less than $1000.

Even at current costs, this acceleration in sequencing has enabled a whole suite of studies into human variation at the genetic level. In the cancer arena, the international cancer genome projects—with which we’ve been involved—show that cancer is a heterogeneous disease. While there are differences in the distribution of mutations in cancers from different tissues, a surprisingly high percentage have mutations in common. [2] This is not obvious from the pathology and can, in many cases, productively inform treatment options and save lives. However, this is just the tip of an iceberg. There are large numbers of human genomics studies around the world producing an explosion of information about how individuals vary in physical and, to some extent, psychological characteristics. These studies are also identifying idiosyncrasies in our DNA that can leave us at risk for complex diseases.

Taking advantage of that information can be useful even at this early stage. In a recent Cell paper [3], the Chair of the Stanford University genetics department gave himself a battery of medical tests and analysed his own genome. By integrating this information, he was able to successfully identify his own type 2 diabetes and take steps to manage its impact.

Genomic stratification – to identify the underlying mutations in cancer – is quickly becoming the standard of care in cancer. Some of these mutations are considered ‘actionable’ because there are existing drugs that have been developed to treat the same mutations in other tissue contexts. Others may predict outcomes in response to existing therapies.

Usage of partial or whole genome sequencing in diagnosing monogenic diseases is also moving quickly. While monogenic diseases, which have catastrophic mutations in protein-coding sequences, are usually individually rare, they collectively account for more than 1% of births in our population. Faster, cheaper sequencing provides the opportunity to analyse an individual’s DNA sequences very quickly. As a result, there are an increasing number of examples in the literature where such information has transformed clinical treatment and the health of the individual.

The bottom line is that we going through the most extraordinary exploration of human genetic programming and genetic diversity in history. This will have an enormous impact on medical practice. Eventually, everybody’s genome will be sequenced and incorporated into their medical record. Clinicians and physicians of the future will be referring to this information as part of standard care for their patients, in conjunction with contextual information such as diet, economic and cultural circumstances.

Where many of the treatments that we traditionally use were pitched at the average of the population, it is now possible to personalise care. This begins with making judgments about people’s drug responses and tuning those accordingly to get the best effective dose and avoiding side effects. It is expected to extend to assessing an individual’s risk of complex diseases like diabetes, osteoporosis and stroke and helping them to take ameliorative behavioural, lifestyle, dietary or pharmaceutical strategies as appropriate to reduce those risks.

There is going to be an extraordinary cultural and operational transition from treatment to health optimisation. The challenge is to translate the literally millions of differences between individual whole genome sequences into simple, lucid, clinically-actionable information that can be accessed at point of care. This means, I think, that in the background, we’re going to see the development of national and international genotype-phenotype databases that will assemble and collate evidence-based information about how human genetic variation indicates disease risk and health futures.

Rather than suggest that this is a threatening development, I think this is a wonderful opportunity for young clinicians to empower medicine through the integration of genomic information with other aspects of practice and care. This is an extraordinary time of technical, intellectual and conceptual change, which offers medical students the opportunity to embrace a career in research and to invest their futures with a major medical research institute. Genomic medicine will have as big an impact on health as antibiotics, and it will be your generation that takes this forward.

References

[1] Wetterstrand KA. DNA Sequencing Costs: Data from the NHGRI Genome Sequencing Program (GSP) Available at: www.genome.gov/sequencingcosts. Accessed 22 April 2013.

[2] Biankin, A. V., Waddell, N., Kassahn, K. S., Gingras, M.-C., Muthuswamy, L. B., Johns, A. L., . . . Grimmond, S. M. (2012). Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. Nature, advance online publication. doi: [10.1038/nature11547].

[3] Chen, R., Mias, G. I., Li-Pook-Than, J., Jiang, L., Lam, H. Y. K., Chen, R., . . . Snyder, M. (2012). Personal Omics Profiling Reveals Dynamic Molecular and Medical Phenotypes. Cell, 148(6), 1293-1307. Retrieved from http://linkinghub.elsevier.com/retrieve/pii/S0092867412001663

Categories
Articles Guest Articles

The impact of the nuclear crisis on global health

Due to my personal concerns regarding the ignorance of the world’s media and politicians about radiation biology after the dreadful accident at Fukushima in Japan, I organized a 2 day symposium at the NY Academy of Medicine on March 11 and 12, 2013, titled ‘The Medical and Ecological Consequences of Fukushima,’ which was addressed by some of the world’s leading scientists, epidemiologists, physicists and physicians who presented their latest data and findings on Fukushima. [1]

Background

The Great Eastern earthquake, measuring 9.0 on the Richter scale, and the ensuing massive tsunami on the east coast of Japan induced the meltdown of three nuclear reactors within several days. During the quake the external power supply was lost to the reactor complex and the pumps, which circulate up to one million gallons of water per minute to cool each reactor core, ceased to function. Emergency diesel generators situated below the plants kicked in but these were soon swamped by the tsunami. Without cooling, the radioactive cores in units 1, 2 and 3 began to melt within hours. Over the next few days, all three cores (each weighing more than 100 tonnes) melted their way through six inches of steel at the bottom of their reactor vessels and oozed their way onto the concrete floor of the containment buildings. At the same time the zirconium cladding covering thousands of uranium fuel rods reacted with water, creating hydrogen, which initiated hydrogen explosions in units 1, 2, 3 and 4.

Massive quantities of radiation escaped into the air and water – three times more noble gases (argon, xenon and krypton) than were released at Chernobyl, together with huge amounts of other volatile and non-volatile radioactive elements, including cesium, tritium, iodine, strontium, silver, plutonium, americium and rubinium. Eventually sea water was – and is still – utilized to cool the molten reactors.

Fukushima is now described as the greatest industrial accident in history.

The Japanese government was so concerned that they were considering plans to evacuate 35 million people from Tokyo, as other reactors including Fukushima Daiini on the east coast were also at risk. Thousands of people fleeing from the smoldering reactors were not notified where the radioactive plumes were travelling, despite the fact that there was a system in place to track the plumes. As a result, people fled directly into regions with the highest radiation concentrations, where they were exposed to high levels of whole-body external gamma radiation being emitted by the radioactive elements, inhaling radioactive air and swallowing radioactive elements. [2] Unfortunately, inert potassium iodide was not supplied, which would have blocked the uptake of radioactive iodine by their thyroid glands, except in the town of Miharu. Prophylactic iodine was eventually distributed to the staff of Fukushima Medical University in the days after the accident, after extremely high levels of radioactive iodine – 1.9 million becquerels/kg were found in leafy vegetables near the University. [3] Iodine contamination was widespread in leafy vegetables and milk, whilst other isotopic contamination from substances such as caesium is widespread in vegetables, fruit, meat, milk, rice and tea in many areas of Japan. [4]

The Fukushima meltdown disaster is not over and will never end. The radioactive fallout which remains toxic for hundreds to thousands of years covers large swathes of Japan and will never be “cleaned up.” It will contaminate food, humans and animals virtually forever. I predict that the three reactors which experienced total meltdowns will never be dissembled or decommissioned. TEPCO (Tokyo Electric Power Company) – says it will take at least 30 to 40 years and the International Atomic Energy Agency predicts at least 40 years before they can make any progress because of the extremely high levels of radiation at these damaged reactors.

This accident is enormous in its medical implications. It will induce an epidemic of cancer as people inhale the radioactive elements, eat radioactive food and drink radioactive beverages. In 1986, a single meltdown and explosion at Chernobyl covered 40% of the European land mass with radioactive elements. Already, according to a 2009 report published by the New York Academy of Sciences, over one million people have already perished as a direct result of this catastrophe. This is just the tip of the iceberg, because large parts of Europe and the food grown there will remain radioactive for hundreds of years. [5]

Medical Implications of Radiation

Fact number one

No dose of radiation is safe. Each dose received by the body is cumulative and adds to the risk of developing malignancy or genetic disease.

Fact number two

Children are ten to twenty times more vulnerable to the carcinogenic effects of radiation than adults. Females tend to be more sensitive compared to males, whilst foetuses and immuno-compromised patients are also extremely sensitive.

Fact number three

High doses of radiation received from a nuclear meltdown or from a nuclear weapon explosion can cause acute radiation sickness, with alopecia, severe nausea, diarrhea and thrombocytopenia. Reports of such illnesses, particularly in children, appeared within the first few months after the Fukushima accident.

Fact number four

Ionizing radiation from radioactive elements and radiation emitted from X-ray machines and CT scanners can be carcinogenic. The latent period of carcinogenesis for leukemia is 5-10 years and solid cancers 15-80 years. It has been shown that all modes of cancer can be induced by radiation, as well as over 6000 genetic diseases now described in the medical literature.

But, as we increase the level of background radiation in our environment from medical procedures, X-ray scanning machines at airports, or radioactive materials continually escaping from nuclear reactors and nuclear waste dumps, we will inevitably increase the incidence of cancer as well as the incidence of genetic disease in future generations.

Types of ionizing radiation

  1. X-rays are electromagnetic, and cause mutations the instant they pass through the body.
  2. Similarly, gamma radiation is also electromagnetic, being emitted by radioactive materials generated in nuclear reactors and from some naturally occurring radioactive elements in the soil.
  3. Alpha radiation is particulate and is composed of two protons and two neutrons emitted from uranium atoms and other dangerous elements generated in reactors (such as plutonium, americium, curium, einsteinium, etc – all which are known as alpha emitters and have an atomic weight greater than uranium). Alpha particles travel a very short distance in the human body. They cannot penetrate the layers of dead skin in the epidermis to damage living skin cells. But when these radioactive elements enter the lung, liver, bone or other organs, they transfer a large dose of radiation over a long period of time to a very small volume of cells. Most of these cells are killed; however, some on the edge of the radiation field remain viable to be mutated, and cancer may later develop. Alpha emitters are among the most carcinogenic materials known.
  4. Beta radiation, like alpha radiation, is also particulate. It is a charged electron emitted from radioactive elements such as strontium 90, cesium 137 and iodine 131. The beta particle is light in mass, travels further than an alpha particle and is also mutagenic.
  5. Neutron radiation is released during the fission process in a reactor or a bomb. Reactor 1 at Fukushima has been periodically emitting neutron radiation as sections of the molten core become intermittently critical. Neutrons are large radioactive particles that travel many kilometers, and they pass through everything including concrete and steel. There is no way to hide from them and they are extremely mutagenic.

So, let’s describe just five of the radioactive elements that are continually being released into the air and water at Fukushima. Remember, though, there are over 200 such elements each with its own half-life, biological characteristic and pathway in the food chain and the human body. Most have never had their biological pathways examined. They are invisible, tasteless and odourless. When the cancer manifests it is impossible to determine its aetiology, but there is a large body of literature proving that radiation causes cancer, including the data from Hiroshima and Nagasaki.

  1. Tritium is radioactive hydrogen H3 and there is no way to separate tritium from contaminated water as it combines with oxygen to form H3O. There is no material that can prevent the escape of tritium except gold, so all reactors continuously emit tritium into the air and cooling water as they operate. It concentrates in aquatic organisms, including algae, seaweed, crustaceans and fish, and also in terrestrial food.  Like all radioactive elements, it is tasteless, odorless and invisible, and will therefore inevitably be ingested in food, including seafood, for many decades. It passes unhindered through the skin if a person is immersed in fog containing tritiated water near a reactor, and also enters the body via inhalation and ingestion. It causes brain tumors, birth deformities and cancers of many organs.
  2. Cesium 137 is a beta and gamma emitter with a half-life of 30 years. That means in 30 years only half of its radioactive energy has decayed, so it is detectable as a radioactive hazard for over 300 years. Cesium, like all radioactive elements, bio-concentrates at each level of the food chain. The human body stands atop the food chain. As an analogue of potassium, cesium becomes ubiquitous in all cells. It concentrates in the myocardium where it induces cardiac irregularities, and in the endocrine organs where it can cause diabetes, hypothyroidism and thyroid cancer. It can also induce brain cancer, rhabdomyosarcomas, ovarian or testicular cancer and genetic disease.
  3. Strontium 90 is a high-energy beta emitter with a half-life of 28 years. As a calcium analogue, it is a bone-seeker. It concentrates in the food chain, specifically milk (including breast milk), and is laid down in bones and teeth in the human body. It can lead to carcinomas of the bone and leukaemia.
  4. Radioactive iodine 131 is a beta and gamma emitter. It has a half-life of eight days and is hazardous for ten weeks. It bio-concentrates in the food chain, in vegetables and milk, then in the the human thyroid gland where it is a potent carcinogen, inducing thyroid disease and/or thyroid cancer. It is important to note that of 174,376 children under the age of 18 that have been examined by thyroid ultrasound in the Fukushima Prefecture, 12 have been definitively diagnosed with thyroid cancer and 15 more are suspected to have the disease. Almost 200,000 more children are yet to be examined. Of these 174,367 children, 43.2% have either thyroid cysts and/or nodules.
    In Chernobyl, thyroid cancers were not diagnosed until four years post-accident. This early presentation indicates that these Japanese children almost certainly received a high dose of radioactive iodine. High doses of other radioactive elements released during the meltdowns were received by the exposed population so the rate of cancer is almost certain to rise.
  5. Plutonium, one of the most deadly radioactive substances, is an alpha emitter. It is highly toxic, and one millionth of a gram will induce cancer if inhaled into the lung. As an iron analogue, it combines with transferrin. It causes liver cancer, bone cancer, leukemia, or multiple myeloma. It concentrates in the testicles and ovaries where it can induce testicular or ovarian cancer, or genetic diseases in future generations. It also crosses the placenta where it is teratogenic, like thalidomide. There are medical homes near Chernobyl full of grossly deformed children, the deformities of which have never before been seen in the history of medicine.
    The half-life of plutonium is 24,400 years, and thus it is radioactive for 250,000 years. It will induce cancers, congenital deformities, and genetic diseases for virtually the rest of time.
    Plutonium is also fuel for atomic bombs. Five kilos is fuel for a weapon which would vaporize a city. Each reactor makes 250 kg of plutonium a year. It is postulated that less than one kilo of plutonium, if adequately distributed, could induce lung cancer in every person on earth.

Conclusion

In summary, the radioactive contamination and fallout from nuclear power plant accidents will have medical ramifications that will never cease, because the food will continue to concentrate the radioactive elements for hundreds to thousands of years. This will induce epidemics of cancer, leukemia and genetic disease. Already we are seeing such pathology and abnormalities in birds and insects, and because they reproduce very fast it is possible to observe disease caused by radiation over many generations within a relatively short space of time.

Pioneering research conducted by Dr Tim Mousseau, an evolutionary biologist, has demonstrated high rates of tumors, cataracts, genetic mutations, sterility and reduced brain size amongst birds in the exclusion zones of both Chernobyl and Fukushima. What happens to animals will happen to human beings. [7]

The Japanese government is desperately trying to “clean up” radioactive contamination. But in reality all that can be done is collect it, place it in containers and transfer it to another location. It cannot be made neutral and it cannot be prevented from spreading in the future. Some contractors have allowed their workers to empty radioactive debris, soil and leaves into streams and other illegal places. The main question becomes: Where can they place the contaminated material to be stored safely away from the environment for thousands of years? There is no safe place in Japan for this to happen, let alone to store thousands of tons of high level radioactive waste which rests precariously at the 54 Japanese nuclear reactors.

Last but not least, Australian uranium fuelled the Fukushima reactors. Australia exports uranium for use in nuclear power plants to 12 countries, including the US, Japan, France, Britain, Finland, Sweden, South Korea, China, Belgium, Spain, Canada and Taiwan. 270,000 metric tons of deadly radioactive waste exists in the world today, with 12,000 metric tons being added yearly. (Each reactor manufactures 30 tons per year and there are over 400 reactors globally.)

This high-level waste must be isolated from the environment for one million years – but no container lasts longer than 100 years. The isotopes will inevitably leak, contaminating the food chain, inducing epidemics of cancer, leukemia, congenital deformities and genetic diseases for the rest of time.

This, then, is the legacy we leave to future generations so that we can turn on our lights and computers or make nuclear weapons. It was Einstein who said “the splitting of the atom changed everything save mans’ mode of thinking, thus we drift towards unparalleled catastrophe.”

The question now is: Have we, the human species, the ability to mature psychologically in time to avert these catastrophes, or, is it in fact, too late?

Disclaimer: The views, opinions and perspectives presented in this article are those of the author alone and does not reflect the views of the Australian Medical Student Journal. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors or omissions.

References

[1] Caldicott H. Helen Caldicott Foundation’s Fukushima Symposium. 2013; Available from: http://www.helencaldicott.com/2012/12/helen-caldicott-foundations-fukushima-symposium/.

[2] Japan sat on U.S. radiation maps showing immediate fallout from nuke crisis. The Japan Times. 2012.

[3] Bagge E, Bjelle A, Eden S, Svanborg A. Osteoarthritis in the elderly: clinical and radiological findings in 79 and 85 year olds. Ann Rheum Dis. 1991;50(8):535-9. Epub 1991/08/01.

[4] Tests find cesium 172 times the limit in Miyagi Yacon tea. The Asahi Shimbun. 2012.

[5] Yablokov AV, Nesterenko VB, Nesterenko AV, Sherman-Nevinger JD. Chernobyl: Consequences of the Catastrophe for People and the Environment: Wiley. com; 2010.

[6] Fukushima Health Management. Proceedings of the 11th Prefectural Oversight Committee Meeting for Fukushima Health Management Survey. Fukushima, Japan2013.

[7] Møller AP, Mousseau TA. The effects of low-dose radiation: Soviet science, the nuclear industry – and independence? Significance. 2013;10(1):14-9.

 

Categories
Feature Articles Articles

Approaching autism

Autism Spectrum Disorder is a social communication disorder in someone displaying repetitive and restrictive interests. Diagnosed in early childhood, children struggle to develop social relationships required for further learning and independent living. This article discusses changes to the diagnosis, how the diagnosis is made, the prevalence, causes and interventions. Importantly, this review guides medical students towards an understanding of what to expect in individuals with autism spectrum disorder and how to interact with them.

What is autism?

Autism is diagnosed according to the American Psychiatric Association (APA) guidelines in the Diagnostic and Statistical Manual of Mental Disorders (DSM), [1] or alternatively, according to the International Classification of Diseases (ICD) published by the World Health Organization. [2] Mostly because of convention, the DSM is more often used in the diagnosis of autism in Australia.

From 2013, ‘autism’ would be a short form of the term Autism Spectrum Disorder (ASD). A diagnosis of ASD applies where there is evidence of functional impairment caused by:

Problems reciprocating social or emotional interaction, including difficulty establishing or maintaining back-and-forth conversations and interactions, inability to initiate an interaction, and problems with shared attention or sharing of emotions and interests with others.

Severe problems maintaining relationships, ranging from a lack of interest in other people to difficulties in pretend play and engaging in age-appropriate social activities, and problems adjusting to different social expectations.

Nonverbal communication problems such as abnormal eye contact, posture, facial expressions, tone of voice and gestures, as well as an inability to understand these. [1]

Additionally, two of the four symptoms related to restricted and repetitive behaviour need to be present:

Stereotyped or repetitive speech, motor movements or use of objects.

Excessive adherence to routines, ritualised patterns of verbal or nonverbal behaviour, or excessive resistance to change.

Highly restricted interests that are abnormal in intensity or focus.

Hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of the environment.

Symptoms must be present in early childhood, but may not become fully manifest until social demands exceed limited capacities. There must be an absence of general developmental delay. Finally, symptoms should not be better described by another DSM-5 diagnosis.

From the criteria it is important to note that there are many combinations of symptoms that can lead to a diagnosis of ASD. Therefore, not only do individuals with ASD share the same degree of uniqueness as the rest of the general population, but even the type of ASD they experience can be unique.

Confusion can arise in the use of the terms ‘autism’ and ‘autism spectrum disorders.’ Part of the reason for this emerges from the subtypes of Pervasive Developmental Disorders (PDD) previously recognised by the APA. PDD previously contained the subtypes Asperger’s Disorder, Childhood Disintegrative Disorder, Autistic Disorder and PDD-Not otherwise specified (NOS). While the ICD also recognizes Atypical Autism, recent changes to the DSM should simplify the nosology. [2]

The current ASD diagnosis criteria came into effect from May 2013 and is expected to identify approximately 90% of children with a clinical diagnosis from the previous DSM-IV. [3] A new diagnosis called Social Communication Disorder (SCD) has been created. Simply put, SCD is ASD, without the restrictive and repetitive interests. It is not yet clear how many children will receive a diagnosis of SCD, nor how many children previously identified with a DSM-IV diagnosis of PDD would meet the criteria for SCD only.

Diagnoses made under DSM-IV guidelines are still valid. A new diagnosis is not required simply because of the change in criteria. However, individuals being assessed for ASD now, and in the future, will be diagnosed under the new criteria.

Features of ASD

Social communication, interaction and motivation

ASD is principally characterized by social communication and interaction deficits. Individuals often experience difficulty with interpreting facial expressions, tone of voice, jokes, sarcasm, gestures and idioms. Imagine the literal meanings of “Fit as a fiddle,” “Bitter pill to swallow” and “Catch a cold.” Some people with ASD may have only limited speech or may be completely non-verbal. [4,5] Echolalia, pronoun reversal, unusual vocalisations and unusual accents are common. [4,5] Alternative, augmentative and visually based communication techniques may help when a child is unable to consistently follow verbal instructions. In this regard, touch-screen portable devices may appeal to their visual and pattern-orientated learning strengths (see Figure 1). [6]

Difficulties with social interactions mean that affected individuals often grow up without a social circle, and as a consequence, miss out on peer-initiated learning opportunities. [7] Such challenges include difficulty with understanding unwritten social rules such as personal space and initiating conversation. [7] They can appear to be insensitive, because they are unable to perceive how someone else is feeling. Turn taking and sharing is not intuitive or learned, and individuals need to be trained how to do this. An inability to express feelings, emotions or needs results in inappropriate behaviour such as unintentionally aggressive actions. [8] This can lead to isolation, a failure to seek comfort from others and signs of low self-esteem. [7] Individuals can also suffer from hypersensitivity to sensory stimuli, which may lead them to prefer limited social contact. Individuals do feel enjoyment and excitement; however, this tends to be a personal experience and often goes unshared, which may be due to a failure to need the reward of another’s attention and praise. [9]

Imagination

Individuals with ASD may experience challenges with social imagination. [10] Individuals are less likely to engage in make-believe play and activities. They are less likely to determine and interpret other’s thoughts, feelings and actions, and as a consequence unable to appreciate that other people may not be interested in their topic of interest.

Individuals with ASD are often unable to predict outcomes, or foresee what might occur next, including hazards. [11] This leads to a difficulty in coping in new or unfamiliar situations, or making plans for the future. Parents, carers and health professionals often need to stick to routines to avoid unpredicted events that could cause distress.

Sensory and motor processing

Sensory information processing is heightened for tactile input, but reduced for social input, in individuals with ASD. [12] Changes in these inputs are understood to contribute to the repetitive and restrictive interest criteria of the diagnosis. Hence, the state of the tactile environment is important to the wellbeing of individuals with ASD, potentially serving as an aggravation by, or as a refuge from, incomprehensible cues. Changes in sensory information processing may present as an inability to distinguish context-relevant stimuli, and varying capabilities and capacity to respond to a stimulus (e.g. ignoring some sounds but over-reactive to others). They may also experience difficulty with proprioception and responding to pain, including temperature extremes. [12,13] Individuals may explore their environment by smelling or mouthing objects, people and surfaces, and as a consequence, develop eating behaviours that relate to smell, texture or flavor, including inedible objects. Participating in repetitive movements such as rocking, bouncing, flapping arms and hands, or spinning with no apparent dizziness is sometimes as a means of coping with stress, or alternatively, could be used as a means of self-stimulus, providing pleasure. [12] Contrary to popular perception, savant skills are uncommon in individuals with ASD. [14]

What causes ASD?

ASD is a multi-factorial disorder. There is no one cause of ASD. The most prominent risk factor is genetics, both familial and de novo. [15] Studies have shown that among monozygotic twins, if one child has ASD, then the other will be affected about 36–95% of the time. [16] In dizygotic twins, if one child has an ASD, then the other is affected up to about 31% of the time. [16] Parents who already have a child with an ASD have a 2%–18% chance of having a second child who is also affected. [17]

In addition to the well-documented increase in chromosomal abnormalities associated with advanced maternal age, the risk of ASD is also associated with advanced paternal age. [18] The current hypothesis to explain this observation is that small, de novo genetic mutations and rearrangements accumulate in the sperm, which are then incorporated into the DNA of the child. [19,20] Other risk factors include premature birth or low birth weight, preeclampsia [21] and in utero exposure to medications, particularly sodium valproate. [22] There is no evidence to support the theory that the measles, mumps and rubella vaccine causes autism. [23]

Three cognitive theories have evolved to explain the behavioural challenges of ASD: the theory of mind deficit, executive dysfunction, and weak central coherence. The first posits that individuals with ASD are unable to recognize mental states in others, leading to social behaviour discordance. [24,25] The second attempts to explain a lack of goal directed behaviour, and lack of behavioural flexibility. [26] Both these cognitive explanations may be underpinned by an early deficit in social motivation, whereby underdevelopment of the brain regions involved in social recognition and response leads to a failure to learn social cues and their contexts. [27] This has been traditionally thought to impact on imitation learning from which social and food reward by infants is derived and goal-directed behaviour emerges, although research in the area is equivocal. [28] Whether this same underdevelopment also delays acquisition of receptive and expressive language is unclear. [29] Finally, the weak central coherence theory is a means of understanding why individuals focus on details and neglect the context. [30] Yet, it could be argued that a neglect of the context emerges from a deficit in social motivation.

Epidemiology

In the community there is considerable concern of an ASD epidemic. Parental reports indicate ASD prevalence may have increased from 1 in 88 in 2007 to 1 in 50 children in 2012. [31] Currently, the prevalence of ASD in Australia is about 1 in 165 children aged 6-12 years. [32] In the USA this prevalence is slightly higher with 1 in 50–88 eight-year olds receiving a diagnosis; [31,33] this breaks down to 1 in 31–54 boys and 1 in 143–252 girls. [31,33]

A true appreciation of the changes in ASD prevalence can only come from understanding the historical basis of the diagnosis. [34,35] In this regard, marked changes in prevalence have been caused by nosology changes (e.g. autism was once called childhood schizophrenia) and a number of changes to the APA PDD criteria in the DSM over the past 30 years. [36] Other contributing factors include demographic variables (e.g. where older individuals may have missed receiving a diagnosis, but receive one now with the help of a retrospective investigation such as archival home video), increased awareness of normal childhood development and developmental disorders, changes in testing and protocols, and the sampling of data, such as parents versus clinicians, or state schools versus all children. Other factors that often go unreported include socioeconomic factors (e.g. those with sufficient knowledge and resources are able to seek out professional assistance and are more likely to receive a diagnosis than those without) and pressure on clinicians to provide a diagnosis, thereby assisting struggling parents access services and financial support. Trying to account for all these factors in an epidemiological study is very difficult. Hence, the true historical prevalence of ASD is difficult to establish. Studies that have tried show no, or a slight, increase in ASD. [35]

How is a diagnosis made?

While parents often suspect developmental delay or ASD, the variability in child development during the first four years can lead to variability in the age of first diagnosis – typically around three years of age. [34] Reliability of the diagnosis also suffers as a consequence. [37] Restrictive and repetitive interests can be difficult to identify before the age of four because even typically developing two- and three-year-olds can show repetitive behaviours. Since the new diagnosis also requires behaviours to be demonstrably incompetent (such as during a child’s interaction at day care), a lag between symptoms and diagnosis is likely to continue.

In Australia, paediatricians, clinical psychologists, psychiatrists and speech pathologists specialising in the field of paediatrics or adolescence make a formal diagnosis of ASD. Further, within these specialisations, diagnoses are likely to be made by practitioners with experience in testing and diagnosing ASD.

A typical diagnostic evaluation involves a multi-disciplinary team including pediatricians, psychologists, speech and language pathologists. Testing takes a number of hours and can be exhausting for subjects, parents and clinicians. Because of this and other factors, waiting times for diagnosis can be up to 24 months across the country, with particular difficulties in rural and remote areas. [38]

In initial consultations, screening tools may be used such as the Autism Behavior Checklist (ABC), Checklist for Autism in Toddlers (CHAT), Modified Checklist for Autism in Toddlers (M-CHAT), Childhood Autism Rating Scale (CARS) and Gilliam Autism Rating Scale (GARS). However, for a diagnosis, the Autism Diagnostic Interview-Revised (ADI-R) and Autism Diagnostic Schedule (ADOS) are used. [39,40]

Differential diagnoses and comorbidities

There is no single test for ASD and there are no unique physical attributes. For this reason differential diagnoses such as hearing and specific language impairments, mutism, environmental conditions such as neglect and abuse, and attachment and conduct disorders need to be excluded. Disorders similar to ASD include Social Communication Disorder and Social Anxiety Disorder. In the latter, communication is preserved but a degree of social phobia persists.

Since ASD diagnoses are made according to a description of a set of behaviours rather than a developmental abnormality or genetic condition, it is not uncommon to find a diagnosis of ASD comorbid with another pre-existing condition. For example, approximately 20% of children with Down syndrome meet the diagnosis for ASD. [41] Theoretically, all children with genetic abnormalities such as Angelman syndrome or Rett syndrome would also meet criteria for a diagnosis for ASD. In the event of an existing condition, a diagnosis of ASD may also be warranted in order to guide the child’s behavioural management and education.

ASD often co-occurs with another developmental, psychiatric, neurologic, or medical diagnosis. [42] The co-occurrence of one or more non-ASD developmental diagnoses with ASD is approximately 80%. Co-morbidities often occur with attention deficit hyperactivity disorder, Tourette syndrome, anxiety disorders and dyspraxia. Although common, the majority (~60%) of children with ASD do not have an intellectual disability (ID; intelligent quotient ≤70). [33] Some individuals with an intellectual disability are likely to always remain dependent on health care services.

There is an increased risk of epilepsy in individuals with ASD. However, the increased co-morbidity of epilepsy is strongly linked to ID – 24% in those with ASD and ID, and 2% with ASD only. [43] There is no evidence that a particular epileptic disorder can be attributed to ASD (or vice versa). [44] The more common presentations include late infantile spasms, partial complex epilepsies and forms of Landau-Kleffner syndrome. Mutations in the tuberous sclerosis genes are particularly associated with ASD and epilepsy. [45]

Gastrointestinal disorders (GID) are a common complication in ASD. [46] Given that some “cognitive” genes of the brain are also expressed in the enteric nervous system, decreased visceral sensitivity, myogenic reflexes or even CNS integration of visceral input may be exacerbated in genetically susceptible individuals. Language impairments may be associated with toilet training difficulties, which can lead to constipation with overflow incontinence and soiling. However, medications and diet are not significantly associated with GID in individuals with ASD. [47]

What treatments are available?

At this point in time, it is thought that biological changes affect the function or structure of the brain over time, leading to different developmental, psychological and behavioural trajectories. There is no cure for ASD, but early intensive behavioural intervention (based on Advanced Behavioural Analysis) is somewhat successful towards promoting learning and independent living. [48] This intervention aims to addressing the core deficits of ASD in a structured, predictable setting with a low student-teacher ratio (initially 1:1). It promotes behavioural systems for generalization and maintenance, promotes family involvement and monitors progress over time. There is some evidence to suggest that participation in social skills groups also improves social interaction. [49] Other intervention strategies are pedagogical approaches to matching faces and actions to meanings.

The Australian Government has made available a support package called Helping Children with Autism. The package includes information, workshops and financial assistance for early intervention services.

At present, pharmacological intervention targets some symptoms associated with ASD. These include serotonin reuptake inhibitors, anti-psychotics, anti-epileptics, mood stabilisers and other medications to treat hyperactivity, aggression and sleep disruption. Given the degree of notable side effects in these pharmacotherapeutics, new generation compounds continue to be tested. There are high rates of complementary and alternative diet use in children with ASD, but a lack of rigorous studies means that the evidence for efficacy is poor. [50,51]

Guidelines on dealing with children with ASD

As medical students and interns, there may be opportunities to participate in a diagnostic clinic or therapy session. Community placements also provide insight into understanding special education interventions, respite and support. However, most interactions would occur during resident training or paediatric rotations. In these situations students will be observing or assisting specialists.

Children with ASD are only likely to be admitted into hospital with a medical problem distinct from their behavioural features. Nevertheless, children with ASD are twice as likely to become inpatients. [52] The more common reasons for hospital admission and general practice visits are seizures, sleep disturbances and constipation. [53]

Parents may describe their child as high-functioning, which tends to imply an IQ >70. This doesn’t usually reflect the social capacity of the child. Ultimately, as with other children, it is important to know the child’s strengths and weaknesses; for example, whether they respond more to visual or verbal communication. Most considerations when working generally with typically developing children also apply to children with ASD and developmental disorders. Suggestions for interacting with individuals with ASD can be found in the Table.

Ultimately, by engaging the parents and working with the child’s strengths, most issues can be resolved. Even for experienced clinicians, interactions can present challenges. It helps to be patient and adaptable. In some cases it may be pointless performing some examinations if doing them would be disruptive and not provide critical medical information. In such cases, working from the collaborative history will have to suffice.

ASD workshops and training opportunities

Workshops and training opportunities for community members range from one-hour presentations to nationally certified training programs. There are currently two nationally accredited training programs: CHCCS413B ‘Support individuals with ASD,’ and CHCEDS434A ‘Provide support to students with ASD.’ Associations around Australia and New Zealand also deliver community education programs and recognized training. The Autism Centre of Excellence (Griffith University, Queensland) provides tertiary training in ASD studies. The Olga Tennison Autism Research Centre (La Trobe University, Victoria) provides behavioural intervention strategy (Early Start Denver Model) training to qualified professionals.

Conferences of note include the annual International Meeting for Autism Research, the biennial Asia Pacific Autism Conference and the Australian Society for Autism Research conferences.

Concluding remarks

Autism is a spectrum disorder. As such, each child is unique. For this reason it is best not to get caught up with the ‘label’, but to focus on the individual’s abilities or disabilities, with an understanding that simplicity, patience and adaptability may be needed. Work with the parents or the carer to achieve the desired outcomes.

Acknowledgements

Thanks to Dr. Elisa Hill-Yardin and Dr. Naomi Bishop for a critical reading of a draft of this manuscript.

Disclosures

Dr. Moldrich is Adjunct Research Fellow of The University of Queensland investigating biological causes of autism. Together with Drs. Hill-Yardin and Bishop, he is co-organiser of autism research conferences. Dr. Moldrich is on the scientific advisory board of the Foundation for Angelman Syndrome Therapeutics.

Correspondence

R Moldrich: randal.moldrich@griffithuni.edu.au

References

[1] American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. 5th ed. Arlington: American Psychiatric Association; 2013.

[2] World Health Organization. International Classification of Diseases. Tenth edition. Geneva: 2010.

[3] Huerta M, Bishop SL, Duncan A, Hus V, Lord C. Application of DSM-5 criteria for autism spectrum disorder to three samples of children with DSM-IV diagnoses of pervasive developmental disorders. Am J Psychiatry. 2012;169(10):1056-64.

[4] Tierney CD, Kurtz M, Souders H. Clear as mud: another look at autism, childhood apraxia of speech and auditory processing. Curr Opin Pediatr. 2012;24(3):394-9.

[5] Boucher J. Research review: structural language in autistic spectrum disorder – characteristics and causes. J Child Psychol Psychiatry. 2012;53(3):219-33.

[6] Kagohara DM, van der Meer L, Ramdoss S, O’Reilly MF, Lancioni GE, Davis TN, et al. Using iPods((R)) and iPads((R)) in teaching programs for individuals with developmental disabilities: a systematic review. Res Dev Disabil. 2013;34(1):147-56.

[7] Volkmar FR. Understanding the social brain in autism. Dev Psychobiol. 2011;53(5):428-34.

[8] Anckarsater H. Central nervous changes in social dysfunction: autism, aggression, and psychopathy. Brain Res Bull. 2006;69(3):259-65.

[9] Tomasello M, Carpenter M, Call J, Behne T, Moll H. Understanding and sharing intentions: the origins of cultural cognition. Behav Brain Sci. 2005;28(5):675-91.

[10] Woodard CR, Van Reet J. Object identification and imagination: an alternative to the meta-representational explanation of autism. J Autism Dev Disord. 2011;41(2):213-26.

[11] Williams JH, Whiten A, Suddendorf T, Perrett DI. Imitation, mirror neurons and autism. Neurosci Biobehav Rev. 2001;25(4):287-95.

[12] Baron-Cohen S, Ashwin E, Ashwin C, Tavassoli T, Chakrabarti B. Talent in autism: hyper-systemizing, hyper-attention to detail and sensory hypersensitivity. Philos Trans R Soc Lond B Biol Sci. 2009;364(1522):1377-83.

[13] Gomes E, Pedroso FS, Wagner MB. Auditory hypersensitivity in the autistic spectrum disorder. Pro Fono. 2008;20(4):279-84.

[14] Howlin P, Goode S, Hutton J, Rutter M. Savant skills in autism: psychometric approaches and parental reports. Philos Trans R Soc Lond B Biol Sci. 2009;364(1522):1359-67.

[15] Betancur C. Etiological heterogeneity in autism spectrum disorders: more than 100 genetic and genomic disorders and still counting. Brain Res. 2011;1380:42-77.

[16] Hallmayer J, Cleveland S, Torres A, Phillips J, Cohen B, Torigoe T, et al. Genetic heritability and shared environmental factors among twin pairs with autism. Arch Gen Psychiatry. 2011;68(11):1095-102.

[17] Ozonoff S, Young GS, Carter A, Messinger D, Yirmiya N, Zwaigenbaum L, et al. Recurrence risk for autism spectrum disorders: a Baby Siblings Research Consortium study. Pediatrics. 2011;128(3):e488-95.

[18] Reichenberg A, Gross R, Weiser M, Bresnahan M, Silverman J, Harlap S, et al. Advancing paternal age and autism. Arch Gen Psychiatry. 2006;63(9):1026-32.

[19] Levy D, Ronemus M, Yamrom B, Lee YH, Leotta A, Kendall J, et al. Rare de novo and transmitted copy-number variation in autistic spectrum disorders. Neuron. 2011;70(5):886-97.

[20] Flatscher-Bader T, Foldi CJ, Chong S, Whitelaw E, Moser RJ, Burne TH, et al. Increased de novo copy number variants in the offspring of older males. Transl Psychiatry. 2011; 1:e34.

[21] Mann JR, McDermott S, Bao H, Hardin J, Gregg A. Pre-eclampsia, birth weight, and autism spectrum disorders. J Autism Develop Disorders. 2010;40(5):548-54.

[22] Nadebaum C, Anderson V, Vajda F, Reutens D, Wood A. Neurobehavioral consequences of prenatal antiepileptic drug exposure. Developmental Neuropsychology. 2012;37(1):1-29.

[23] Demicheli V, Rivetti A, Debalini MG, Di Pietrantonj C. Vaccines for measles, mumps and rubella in children. Cochrane Database Syst Rev. 2012;2:CD004407.

[24] Constantino JN. Social Impairment. In: Hollander E, Kolevzon A, Coyle JT, editors. Textbook of Autism Spectrum Disorders. Arlington, VA, USA: American Psychiatric Publishing; 2011. p. 627.

[25] Baron-Cohen S, Leslie AM, Frith U. Does the autistic child have a “theory of mind”? Cognition. 1985;21(1):37-46.

[26] Hill EL. Executive dysfunction in autism. Trends in Cognitive Sciences. 2004;8(1):26-32.

[27] Scott-Van Zeeland AA, Dapretto M, Ghahremani DG, Poldrack RA, Bookheimer SY. Reward processing in autism. Autism Research. 2010;3(2):53-67.

[28] Nielsen M, Slaughter V, Dissanayake C. Object-directed imitation in children with high-functioning autism: testing the social motivation hypothesis. Autism Research. 2013;6(1):23-32.

[29] Sassa Y, Sugiura M, Jeong H, Horie K, Sato S, Kawashima R. Cortical mechanism of communicative speech production. NeuroImage. 2007;37(3):985-92.

[30] Happe FG. Studying weak central coherence at low levels: children with autism do not succumb to visual illusions. A research note. J Child Psychol Psychiatry. 1996;37(7):873-7.

[31] Blumberg SJ, Bramlett MD, Kogan MD, Schieve LA, Jones JR. Changes in Prevalence of Parent-reported Autism Spectrum Disorder in School-aged U.S. Children: 2007 to 2011–2012. Hyattsville: Centers for Disease Control and Prevention, 2013 March 20, 2013. Report No.: 65.

[32] Williams K, MacDermott S, Ridley G, Glasson EJ, Wray JA. The prevalence of autism in Australia. Can it be established from existing data? J Paediatric Child Health. 2008;44(9):504-10.

[33] Baio J. Prevalence of Autism Spectrum Disorders — Autism and Developmental Disabilities Monitoring Network, 14 Sites, United States, 2008. Atlanta, USA: Centers for Disease Control and Prevention, 2012 March 30, 2012. Report No.: 61(SS03).

[34] Fountain C, King MD, Bearman PS. Age of diagnosis for autism: individual and community factors across 10 birth cohorts. J Epidemiol Community Health. 2011;65(6):503-10.

[35] Rutter M. Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatrica. 2005;94(1):2-15.

[36] Evans B. How autism became autism: The radical transformation of a central concept of child development in Britain. Hist Human Sci. 2013;26(3):3-31.

[37] van Daalen E, Kemner C, Dietz C, Swinkels SH, Buitelaar JK, van Engeland H. Inter-rater reliability and stability of diagnoses of autism spectrum disorder in children identified through screening at a very young age. Euro Child Adolescent Psychiatry. 2009;18(11):663-74.

[38] Australian Advisory Board on Autism Spectrum Disorders. The Prevalence of Autism in Australia. Can it be established from existing data? 2007. Available from: http://www.autismadvisoryboard.org.au.

[39] Lord C, Rutter M, DiLavore P, Risi S. Autism Diagnostic Observation Schedule (ADOS). Los Angeles: Western Psychological Services; 1999.

[40] Rutter M, Le Couteur A, Lord C. Autism Diagnostic Interview–Revised (ADI-R). Los Angeles: Western Psychological Services; 2003.

[41] Moss J, Richards C, Nelson L, Oliver C. Prevalence of autism spectrum disorder symptomatology and related behavioural characteristics in individuals with Down syndrome. Autism. 2012;

[42] Levy SE, Giarelli E, Lee LC, Schieve LA, Kirby RS, Cunniff C, et al. Autism spectrum disorder and co-occurring developmental, psychiatric, and medical conditions among children in multiple populations of the United States. J Develop Behav Pediatrics. 2010;31(4):267-75.

[43] Woolfenden S, Sarkozy V, Ridley G, Coory M, Williams K. A systematic review of two outcomes in autism spectrum disorder – epilepsy and mortality. Developmental Medicine Child Neurol. 2012;54(4):306-12.

[44] Deonna T, Roulet E. Autistic spectrum disorder: evaluating a possible contributing or causal role of epilepsy. Epilepsia. 2006;47 Suppl 2:79-82.

[45] Numis AL, Major P, Montenegro MA, Muzykewicz DA, Pulsifer MB, Thiele EA. Identification of risk factors for autism spectrum disorders in tuberous sclerosis complex. Neurology. 2011;76(11):981-7.

[46] Buie T, Campbell DB, Fuchs GJ, 3rd, Furuta GT, Levy J, Vandewater J, et al. Evaluation, diagnosis, and treatment of gastrointestinal disorders in individuals with ASDs: a consensus report. Pediatrics. 2010;125 Suppl 1:S1-18.

[47] Gorrindo P, Williams KC, Lee EB, Walker LS, McGrew SG, Levitt P. Gastrointestinal dysfunction in autism: parental report, clinical evaluation, and associated factors. Autism Research. 2012;5(2):101-8.

[48] Reichow B, Barton EE, Boyd BA, Hume K. Early intensive behavioral intervention (EIBI) for young children with autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2012;10:CD009260.

[49] Reichow B, Steiner AM, Volkmar F. Social skills groups for people aged 6 to 21 with autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2012;7:CD008511.

[50] Millward C, Ferriter M, Calver S, Connell-Jones G. Gluten- and casein-free diets for autistic spectrum disorder. Cochrane Database Syst Rev. 2008(2):CD003498.

[51] James S, Montgomery P, Williams K. Omega-3 fatty acids supplementation for autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2011(11):CD007992.

[52] Bebbington A, Glasson E, Bourke J, de Klerk N, Leonard H. Hospitalisation rates for children with intellectual disability or autism born in Western Australia 1983-1999: a population-based cohort study. BMJ Open. 2013;3(2):10.1136/bmjopen-2012-002356.

[53] Kohane IS, McMurry A, Weber G, MacFadden D, Rappaport L, Kunkel L, et al. The co-morbidity burden of children and young adults with autism spectrum disorders. PLoS One. 2012;7(4):e33224.


Categories
Feature Articles Articles

The B Positive Program as a model to reduce hepatitis B health disparities in high-risk communities in Australia

As the epicentre for the highest incidence of liver cancer diagnosis in New South Wales, southwest Sydney is simultaneously home to a large number of first generation migrants from Southeast Asia. Alarmingly, these individuals are six to twelve times more likely to be diagnosed with liver cancer than Australian born individuals. This article aims to explore some of the challenges in diagnosing and managing hepatitis B in culturally and linguistically diverse (CALD) communities as well as to introduce the B Positive Program, a health initiative by the Cancer Council of New South Wales, as a model to address chronic hepatitis B related health issues.

Challenges in Diagnosing and Managing Hepatitis B Infection in High Risk Communities in Australia
While hepatitis B vaccination is part of the immunisation program for infants and school-aged children in Australia, the incidence of hepatitis B induced hepatocellular carcinoma (HCC), the most common form of liver cancer, continues to be on the rise. This surge is largely attributed to chronic hepatitis B (CHB) infection amongst the migrant population from endemic areas such as Southeast Asia. [1] Alarmingly, these migrants are six to twelve times more likely to be diagnosed with liver cancer than Australian born individuals. [2] It is estimated that 90% of individuals acquire CHB at birth through mother-to-infant transmission.  [3] Thus, most  individuals suffering from CHB are unaware of their status due to the insidous nature of the disease in which individuals are asymptomatic until late adulthood. By the time CHB sufferers present for medical attention, a signifiant proportion of individuals have developed advanced HCC and treatment options are limited and survial rates are poor. In order to reduce the morbidity and mortality related to CHB related liver cancer, early screening, surveillance and treatment of high risk populations while in the asymptomatic phase are strongly indicated.

The National Cancer Prevention Policy for Liver Cancer recommend that hepatocellular carcinoma surveillance be based on abdominal ultrasound in high-risk groups at 6-month intervals. Blood tests screening for hepatitis B antigen and antibodies are used to diagnose CHB and individuals who are at high risk of hepatocellular carcinoma. If diagnosed early, antiviral agents and regular monitoring are extremely effective in preventing progression of CHB to HCC. As well, low grade HCC can be treated curatively by surgical resection, liver transplantation and percutaneous ablation.

Despite these guidelines and treatment options, it is well established that the culturally and linguistically diverse (CALD) communities in Australia remain undiagnosed or improperly managed due to difficulties in seeking equitable medical services. The following article aims to explore some of the challenges in diagnosing and managing hepatitis B in CALD communities as well as to introduce the B Positive Program, an ongoing health initiative by the Cancer Council of New South Wales, as a model to address chronic hepatitis B related health issues.

Language Barrier and Cultural Differences

Language barrier and cultural differences are often cited as two main challenges that adversely affect the diagnosis and management of hepatitis B infections in at-risk communities. [2,4] Due to language barriers, it is often difficult for patients to communicate with their healthcare providers unless the latter is well versed in the language. In these circumstances, an interpreter, often the patient’s family or friend, assumes the role of facilitating communication unless professional medical interpreters are available. This can be problematic because these novice interpreters might be unfamiliar with medical jargon and may misconstrue or censor physician messages. [4] In addition, the patient’s confidentiality and autonomy can be compromised when family or friends are involved. A systematic review study showed that patients benefit from professional interpreters instead of their family or friends. [5] At present, the prevailing solution for balancing patient confidentiality and autonomy while preserving cultural traditions for patients with limited English abilities is to consult language concordant healthcare providers. [6]

Stigmatization

Fear of stigmatization is a legitimate concern that individuals in CALD communities may experience. For example, a Chinese study conducted by Chao et al. showed that in China, healthcare professionals reported positive hepatitis B surface antigen (HBsAg) results to 38% and 25% of patients’ employers and schools respectively. [7]  Although this sort of disclosure practice is considered a breach of patient confidentiality in Australia, migrants coming from hepatitis B endemic countries may be reluctant to seek testing because of the aforementioned practices in their home countries. As a consequence, failure to screen and intervene promptly may result in chronic hepatitis B sufferers seeking health professionals as a last resort and possibly present at more advanced disease states. Presentation at these late stages would confer a worse prognosis to the patient and also increase the burden and cost to the healthcare system.

Knowledge Gaps amongst Healthcare Professionals

Avoiding disease progression is largely dependent on early recognition, monitoring and intervention. Unfortunately, some health professionals have unsatisfactory levels of knowledge. A study conducted by Stanford University in collaboration with the Asian Liver Centre showed that 34% (n=250) healthcare professionals in China who attended the ‘China National Conference on the Prevention and Control of Viral Hepatitis’ failed to recognize the natural history of hepatitis B infection or that a vaccine can be used as a prophylaxis for individuals who are seronegative. [7]

Not surprisingly, within Australia, similar surveys have shown similar gaps in knowledge amongst general practitioners. [8] Due to lack of knowledge, general practitioners may neglect treatment for individuals suffering from chronic hepatitis B or make inappropriate referrals to specialists for patients who are seronegative. In a system that is already overstretched with long waiting periods, this can be highly problematic. In addition, a major concern is that healthcare professionals fail to recognise that effective therapies are available for chronic hepatitis B and that hepatocellular carcinoma diagnosed at an early stage can be effectively treated especially with timely diagnosis, surveillance and treatment using antiviral agents and Fibroscan. Fibroscan is an accurate noninvasive investigation that is used regularly to assess the degree of liver scarring based on ultrasound technology. All healthcare professionals should be aware that recent developments in hepatitis B management, like antiviral therapy and FibroScan, have been extremely effective in preventing, monitoring and controlling the disease to progress to cirrhosis, liver failure and liver cancer amongst chronically infected individuals. The concept of “healthy carriers” no longer holds true. Yet, if healthcare practitioners are not imparted with this important knowledge, the wellbeing and health of many individuals suffering from chronic HBV will continue to be in jeopardy.

An added layer of complexity lies in the frequent use of complementary and alternative medical therapies within CALD communities. A 2012 study conducted by Guirgis et al. indicated conflicting advice about hepatitis B management given by conventional and complementary medical practitioners within Sydney. [9] The contradictory information patients receive can negatively affect their screening or management intentions. Hence, it is important to reconcile any conflicting management strategies by not only educating conventional medicine practitioners but also complementary medicine practitioners about hepatitis B screening and management so as to allow the two systems to co-exist and complement one another.

B Positive Program – A Program to Reduce Health Disparities in Hepatitis B Care

Given the increased incidence of hepatocellular cancer is clustered within specific geographical and ethnic regions within Sydney, the B Positive program is a good model in reaching a vulnerable Southeast Asian audience within New South Wales. The program, spearheaded by the Cancer Council of New South Wales, employs various strategies to address access issues at the patient, community and health professional levels.

At the patient level, the program initiates numerous educational campaigns and materials to educate the at-risk population and to remove the stigmatization of hepatitis B. One of the strengths of the program is the use of educational materials that are culturally and language concordant. For example, one of the campaign posters features Andy Lau, a prominent Chinese entertainer within the Asian community, as an individual with hepatitis B. Placing a public figure in the spotlight helps to demystify the condition for the CALD community and can demonstrate to carriers that medical therapy is effective given proper management and timely diagnosis. This campaign was highly effective and recently garnered the NSW Multicultural Health Communication Award 2013.

Another educational strategy employed by the program was the distribution of chopsticks engraved with the phrase “one cannot spread hepatitis B by sharing food” in Vietnamese and Chinese to shed light on the mode of transmission for the virus. A further strategy that the Cancer Council NSW employed was to collaborate and engage with Asian community-based health organizations like CanRevive and Australian Chinese Medical Association during outreach programs to enhance their cultural authenticity and receptivity within the CALD community.

At the community level, the program has recently developed a pilot project in May 2013 to engage high-risk migrant communities by creating a high school certificate course for south-west Sydney students called “Animating Hepatitis B”. This course involves ten weeks of lessons on hepatitis B and animation production before the high school students  create short animations to deliver hepatitis B health facts to their community.

At the health professional level, the program also assists general practitioners to better identify and screen patients belonging to high-risk groups. Community nurses visit medical clinics to remind general practitioners about enrolling at-risk patients into screening programs. The program also encourages regular monitoring programs of chronic hepatitis B patients for surveillance of hepatocellular carcinoma. General practitioners are also offered Hepatitis B seminars through the Continuing Medical Education Program, so that their knowledge is up to date.

Conclusion

With the appropriate use of cultural and language concordant educational campaigns and outreach programs for at-risk individuals, community healthcare workers to deliver these programs, community engagement and continuing medical education opportunities for healthcare professionals, the prospect of reducing the disparities in hepatitis B care within the CALD communities in Australia is highly positive.

Acknowledgements

Many thanks to Dr. Monica Robotin, Ms. Debbie Nguyen, Dr. Simone Strasser, Dr. Jacob George and Dr. Lilon Bandler for their guidance, mentorship and support.

Conflict of interest

None declared.

Correspondence

G Fong: gfon9247@uni.sydney.edu.au

References

[1] Robotin M, Patton Y, Kansil M, Penman A, George J. Cost of treating chronic hepatitis B: comparison of current treatment guidelines. World J. Gastroenterol. 2012 Nov; 14;18(42) :6106-13.

[2] Bosch FX, Ribes J, Diaz M, Cleries R. Primary liver cancer: worldwide incidence and trends. Gastroenterology. 2004 Nov;127(5 Suppl 1):S5-S16.

[3] Gellert L, Jalaludin B, Levy M. Hepatocellular carcinoma in Sydney South West: late symptomatic presentation and poor outcome for most. Intern. Med. 2007 Aug;37(8):516-22.

[4] Ngo-Metzger Q, Massagli MP, Clarridge BR, Manocchia M, Davis RB, Iezzoni LI, et al. Linguistic and cultural barriers to care. J Gen Intern Med. 2003 Jan;18(1):44-52.

[5] Karliner LS, Jacobs EA, Chen AH, Mutha S. Do professional interpreters improve clinical care for patients with limited English proficiency? A systematic review of the literature. Health Serv Res. 2007 Apr;42(2):727-54.

[6] Wilson E, Chen AH, Grumbach K, Wang F, Fernandez A. Effects of limited English proficiency and physician language on health care comprehension. J Gen Intern Med. 2005 Sep;20(9):800-6.

[7] Chao J, Chang ET, So SK. Hepatitis B and liver cancer knowledge and practices among healthcare and public health professionals in China: a cross-sectional study. BMC Public Health. 2010 Feb;10:98.

[8] Guirgis M, Yan K, Bu YM, Zekry A. General practitioners’ knowledge and management of viral hepatitis in the migrant population. Intern. Med. 2012 May;42(5):497-504.

[9] Guirgis M, Nusair F, Bu YM, Yan K, Zekry AT. Barriers faced by migrants in accessing healthcare for viral hepatitis infection. Intern. Med. 2012 May;42(5):491-6.

Categories
Feature Articles Articles

Oral Health – An important target for public policy?

Introduction

A healthy mouth is something we take for granted. We use our mouths to speak, to eat and to socialise without pain or significant embarrassment. Yet when oral disorders develop the impacts can extend well beyond the domains of speech, chewing, and swallowing to sleep, productivity, self-esteem and consequently quality of life. Despite the significant improvements made in oral health on a national scale over the last 20 years, there are still persistently high levels of oral disease and disability among Australians. This is most evident among Aboriginal and Torres Strait Islander peoples. This paper aims to review current medical literature concerning the overlap between oral health and Indigenous health outcomes and whether it may represent an important target for public health policy.

Methodology

A literature review was performed through a search of The Cochrane Library, Google Scholar and Ovid Medline as well as government databases such as the Australian Institute of Health and Welfare. The terms used in the searches included: ‘Indigenous health’, ‘Aboriginal and Torres Strait Islanders’, ‘oral health’, ‘dental caries’, ‘cardiovascular disease’ and ‘education’. Limits were also set to include only studies published in the English Language and to papers published between 1995 and 2013.

Results

Searches using combinations of the above keywords yielded more than 100 results. Article titles and abstracts were analysed for relevance to the research question and in particular any reference to Indigenous health. Specific key word limits such as ‘education’ and ‘Indigenous health’ were used to restrict the yield. Relevant articles were collated from the individual searches and bibliographies were searched for any additional points of interest. This process yielded the 17 papers reviewed for this paper.

Discussion

Indigenous Health

In 2004-2008 the age-standardised death rate for Indigenous people was 1.8 times that of the non-Indigenous population; a representation of just one aspect of the ongoing issue of Indigenous disadvantage in Australia. [1] In terms of the domain of oral health there is also a wide discrepancy between both population groups. However, current literature suggests that, in the past, Indigenous Australians actually enjoyed better oral health than those who were non-Indigenous. [2] Historically, throughout the 19th and 20th centuries caries was considered to be a “disease of affluence” [3] whereas today it could potentially be a better “indicator of deprivation.” [4] Foods rich in fermentable carbohydrates are plentiful in Indigenous communities today and so is dental decay. [3] The current Indigenous health situation provides the perfect example of how a non-Western society can be detrimentally impacted upon by the introduction of Western lifestyle [5] and whilst it is not possible to discuss every aspect of this complex issue, the importance of oral health in these communities is something that requires further consideration.

The risk factors for poor oral health are the same whether someone is Indigenous or not, yet there is a disparity between the standard of oral health of both groups. According to the World Health Organisation (WHO) oral health is “being free of chronic mouth and facial pain…and disorders that affect the mouth and oral cavity.” [6] The ‘Oral health of Aboriginal and Torres Strait Islander children’ report, published by the Australian Institute of Health and Welfare, found that a higher percentage of Aboriginal and Torres Strait Islanders had experienced dental caries than other Australian children aged between four and 14 years. [7] The report further stated that children aged less than five years had almost one and a half times the rate of hospitalization for dental care when compared to their non-Indigenous counterparts. [7] A rising trend was also demonstrated in the prevalence of caries among Indigenous children, particularly in the deciduous dentition. [7] In extrapolating the causes of these inequalities it is important to consider current structural and social circumstances. These social determinants of health include aspects like socioeconomic status, transport and access, racism and housing and with the recognition of these inequalities being embedded in “a history of conflict and dispossession, loss of traditional roles…and passive welfare” a more accurate snapshot of the complicated Indigenous situation can be established. [8]

In order to best understand the issues of Indigenous health it is also important to understand how Indigenous people themselves conceptualise health. The traditional Indigenous notion of health is holistic and encompasses everything from a person’s life, body and environment to relationships, community and law; [3] a significant overlap with the social determinants model mentioned above. Whilst following a reductionist approach to medical care may be helpful in treating and managing disease, alone it is inadequate in addressing health disadvantage at a population level where a more holistic method of interpretation is required. The relationship between oral health and one’s systemic health illustrates an important area where population-focused medicine could potentially cause a reduction in rates of morbidity and mortality across multiple medical domains. Current medical research has, for example, confirmed an association exists between cardiovascular disease and periodontal disease. [9] A large retrospective cohort study performed by Morrison and colleagues (1999) reported an association between poor dental health and an increase in the incidence of fatal coronary heart disease. [10] The relationship was assessed using Poisson regression and results were adjusted for age, sex, diabetes status, serum total cholesterol, smoking and hypertensive status. [10] Rate ratios of 2.15 (95% confidence interval (CI): 1.25-3.72) and 1.90 (95% CI: 1.17-3.10) were observed in the gingivitis and edentulous status groups respectively and supported a positive association with fatal coronary heart disease. [10] A study by Joshipura and colleagues (2003), looking at 41,380 men who were free of cardiovascular disease and diabetes mellitus at baseline, suggested that periodontal disease and fewer teeth may also be associated with an increased risk of stroke. [11] During the follow up period, 349 cases of ischaemic stroke were reported, and men who had 24 or less teeth at baseline were at a higher risk of stroke than those with at least 25 teeth (hazard ratio: 1.57; 95% CI: 1.24-1.98). Furthermore, the addition of dietary factors to the model only changed the hazard ratios slightly. [11] Similar relationships have been established in linking oral infection to diabetes mellitus, low birth weight babies and disorders like otitis media and delayed growth. [3] The fact that the area of oral health has been identified as a potential risk factor for so many medical conditions highlights its importance as a target in population health.

The role of education

WHO defines health as “a state of complete physical, mental and social well being and not merely the absence of disease or infirmity.” [6] Whilst “population” is the “total number of people or things in a given place.” [12] So essentially, putting these two terms together there is an orientation towards “preventing disease, prolonging life and promoting health through organised efforts and informed choices” among whole groups rather than individuals. [12] Many of the oral health problems faced by these communities have overlapping risk factors with wider general health conditions [3] and whilst this may be a reflection of the huge amount of work that is to be done it may also be viewed as a golden opportunity, to bring positive change through the many domains of health. Improving oral health through a campaign against alcohol and tobacco will not only have positive ramifications for oral health but its effects may also be seen in the areas of general health and wellbeing. The promotion of better oral hygiene through healthier eating may also have positive developments in the rates of obesity and type two diabetes mellitus.

It is also important to mention the role of education in achieving these goals, as this tool is often the key to someone gaining the power and knowledge to change their life. Education to create awareness on how dental hygiene can improve all domains of life is important in empowering people from a population perspective. Previous studies looking at the oral health of Indigenous Australians in Port Augusta, South Australia, have revealed associations between low oral health literacy scores and self-reported oral health outcomes. [13-15] It is studies like these that have prompted the need for targeted interventions that use tailored communication and training techniques to improve oral health literacy; however, there remain few interventions actually targeting oral health literacy in Indigenous populations. [16]

Conclusion

Indigenous health is a complex and often controversial topic and there is much debate as to what actually needs to be done to address the huge gap. Oral health is an important field of health care that has associations with many systemic conditions and thus may provide an appropriate target for effective public health policy. Perhaps a fault in our current health care system is that the dental and medical care fields have evolved quite separately and thus many people may habitually fail to understand how a simple cavity can be linked to the rest of their being. [17] Even in the Medicare system today there are no provisions for any preventative oral health services; with the exception for low income earners being entitled to concessions for public dental treatment through the public hospital system. [3] Oral health is an integral aspect of general health and thus should be an important public health goal; especially in Indigenous communities where the high prevalence of oral disease could be prevented through population-level interventions.

Conflict of interest

None declared.

Correspondence

L Mclean: lsmcl2@student.monash.edu

References

[1] Thomson N, MacRae A, Brankovich J, Burns J, Catto M, Gray C et al. Overview of Australian Indigenous health status 2011. Perth: Australian Indigenous HealthInfoNet; 2012.

[2] Harford J, Spencer J, Roberts-Thomson K. Oral health, In: The health of Indigenous Australians, N. Thomson (Ed.). South Melbourne: Oxford university press; 2003. p.313-338.

[3] Shearer M and Jamieson L. Indigenous Australians and Oral Health, Oral Health Care – Prosthodontics, Periodontology, Biology, Research and Systemic Conditions [monograph on Internet]. n/a: InTech; 2012 [cited 2012 Jun 13]. Available from: http://www.intechopen.com/books/oral-health-care-prosthodontics-periodontology-biology-research-and-systemic-conditions/indigenous-australians-and-oral-health

[4] Williams S, Jamieson L, MacRae A, & Gray C. Review of Indigenous oral health [monograph on Internet]. Australian Indigenous HealthInfoNet; 2011 [cited 2012 Jun 13]. Available from: http://www.healthinfonet.ecu.edu.au/uploads/docs/oral_health_review_2011.pdf

[5] Irvine J, Kirov E, Thomson, N. The Health of Indigenous Australians. Melbourne: Oxford University Press; 2003.

[6] World Health Organisation. Oral Health: Fact sheet No. 318 [homepage on Internet]; 2007 [cited 2012 Jun 13]. Available from: http://www.who.int/mediacentre/factsheets/fs318/en/index.html

[7] Australian Institute of Health and Welfare, Dental Statistics and Research Unit: Jamieson LM, Armfield JM, Roberts-Thomson KF. Oral health of Aboriginal and Torres Strait Islander children. Canberra: Australian Institute of Health and Welfare (Dental Statistics and Research Series No. 35); 2007. AIHW cat. No. DEN 167.

[8] Banks G. Overcoming indigenous disadvantage in Australia. Address to the second OECD world forum on statistics, knowledge and policy, measuring and fostering the progress of societies. Measuring and fostering the progress of societies; 27-30 Jun 2007. Istanbul, Turkey.

[9] Demmer RT, Desvarieux M. Periodontal infections and cardiovascular disease. J Am Dent Assoc. 2008 Mar;139(3):252.

[10] Morrison HI, Ellison LF, Taylor GW. Periodontal disease and risk of fatal coronary heart and cerebrovascular diseases. J Cardiovasc Risk 1999;6(1):7-11.

[11] Joshipura KJ, Hung HC, Rimm EB, Willett WC, Ascherio A. Periodontal disease, tooth loss, and incidence of ischemic stroke. Stroke 2003;34(1):47-52.

[12] Queensland Health. Understanding Population Health [monograph on Internet]. Queensland: Queensland Health; [cited 2012 Jun 10]. Available from: http://www.health.qld.gov.au/phcareers/documents/background_paper.pdf

[13] Jamieson LM, Parker EJ, Richards L. Using qualitative methodology to inform an Indigneous owned oral health promotion initiative. Health Prom Int 2008; 23:52-59.

[14] Williams SD, Parker EJ, Jamieson LM. Oral health-related quality of life among rural-dwelling Indigenous Australians. Aust Dent J 2010; 55:170-176.

[15] Parker EJ, Jamieson LM. Associations between Indigenous Australian oral health literacy and self-reported oral health outcomes. BMC Oral Health 2010; 10:3.

[16] Parker EJ, Misan G, Chong A, Mills H, Roberts-Thomson K, Horowitz A et al. An oral health literacy intervention for Indigenous adults in a rural setting in Australia. BMC Public Health 2012; 12:461.

[17] Widdop, F. Crossing divides: an ADRF perspective [monograph on Internet]. Australian Dental Association. Australia: Australian Dental Association; 2005 [cited 2012 Jun 13]. Available from: http://www.ada.org.au/app_cmslib/media/lib/0702/m47474_v1_crossingdividesanadrfperspective.pdf

 

Categories
Articles Feature Articles

See no evil, hear no evil, speak no evil: Tanzania’s struggles with the HIV epidemic

Nestled on the south-eastern slopes of Mt Kilimanjaro in Northern Tanzania, the sprawling village of Machame emerges from the surrounding rainforest. This village is home to the Machame Hospital, where I was fortunate enough to undertake a month-long elective before commencing my final year of medical school. This elective was a challenging, yet enriching experience, and helped me gain a glimpse into some of the major public health issues affecting the country.

The century-old Machame Hospital is a 120-bed facility that provides essential healthcare to over 150,000 people from the surrounding area. Although severely under-resourced, the hospital was a bustling hive of activity that provided me with a taste of Tanzanian medical, surgical and obstetric services. The locals were exceptionally friendly and welcoming and I was able to get involved in all aspects of hospital functioning including attending clinics, contributing to ward rounds, assisting in surgery and conducting outreach clinics in the community.

Throughout my time there it quickly became apparent that the gravest problem facing the community of Machame, as with much of Tanzania, is that of HIV/AIDS. Indeed, the most recent epidemiological data estimate the national adult prevalence to be 5.7%. [1] This figure, however, is likely to be an underestimation given the prevailing social stigma associated with being HIV-positive and the resultant reluctance of people to come forward for testing.

In Tanzania, HIV is a dirty word. Many of the doctors and health workers were loath to refer to it by name (virusi vya ukimwi or VVU in Swahili), especially around patients. It was often alluded to by euphemisms, becoming the great unspoken problem. Many Tanzanians have a very poor understanding of its natural history or transmission and this engenders great fear, especially as many have witnessed the devastating effects of the disease firsthand. [2,3] When it comes to HIV, unfortunately many Tanzanians really do ‘see no evil, hear no evil, and speak no evil.’

Machame Hospital’s HIV clinic was housed in a little hut ten metres from the main hospital complex itself – an apt demonstration of the social segregation of AIDS sufferers. Accommodating patients with HIV within the main facility may discourage others from presenting for fear of contracting the condition while in hospital. The locals were also worried about being sighted at known HIV treatment or testing locations for fear of social repercussions. The building was instead known as the Centre for Disease Control, a deliberately ambiguous name that enabled patients to attend appointments without fear of being stigmatised as a carrier.

During my elective I also had the opportunity to assist with HIV screening using finger-prick antibody testing. Under the auspices of a general clinic, we would travel to different locations around the village and set up a consulting area. It almost seemed that an unspoken agreement existed between the patients and medical staff to ensure HIV testing was conducted surreptitiously, with the testing area tucked away up the back and never mentioned by name. This made the process all very secretive, ensuring that full, informed consent was often overlooked. Despite this, many seemed to know what was going on and, fortunately, people from the village willingly came forward to be tested.

I met numerous patients during my elective but the most confronting case I saw was that of a two-year-old boy infected with HIV. The child’s mother had already died from complications of AIDS and the grandmother, distraught and surfeited, had brought him in asking for an ‘injection to kill her baby’ because she could no longer bear to see him so sick. He had already lost 30% of his 10kg body weight within the last month and cried throughout the whole consultation. Apart from being deeply tragic on a human level, seeing patients such as this made me frustrated as this situation might have been prevented. Perhaps the greatest tragedy of medicine in the developing world is when medical knowledge exists to provide a solution, but is not implemented due to a lack of financial or educational resources.

Fortunately, there were also many uplifting cases that did highlight the tangible benefits of effective medical therapy. One 38-year-old presented to the hospital with a paltry CD4 count of 1 (the normal adult range being between 500 and 1,300 cells per microlitre [4]). He was commenced on anti-retroviral therapy and is now doing well, able to again provide for his wife and son.

There are certainly many challenges that Tanzanian health authorities continue to face in the fight against HIV/AIDS.

Firstly, the lack of health resources in the country limits the capacity for investigations. For example, in Machame it was not possible to measure HIV viral loads, a test routinely performed in Australia to monitor disease progress. CD4 counts alone stand as the only available measure of treatment efficacy. Secondly, patients perceive little incentive to continue taking anti-retroviral medication if they do not feel that it is improving their well-being, as the notions of prevention and maintenance therapy are generally poorly understood. This generates significant compliance challenges that undermine the delivery of treatment.

For its part, the government provides all HIV medication free of charge. Although this is an excellent initiative, it makes the reluctance of people to get tested and treated harder to fathom, especially considering the effectiveness of pharmacotherapy. For example, the rate of vertical transmission from untreated mother to child is 25-35%, but this can be reduced by up to two-thirds with Highly Active Anti-Retroviral Therapy during pregnancy and six months of breastfeeding. [5]

Thirdly, the considerable social stigma and widespread reluctance to discuss HIV act as a significant barrier to primary and secondary prevention strategies. Public education about HIV/AIDS is severely limited and it is difficult to counsel patients about preventing transmission of the illness when sex remains a taboo subject. Many people are tragically unaware of the role of unprotected heterosexual intercourse in spreading infection, in spite of it being the most common mode of transmission. [1]

There is also an issue of protection for health care workers. I noticed a marked contrast in attitudes towards personal safety and infection control between my time in both the Australian and Tanzanian systems. In Australia, additional precautions are taken for patients with diseases like HIV. Such measures include isolating infectious or immunodeficient patients, collection and incineration of contaminated medical waste, use of personal protective equipment and safe handling of sharps. None of these methods were routinely observed to be practiced during my time in Tanzania and it raised concerns about the rate of potentially preventable transmission amongst hospital staff. Indeed, a recent study of two other Tanzanian hospitals found that nearly half of all healthcare workers experienced at least one occupational injury, such as a needle-stick injury, over a twelve-month period. [6] Clearly, efforts need to be made to improve safety procedures and staff awareness.

Overall, reducing the impact of HIV will depend on multiple approaches with a focus on adherence to treatment, early testing and mitigation of high-risk behaviours. Such improvement can only be achieved through education and good public health initiatives.

My time in Tanzania as an elective medical student proved to be a humbling and eye-opening exposure to global health, with a particular focus on HIV/AIDS. By far the most incredible words I have ever learnt to say are hakuna shida, as this was the Swahili phrase I used to inform patients that their HIV test was negative. People were so pleased to hear this that several patients cried with joy or hugged me upon learning the good news. In a beautiful moment of symmetry to my previous HIV clinic, I saw another lady accompanying her grandchild who had lost his mother to AIDS. This time the boy was negative and, upon hearing this, the grandmother burst into joyous tears. These experiences have helped change my perspective on medicine and what I take for granted in Australia. I look forward to potentially returning in the future and to help get people talking about HIV.

Acknowledgements

I would like to thank the Insight Global Health Group for providing financial support for this elective through the Insight Development Grant.

Conflict of interest

None declared.

I especially want to acknowledge the significant contribution of colleague Justin Mencel, who undertook the elective with me and helped organise it. Additionally, I would like to recognise the warmth and generosity with which we were welcomed by the whole community, in particular by Hospital Patron Mr Edward Mushi.

Correspondence

M Weightman: michael.weightman@student.adelaide.edu.au

References

[1] Tanzania Commission for AIDS, Zanzibar AIDS Commission, National Bureau of Statistics (Tanzania), Office of the Chief Government Statistician, Macro International Inc. Tanzania HIV/AIDS and malaria indicator survey 2007-08. Dar es Salaam, Tanzania: Macro International Inc; 2008.

[2] Amuri M, Mitchell S, Cockcroft A, Andersson N. Socio-economic status and HIV/AIDS stigma in Tanzania. AIDS Care 2011;23(3):378-82.

[3] Ostermann J, Reddy E, Shorter M, Muiruri C, Mtalo A, Itemba D et al. Who tests, who doesn’t, and why? Uptake of mobile HIV counseling and testing in the Kilimanjaro Region of Tanzania. PLoS One 2011;6(1):e16488.

[4] Coffey S, editor. Guide for HIV/AIDS Clinical Care. Rockville, MD, USA: US Department of Health and Human Services, Health Resources and Services Administration, HIV/AIDS Bureau; 2011.

[5] Siegfried N, van der Merwe L, Brocklehurst P, Sint T. Antiretrovirals for reducing the risk of mother-to-child transmission of HIV infection. Cochrane Database Syst Rev 2011;2011(7):1-122.

[6] Mashoto K, Mubyazi G, Mohamed H, Malebo H. Self-reported occupational exposure to HIV and factors influencing its management practice: a study of healthcare workers in Tumbi and Dodoma Hospitals, Tanzania. BMC Health Serv Res 2013;13(1):276.

Categories
Feature Articles Articles

Reproductive Healthcare in Latin America: Perspectives from a Guatemalan Elective

If medicine is to fulfill her great task, then she must enter the political and social life.

—Rudolf Virchow, founder of modern pathology

An overseas elective is a time to experience medicine in another setting, and it is as much about the setting as it is about the medicine. While gunshot wounds in Johannesburg, and tropical diseases in East Timor, are the often the draw cards when we are planning an elective, it is witnessing the social conditions that lead to those health problems that really change our outlook. Rudolph Virchow was right about many things, but this dictum seems to go unheeded in much of our medical education. Perhaps that is best; there doesn’t seem to be much space in the curriculum for a quick course on East Asian history, Latin American politics or economic development. It does mean, however, that for many of us, our elective becomes a crash course on the political and social life we aren’t taught about in medical school.

After some deliberation, I decided on a women’s health elective in Guatemala. It seemed like a good chance to spend some time learning about a single public health issue in more depth, and at the time I was interested in how cervical cancer, a disease so preventable in our own country, could be such a significant killer of women in the developing world. Some quick research led me to believe Guatemala was no different. Once I arrived, however, I discovered that most of the women in that area of Guatemala, Antigua, a wealthy area popular with tourists, were already engaged by cervical cancer screening programs. While the hospital I was working at openly encouraged women to be screened for cervical cancer, there was an issue that no one seemed to be talking about. An issue that inextricably links medicine to the political and social lives of women. Contraception.

In the first week I went out on a few visits with the social worker to the villages surrounding Antigua where most of the patients lived. As we walked farther from the edge of town the roads diminished to dirt tracks, the cinder block houses became tin shacks. We spoke mostly to women and many of their stories were similar; they worried when their husbands would next get regular work, whether there would be enough money for food, whether they could continue to afford to send their children to school. It also seemed as if every family had upwards of five or six children, many of them only a year or two apart. The doctors at the hospital had said they did not discuss family planning with the women because it was a cultural issue, and they did not want to alienate the community. Although the hospital was run by a Christian non-profit based in the United States (US), the director stated the practices at the hospital were not guided by religious belief. The doctors and health workers at the hospital would not raise the issue of contraception with patients. If women requested contraception the hospital would refer them to another US-based non-governmental organization (NGO), WINGS, that dealt with family planning amongst other reproductive health issues, and had limited funding and scope. Walking through those tin shacks and dirt lanes family planning seemed much more than a cultural issue, it seemed to be about gender, politics, economics, education, religion and history too.

Guatemala has one of the highest fertility rates in Latin America of four children per woman. [1] Amongst Indigenous women that rate is 6.8, and in some rural areas is reported to be as high as 10 per woman. Indeed the Indigenous population, mostly Maya, make up approximately 50% of Guatemala’s population, of which 80% live rurally. [2] As is true almost universally for Indigenous populations, they suffer from significantly poorer health parameters, which can be traced back to a brutal colonial history followed by a 36-year civil war, and the ongoing economic and educational disparities related to this.

On a quest to find out more about contraceptive use, I decided to spend the remainder of my elective with another NGO, Maya Gift, doing village clinics in the Lago de Atitlan region of the Guatemalan highlands, where the population is largely Indigenous and the fertility rates are highest. Maternal mortality rate (MMR) in this region is up to 534 per 100 000, compared to 120 per 100 000 in Guatemala as a whole, or 7 per 100 000 in Australia. [3] Most births are not attended by a skilled midwife, but by a comadrona, a traditional birth attendant. In Guatemala, 59% of births are attended by a traditional birth attendant only, in rural areas this percentage is thought to be much higher. [4] The high fertility rates, combined with high maternal mortality rates, result in a 1 in 20 lifetime chance of dying in childbirth in the highlands surrounding Atitlan. [5] That is significantly higher than the 1 in 190 lifetime risk in Guatemala as a whole, or the 1 in 8100 lifetime risk of dying in childbirth in Australia. [3]

Given the incredible impact of pregnancy on women’s lives in this part of the world it seemed strange for health organizations to not actively discuss the issue, or to consider it as purely cultural. It seemed like these women were missing out on a basic element of healthcare, but were they really? What does contraceptive use mean to the individual and the society they live in.

A revolutionary pill

Family planning may date back to the fertility goddesses of ancient Egypt, but modern family planning methods started in the 1960s with the contraceptive pill. The availability of effective contraception had far reaching consequences for role of women in society, particularly in terms of marriage and the workforce. [6]

It was not long before family planning entered the domain of public health. Amid concerns about rapid population growth, international family planning programs in the 1960s and 70s were framed with population policies, with the focus on reaching demographic and fertility targets. In this context some nations adopted coercive population control policies that violated human rights and often targeted sections of the population based on race and socioeconomic status. [7] This sort of practice is completely at odds with the family planning efforts of the majority of governments and public health organizations today.

Family planning in 2012

The marked shift in the basis of family planning policy from population control to human rights was clearly demarcated in 1994 by the Program of Action of International Conference on Population and Development in Cairo. [8] Here, 179 countries signed on to a Program of Action that framed family planning as a women’s health issue rather than a purely demographic issue. For the first time, universal access to contraceptives was set as the goal, rather than the population targets set in the past. From this conference onwards the focus has been on autonomy, choice and improving access.

With this approach in mind, the benefits of family planning programs in developing countries have been marked. In development terms family planning provides one of the best returns for investment of any public health measure. [9] When women are given access to modern family planning methods they have fewer children and those children go on to be better educated and healthier, suffering significantly less from malnutrition. The most well known cases are perhaps in South East Asia, where countries like Thailand dropped their fertility rate from 6.3 in 1967 to 1.7 in 2003. [10] In this setting the decrease in fertility was associated with an explosion in economic growth, leading to a phenomenon known as the ‘demographic dividend’. [11] This phenomenon occurs in countries with high fertility rates, where an increased investment in family planning results in a significant fertility drop across one generation. [12] As a greater proportion of the population are at working age relative to dependants, there may be more funds to spend on health and education. This raises the ‘human capital’ of the population, as those children who have grown up an environment with increased access to health and education become more economically productive than their predecessors.

Despite the knowledge of the profound effect of family planning on economic development, funding for programs was slowly eroded from the 1980s onwards. [13] This was in part due to the redirection of funds to fight the AIDS epidemic, and in part due to the political rise of the Christian right in US politics. The Christian right lobbied to block US funding to the United Nations Population Fund (UNFPA), a key reproductive health body, and prevented the United States Agency for International Development (USAID) funding any organisations that were linked with abortion. Many of those organisations were also key providers of less controversial aspects of family planning, including the contraceptive pill and injectable contraceptives. [14]

In 2012, however, family planning was placed back on top of the development agenda, when Melinda Gates, of the Bill and Melinda Gates Foundation, the largest philanthropic organization in the world, decided to make family planning her signature issue, investing several billion dollars in the cause. Gates highlighted the key issues in her first public speech on the topic: accessibility, education and above all, removing the taboo surrounding contraception. [15] At the landmark London Summit on Family Planning in July 2012, organized by the Gates Foundation, world leaders gathered to orchestrate a plan to address the enormous unmet need for contraceptives. It is estimated that 222 million women who would like to use contraception do not have access to it. Of the 210 million pregnancies each year, 80 million are estimated to be unintended. Furthermore, there are 22 million unsafe abortions occurring each year, resulting in 47,000 deaths. [13]

There is, of course, another reason family planning has been put back on the agenda: climate change. Uncontrolled population growth has been touted as one of the most significant contributors to carbon emissions. [16] A 2011 UN report on the predicted population of the world in 2050 outlined the variability in our global future. [17] The report released three variants of estimated population, a smaller, medium and large variant, 8.1 billion, 9.3 billion and 10.6 billion, respectively. The medium variant, largely held to be the most likely, relies on fertility rates in high fertility countries dropping from an average of 4.9 children per woman to 2.8. Family planning services in high fertility countries in Africa and Asia will need to be expanded if they are to meet this need. Alarmingly, Africa, which struggles to provide food and water to its inhabitants today, could see its population more than triple, from 1 billion today to 3.6 billion by 2100. [18]

The global, the local

For the women of the Lago de Atitlan region of Guatemala these global issues are largely esoteric. The inaccessibility of contraception at the local level is made up of a different set of factors, albeit related to these global issues. After talking with these women for a few weeks it seemed that the barriers to contraceptive use could be broadly broken down into economic, educational, cultural, historical and geographical obstacles.

In this area of Guatemala, generally only the males worked for a paid wage, which for a campesino (rural labourer) was US$150 per month. [19] Speaking with the campesinos who came to the clinic, it seemed this wage would often need to support families with six or more children and dependant grandparents. An average workday involved 12 hours of backbreaking labour, carrying 60kg sacks of coffee back and forth. Speaking with the women it was clear they worked just as hard: labouring, preparing meals and selling food in the bigger towns. In this environment it seemed there was rarely a free morning, or spare funds, to go and get an injection of depot contraceptive at the clinic in the next town. Contraception would have to be cheaper, or free, and more accessible if they were to use it consistently.

Inextricably linked to the economic disadvantage of rural Guatemala was the educational disadvantage. Many families could not afford to send their children to school, which although free, required purchasing shoes, uniforms, books and supplies. The average amount of schooling is 4.28 years per person. [20] Illiteracy rates are amongst the highest in Latin America; 21.8% for men and 39.8% for women. [21] It is estimated that two million children of school age are not attending school. The majority of these are Indigenous girls living in rural areas, the very demographic that go on to experience poor reproductive health and the highest fertility rates. [22] These educational disparities are apparent in every aspect of health and particularly in reproductive health. Myths of contraceptive side effects abound in such an environment. Some I commonly heard were that contraceptives can give you cancer, can cause irreversible infertility, or can cause menstrual blood to collect in the uterus and make a woman sick.

Perhaps the most commonly referred to barriers to contraception are culture and religion. In fact, it was the reason the doctors in Antigua gave me for not discussing contraception with their patients. Certainly the Guatemalans are very religious people, 55-60% are Catholic and 40% are Evangelical Christian. [23] There is also a strong machismo culture, as in much of Latin America, and virility is associated with manhood. Culture, however, has proven to be exquisitely sensitive to change when it comes to contraception. In historically strong Catholic countries like Ireland and Italy contraceptive use rates have grown to mirror other developed countries. In 2010, 94% of sexually active adults trying to avoid pregnancy in Ireland had used contraception in the previous year. [24] Similarly, 85% of Catholics in the United States no longer believe that the use of contraception is immoral. I think this signifies that when people are educated and have access to contraception, they are willing to integrate different forms of knowledge into their own belief systems and practices. Attributing the low rate of contraceptive use as religious in origin seems overly simplistic, given members of the same religion in another cultural and economic environment make different decisions.

Lastly, nothing can be discussed in relation to Guatemala without mentioning history and geography. The Indigenous Guatemalans bore the brunt of a brutal 36-year civil war, which only ended in 1996. Assumed to have sided with the left wing guerrillas, who supported more populist policies, the Indigenous were targeted by the right wing military government. [25] Some of the towns in the Lago de Atitlan region were the sites of acts of genocide by the government. It goes without saying that public health, and family planning, for these people was not a priority for the Government. Aside from small NGOs that carried out work in the Atitlan region throughout the violence, the health system of the region has been developed from scratch since 1996 and remains grossly underfunded. The Atitlan region remains one of the poorest in a country with one of the most unequal distributions of wealth in the world. Contributing further to the disadvantaged health status of these people is the difficulty of accessing services in larger towns. Seemingly regular natural disasters have severely damaged what little infrastructure there was connecting small mountain villages. Even the shortest of distances can take hours to travel, and poor roads and lack of transport are yet another barrier to delivering effective healthcare.

Xocomil: wind of change

Despite all these barriers to accessing contraception, it seems there is real hope. Many of the Guatemalans I met believed the end of the Mayan calendar on winter solstice 2012 would bring change, a new world, and an end to the old world of inequality and injustice. Thinking of the immense change contraception brought to many countries, and the very real possibility that this will soon be available to women in developing countries, I found myself sharing in the optimism.

But optimism should never breed complacence, and the struggle to make contraception universally available to women continues. Continued progress towards this goal raises new obstacles. After all, it was only recently in the United States, where contraception has been available since the 1960s, that there was a push to remove the requirement for health insurers to cover contraception from the Affordable Care Act.  We cannot afford to forget Virchow’s words now. In order to fulfil our tasks as future medical professionals, we must not forget the political and social life of the world we live in.

The Xocomil is the midday wind that crosses Lake Atitlan. The local Mayan people believe the wind carries away sin and the souls of lives lost in the lake. It is famous in the region and is a symbol of change and vitality.

Acknowledgements

Lyle and Andree at Maya Gift for giving me the opportunity to travel to villages as part of my elective.

Conflict of interest

None declared.

Correspondence

C McHugh: catemchugh@icloud.com

References

[1] UNICEF. At a glance: Guatemala. 2012; Available from: http://www.unicef.org/infobycountry/guatemala_statistics.html.

[2] Metz B. Politics, population and family planning in Guatemala: Ch’orti’ Maya experiences. Human Organization. 2001;60(3).

[3] Organization WH, UNICEF, UNFPA, Bank TW. Trends in maternal mortality: 1990 to 2010 2012.

[4] Walsh L. Beliefs and Rituals in Traditional Birth Attendant Practice in Guatemala. Journal of Transcultural Nursing. 2006;17(2):148-54.

[5] Pfeiffer E. Guatemala. Minnesota Curamericas Guatemala; 2010 [cited 2013]; Available from: www.curamericas.org/our-work/guatemala.

[6] Goldin C, Katz L. The Power of the Pill: Oral Contraceptives and Women’s Career and Marriage Decisions. Journal of Political Economy. 2002;110(4):730-70.

[7] Santhya K. Changing Family Planning in India: An Overview of Recent Evidence. New Delhi: Population Council, 2003.

[8] Greene M, Joshi O, Robles O. By Choice, Not By Chance: Family Planning, Human Rights and Development. New York: 2012.

[9] Singh S, Darroch JE. Adding It Up: Costs and Benefits of Contraceptive Services. Estimates for 2012. New York: Guttmacher Institute; 2012 [cited 2013 July 6]; Available from: www.guttmacher.org/pubs/AIU-2012-estimates.pdf.

[10]  SEARO. Thailand and Family Planning: An Overview. New Delhi: World Health Organization; 2003.

[11] Atinc TM. Realizing the Demographic Dividend: Challenges and Opportunities for Ministers of Finance and Development. Word Bank Live2011 Available from: http://live.worldbank.org/realizing-demographic-dividend-challenges-and-opportunities-ministers-finance-and-development.

[12] Bloom DE, Canning D, Sevilla J. The Demographic Dividend: A New Perspective on the Economic Consequences of Population Change. RAND Corporation 2003.

[13] Family Planning: An Overview. The Bill and Melinda Gates Foundation; 2012; Available from: http://www.gatesfoundation.org/familyplanning/Pages/overview.aspx.

[14] Douglas E. USAID Halts Supply of Contraceptives to Marie Stopes in Six African Countries. RH Reality Check. 2008.

[15] Gates M. Let’s put birth control back on the agenda: TED; 2012.

[16] Simmons A. 7 challenges for 7 billion. ABC News; 2011 [cited July 6 2013]; Available from: www.abc.net.au/news/2011-11-02/7-issues-facing-7-billion-people/3610318.

[17] World Population Prospects: The 2010 Revision, Highlights and 2011.

[18] Gillis J, Dugger C. UN forecasts 10.1 billion by Century’s End. 2011 [cited 2013 July 6]; Available from: www.nytimes.com/2011/05/04/world/04population.html?_r=0.

[19] Schieber B. Guatemala: 60 percent of workers earn less than minimum wage. The Guatemala Times. 2011 Wednesday 16th November

[20] Edwards J. Education and Poverty in Guatemala. World Bank, 2002.

[21] Literacy: Guatemala. 2012 [cited 2013 July 6]; Available from: www.cia.gov/library/publications/the-world-factbook/fields/2103.html.

[22] Hallman K, Peracca S. Indigenous Girls in Guatemala: Poverty and Location. In: Lewis M, Lockheed M, editors. Exclusion, Gender and Education: Case Studies from the Developing World. Washington: Centre for Global Development; 2007.

[23] International Religious Freedom Report: Guatemala. Washington US Department of State; 2006 [cited July 6 2013]; Available from: www.state.gov/j/drl/rls/irf/.

[24] McBride O, Morgan K, McGee H. Irish Contraception and Crisis Pregnancy Study. Health Service Executive, 2010.

[25] Manz B. Refugees of a Hidden War: The Aftermath of the Counterinsurgency in Guatemala. Albany, New York: State University of New York; 1988.

Categories
Feature Articles Articles

Probiotics: A New Recommendation with Proton Pump Inhibitors?

Introduction

Clostridium difficile-Associated Diarrhoea (CDAD) is becoming a worldwide epidemic with significant patient morbidity and mortality, as well as increasing the costs to health care systems. Although CDAD is generally associated with antibiotic use, there are multiple studies demonstrating that proton pump inhibitors (PPIs) may also be linked with CDAD. This is particularly worrisome for physicians in general practice, where PPIs are among the most frequently prescribed drugs. [1]

Clostridium difficile is a gram-positive, spore-forming, anaerobic bacillus that may cause gastrointestinal infections with poor patient outcomes and significant medical costs. [2,3] In one study, 3% of C. difficile infections resulted in death or admission to an Intensive Care Unit. [4] In 2002, another study demonstrated a mortality rate of 15.7% due to C. difficile colitis. [5] Although there is no complete cost analysis done in Australia, the figures emerging from the United States are staggering, with the average C. difficile infection cost ranging between $10,970-$29,000 per patient [6,7] and the estimated annual cost of $55 million in the state of New York alone. [7]

The mechanism of infestation and standard treatment

C. difficile enters the human body by spores which are ingested orally. Five percent of the population carries C. difficile asymptomatically due to growth-regulation by gastrointestinal flora. [8] In the presence of antibiotics, normal flora may be reduced, allowing an over-colonization of C. difficile. Typically, C. difficile is treated with a 10-day course of metronidazole for less severe infections, or with vancomycin for severe infections, with recurrence rates as high as 25%. [9]

PPIs and the link with C. difficile

PPIs are a class of drugs frequently prescribed in the general practice setting for Gastro-Oesophageal-Reflux-Disease (GORD), [10] peptic ulcer disease [11] and related conditions. [12] PPIs inhibit the hydrogen-potassium ATPase of parietal cells in the stomach, decreasing gastric acid production, thereby settling acid-related gastric symptoms. General practitioners are prescribing PPIs with increasing frequency. This is not surprising, as between 3% and 7% of the population suffer from GORD. [13] The mechanism by which PPIs may lead to C. difficile colitis is unclear; it may be that reduced stomach acidity allows more of the bacterial spores to survive, thereby increasing bacterial load in the gastrointestinal system. [14]

There are multiple studies demonstrating a link between C. difficile and PPIs. [15-18] In one meta-analysis of case-control and cohort studies, it was shown that PPIs imparted a relative risk of 1.69 for the development of C. difficile infection. [19] Another meta-analysis published by Kwok et al. (2012)  suggested a 70% increase in risk of this infection. [20] Given the considerable risk of developing CDAD in association with PPIs, and the morbidity and mortality associated with CDAD, it is recommended that general practitioners use caution when prescribing these medications, observe patients for secondary diarrhoea and investigate with C. difficile cytotoxin assays.

A multi-center case control trial from the Netherlands identified that the greatest risk for development of C. difficile infection was within the first three months after initiation of antibiotics, with the risk peaking at one month and declining between one and three months. [21] According to this study, third-generation cephalosporins and carbapenems were associated with the greatest risk of CDAD.[21] Other risk factors for CDAD include living in long term care facilities, major bowel diseases such as Inflammatory Bowel Disease (IBD), colorectal cancer, radiation and chemotherapy, and age, with highest risk beyond the age of 65 years. [22] It is yet to be determined if similar risk factors are involved in the development of PPI-associated diarrhoea.

It should be noted that the meta-analytic link between PPIs and CDAD is criticized, as there are multiple methodological problems with many of the studies involved. [23] One criticism is that duration and dose of PPI exposure were not variables considered in the meta-analyses; therefore, the exposure-dependent and dose-dependent relationship cannot be established. [23] Further research is required to determine whether there is a causal relationship between PPI use and CDAD.

What can physicians do in the meantime while the link is investigated?

There may be a role for probiotics in the prevention of PPI related CDAD. Probiotics are broadly defined as live microorganisms that exert beneficial effect on the host. [24-26] The mechanism for this is unclear, but may involve the suppression of pathogenic bacteria and/or suppression of inflammation in the gut. [27] There are a wide range of probiotics marketed today to improve immune function including Bifidobacterium lactis, Lactobacillus reuteri, Lactobacillus rhamnosus and others for diarrhoea including Saccharomyces boulardii, Lactobacillus casei, Lactobacilus acidophilus and others. Lactobacillus, bifidobacteria and certain yeasts (eg: Saccharomyces) are the most common microbes used in commercial probiotics. These can be consumed as part of fermented foods, such as yogurt, or directly as supplements. Recommendation of the probiotic S. boulardii with antibiotics has shown a significant reduction in the incidence of antibiotic-associated-diarrhoea in two separate double-blind placebo controlled studies. [28,29] A meta-analysis reveals nine studies have shown use for both S. boulardii and lactobacilli in the prevention but not the treatment of CDAD. [30]

At this point there is no research examining the effects of probiotics regarding the prevention of PPI associated CDAD; however, it is reasonable to presume there may be a role for S. boulardii and lactobacilli in balancing the gastrointestinal tract flora whether the disruption of its microenvironment is secondary to antibiotics or PPIs. If future research demonstrates a similar reduction in PPI-related CDAD, as has been documented with antibiotic-related CDAD, there may be grounds for adjustment of future clinical recommendations to include probiotics with PPIs in the general practice setting.

In general practice, deciding whether to prescribe any medication requires evaluation of risks and benefits to the patient. As minimal risks have been reported in healthy individuals with probiotic use, [31] and given the potential benefit to reduce the incidence of CDAD, research needs to be done to determine whether there is benefit to prophylactically recommending S. boulardii with PPIs. It would be logistically difficult to ensure compliance and no use of alternate anti-acid medication in a randomly controlled longitudinal trial in the development of C. difficile infection. However, a well controlled prospective cohort study may minimize confounding factors and suggest causality by examining patients with limited comorbidities.

The risks of recommending probiotics

There are no systematic reviews demonstrating risk of probiotics; however, general practitioners should be aware that multiple case studies indicate there may be a risk of recommending probiotics in immunocompromised patients. These include cases of hepatic abscesses and pneumonia, [32] probiotic sepsis [33,34] and S. boulardii fungaemia. [35,36] There are no cases of such probiotic sepsis or fungaemia in healthy individuals.

Conclusion

Probiotics have been recommended in the prevention but not the treatment of C. difficile infection associated with antibiotics. While the pathogenesis of PPI-related CDAD is unknown, it presumably involves the disruption of gastrointestinal flora, which is potentially amenable to probiotic supplementation. Given minimal documented risks of probiotics in immunocompetent individuals, research needs to determine whether there are direct benefits of the use of probiotics in the prevention of PPI-related CDAD. Such recommendation on the part of the general practitioner may reduce morbidity and mortality associated with CDAD and reduce costs to the health care system.

Conflict of interest

None declared.

Correspondence

C Oitment: colby.oitment@uqconnect.edu.au

References

[1] Ahrens D, Behrens G, Himmel W, Kochen M, Chenot JF. Appropriateness of proton pump inhibitor recommendations at hospital discharge and continuation in primary care.  Int J Clin Prac. 2012; 66(8):767-773. DOI: 10.1111/j.1742-1241.2012.02973.x

[2] Miller M, Gravel D , Mulvey M, Taylor G, Boyd D, Simor A, et al. Health care-associated Clostridium difficile infection in Canada: patient age and infecting strain type are highly predictive of severe outcome and mortality. Clin Infect Dis. 2010; 50: 194-200.

[3] Dubberke ER, Reske KA, Olsen MA, McDonald LC, Fraser VJ. Short- and long-term attributable costs of Clostridium difficile-associated disease in nonsurgical inpatients. Clin Infect Dis. 2008; 46: 497-504.

[4] Rubin MS, Bodenstein LE, Kent KC. Severe Clostridium difficile colitis. Dis Colon Rectum. 1995; 38(4): 350-354.

[5] Morris AM, Jobe BA, Stoney M, Sheppard BC, Deveney CW, Deveney KE. Clostridium difficile colitis: an increasingly aggressive iatrogenic disease? Arch Surg. 2002; 137(10): 1096-1100.

[6] McFarland LV, Surawicz CM, Rubin M, Fekety R, Elmer GW, Greenberg RN. Recurrent Clostridium difficile disease: epidemiology and clinical characteristics. Infect Cont Hosp Epidemiol. 1999; 20(1): 43-50.

[7] Lipp MJ, Nero DC, Callahan MA. The impact of hospital-acquired Clostridium difficile. J Gastroenterol Hepatol. 2012; 27(11): 1733-1737.

[8] Bartlett JG. Clostridium difficile: clinical considerations. Rev Infect Dis. 1990;12 (2):243-251.

[9] Bricker E, Garg R, Nelson R, Loza A, Novak T, Hansen J. Antibiotic treatment for Clostridium difficile-associated diarrhoea in adults. Cochrane Database of Syst Rev. 2007; (3): CD004610.

[10] McKeage K, Blick SK, Croxfall JD, Lyseng-Williamson KA, Keating GM. Esomeprazole: a review of its use in the management of gastric-acid related diseases in adults. Drugs. 2008; 68: 1571-1607.

[11] Saha SK, Saha SK, Masud H, Islam N, Ralhan AS, Roy PK, Hasan M. To compare the efficacy of triple therapy with furazolidone amoxicillin and omeprazole for two weeks and three weeks in the eradication of Helicobacter pylori in Bangladeshi duodenal ulcer patients. Bangladesh Med Res Counc Bull. 2011; 37(3): 83-87.

[12] Gerson LB, Mitra S, Blecker WF, Yeung P. Control of intra-esophageal pH in patients with Barrett’s esophagus on omeprazole sodium bicarbonate therapy. Ailment Pharmacol Ther; 2012; 35(7): 803-809.

[13] Digestive diseases in the United States: Epidemiology and Impact. NIH. 1994; 94-1447.

[14] Stevens V, Dumyati G, Brown J, Wijgaarden E. Differential risk of Clostridium difficile infection with proton pump inhibitor use by level of antibiotic exposure. Pharmacoepidemiol Drug Saf. 2011; 20(10): 1035-1042.

[15] Rotamel A, Poritz LS, Messaris E, Berg A, Stewart DB. PPI Therapy and Albumin are Better Predictors of Recurrent Clostridium difficile Colitis than Choice of Antibiotics. J Gastrointest Surg. 2012; 16(12): 2267-2273.

[16] Leonard AD, Ho KM, Flexman J. Proton pump inhibitors and diarrhoea related to Clostridium difficile infection in hospitalized patients: a case-control study. Intern Med J. 2012; 42(5): 591-594.

[17] Keuhn BM. Reflux drugs linked to C. difficle-related diarrhea. JAMA. 2012; 307(10): 1014.

[18] Kim YG, Graham DY, Jang BI. Proton pump inibitor use and recurrent Clostridium difficile-associated disease: a case-control analysis matched by propensity score. J Clin Gastroenterol. 2012; 46(5): 397-400.

[19] Janarthanan S , Ditah I , Adler DG, Ehrinpreis MN. Clostridium difficile associated

diarrhea and proton pump inhibitor therapy – a meta-analysis. Am J Gastroenterol. 2012; 107:1001-1010.

[20] Kwok CS , Arthur AK , Anibueze CI, Singh S, Cavallazzi R, Loke YK. Risk of Clostridium difficile infection with acid suppression agents and antibiotics: meta-analysis. Am J Gastroenterol. 2012; 107:1011-1019.

[21] Grigorios I, Leontiadis I, Miller M, Howden C. How Much Do PPIs Contribute to C. difficile Infections? The Am J Gastroenterol. 2012;107:1020-1021.

[22] Pillai A, Nelson RL. Probiotics for the treatment of Clostridium difficile-associated colitis in adults. The Cochrane Library. 2008; 3: 1-18.

[23] Hensgens MPM, Goorhuis A, Dekkers OM, Kuijper EJ. Time interval of increased risk for Clostridium difficile infection after exposure to antibiotics. J Antimicrob Chemother. 2011; 1-7

[24] Bartlett JG, Gerding DN. Clinical recognition and diagnosis of Clostridium difficile infection. Clin Infect Disease 2008; 46: s12-s18

[25] Dinleyici EC, Eren M, Ozen M, Yargic ZA, Vandenplas Y. Effectiveness and Safety of Saccharomyces boulardii for Acute Infectious Diarrhea. Expert op on boil therapy. 2012: 12(4); 395-410.

[26] Vitetta L. Probiotics, prebiotics and gastrointestinal health. Medicine Today. 2008;9(9): 65-70.

[27] Avadhani A, Miley H. Probiotics for prevention of antibiotic-associated diarrhea and Clostridium difficile-associated disease in hospitalized adults–a meta-analysis. J Am Acad Nurse Pract. 2011;23(6):269-274.

[28] Surawicz CM, Elmer GW, Speelman P, McFarland L, Chinn J, van Belle G. Prevention of antibiotic-associated diarrhoea by Saccharomyces boulardii: a prospective study. Gastro. 1989; 96: 981-988.

[29] McFarland LV, Surawicz CM, Greenberg RN, Elmer GW, Moyer KA, Melcher SA, et al. Prevention of B-lactam-associated diarrhoea by Saccharomyces boulardii compared with placebo. Am J Gastroenterol 1995; 90: 439-448.

[30] D’Souza AL, Rajkumar C, Cooke J, Bulpitt CJ. Probiotics in prevention of antibiotic associated diarrhea: meta-analysis. BMJ. 2002. 8; 324(7350): 1361

[31] Das RR, Naik SS, Singh M. Probiotics as additives on therapy in allergic airway diseases: a systematic review of benefits and risks. Biomed Res Int. 2013; Vol 2013, Article ID 231979, 10 pages. DOI: 10.1155/2013/231979.

[32] Kunz AN, Noel JM, Fairchok MP. Two cases of Lactobacillus bacteremia during probiotic treatment of short gut syndrome. J Pediatr Gastroenterol Nutr 2004;38:457-458.

[33] De Groote MA, Frank DN, Dowell E, Glode MP, Pace NR. Lactobacillus rhamnosus GG bacteremia associated with probiotic use in a child with short gut syndrome. Pediatr Infect Dis J. 2005;24:278-280.

[34] Hennequin C, Kauffmann-Lacroix C, Jobert A, Vlard JP, Ricour C, Jacquemin JL, et al. Possible role of catheters in Saccharomyces boulardii fungemia. Eur J Clin Microbiol Infect Dis. 2000;19:16-20.

[35] Bassetti S, Frei R, Zimmerli W. Fungemia with Saccharomyces cerevisiae after treatment with Saccharomyces boulardii. Am J Med 1998;105:71-72.

[36] Niault M, Thomas F, Prost J, Ansari FH, Kalfon P. Fungemia due to Saccharomyces species in a patient treated with enteral Saccharomyces boulardii. Clin Infect Dis. 1999; 28: 930.

 

Categories
Feature Articles Articles

Evidence based practice; keep it simple stupid

Learning and implementing evidence based practice is an expected component of good medical practice. Synthesising evidence in an effective and timely manner is a skill that is growing in importance and relevance. Evidence based practice is widely included in medical school curricula, and information literacy skills are known to be difficult to acquire. We provide a fresh look at a streamlined approach to evidence based practice, using a ‘real world’ case study.

Introduction

The importance of evidence based practice (EBP) is ever increasing. [1,2] However, the complexities of collecting, interpreting and synthesising information may be time consuming and laborious. [3] Information literacy skills are known to be difficult to learn. [4] In an effort to condense the process, a variety of models have been designed for evidence retrieval, including the 4S, [5] the 5S, [6] and more recently the 6S pyramid (Fig. 1). [7] In this article we will focus on the 6S pyramid and its application to a clinical case.

The technology explosion of the last decade has increased access to information for clinicians in almost all settings. The rapid development of handheld electronic devices, paired with the licenses to evidence based databases being held by many universities and institutions, results in information being easier to access. The problem then arises of how to find the best information for a clinical scenario in the swiftest manner. The 6S pyramid is useful as it provides a guide showing where to look first; additionally, it tracks the integration of research into clinical practice, with a decision support system at the pinnacle. An example of this is the ‘PrimaryCare Sidebar’ [8] integrating evidence based guidelines into the clinical data already in the patient record. Although the tip of the pyramid is not always readily available, as we step down the pyramid there are a variety of other evidence based tools available, including Dynamed, [9] BMJ Clinical Evidence, [10] and the Therapeutic Guidelines. [11] Further down the pyramid are reliable resources such as PubMed [12] and the Cochrane Database of Systematic Reviews, [13] which are freely available online.

This article presents a streamlined approach to EBP, demonstrating the multistep process via a clinical case. One of the most difficult aspects of evidence based practice, translating medical jargon and statistics into ‘layman’s terms’ with the goal of empowering the patient to make an informed decision, is demonstrated. Our aim is to demystify EBP and its application for medical students and practitioners, thereby encouraging a wider application in day-to-day clinical work.

Case Details

Mrs SJ is a 62yo Caucasian female who is fairly new to the practice; she presents to discuss the topic of her back pain. SJ reports a three year history of bilateral lumbar radiculopathy; MRI showed degenerative spinal canal stenosis at L5/S1 and nerve conduction studies confirmed neural involvement. Failing a period of conservative measures and continuing to report severe pain, SJ underwent an L5/S1 laminectomy and posterior fusion.

Postoperatively, SJ reported minor relief of her symptoms; she continues to have 6/10 bilateral leg pain on a daily basis. The surgeon advised SJ there was no role for further operative procedures and SJ confirmed she did not want to even consider another procedure. Following the surgery she trialled gabapentin, with minimal effect. Since then she has been attempting to manage her pain with paracetamol, which has only had a partial effect.

Although not under any major financial stress, SJ felt the benefit of the gabapentin did not justify the cost, contributing to cessation of the medication. As an adjunct to pharmacotherapy, SJ had five sessions of physiotherapy addressing postural correction and stretching. She felt there was no benefit from this treatment.

SJ has an otherwise unremarkable medical history, is not on any regular medication and has no allergies. She lives with her husband, who is well. Friends have mentioned other drugs that they found effective for their pain, and she asks why she shouldn’t use them.

Determining a specific, targeted question

Before we seek our answers, we need to define the question/s. [14] This will lead us to a more precise, relevant answer, and save time sifting through irrelevant information.

In patients with chronic lumbar neuropathic pain (radiculopathy), what are the pharmacological options? This question is really what the patient has asked; however, our clinical problem is: what are the pain management options (pharmacological and non-pharmacological) in a patient with radiculopathy who has failed surgical therapy. In practice, we may choose to enquire about the pharmacotherapy about which Mrs SJ has asked; however, a holistic approach to the longterm management of this patient would involve a review of all options, including those that are non-pharmacological. In order to stay focused on the purpose of this article, which is the process of EBP and not the best practice treatment for lumbar radiculopathy, we will focus on pharmacotherapy only.

PICO:

  • Population: Chronic radiculopathy, unsuccessful lumbar surgery, menopausal women
  • Intervention: Medication, not gabapentin
  • Comparator: No medication, paracetamol
  • Outcome: Pain reduction and quality of life improvement. [15]

Collecting the evidence

In order to approach this therapy question, we started as high up the pyramid as possible. When creating a search we used keywords that were defined during the formulation of our targeted (PICO) question. Boolean operators (AND, OR, NOT) are also useful and function well in most search engines. Dynamed contained a topic entitled ‘Lumbar spinal stenosis,’ and the treatment section covered some information about medications, but this was not complete. Using BMJ Clinical Evidence (a clinical guideline tool) we searched ‘chronic pain.’ That search led us to the topic ‘chronic pain syndromes,’ and, although there wasn’t a direct answer to our question, under the treatment section we found an international guideline dated 2007.

Now that we knew guidelines existed on the topic, we searched Medline for a more recent version. This led us to three international guidelines. We used the 2010 paper ‘Recommendations for the pharmacological management of neuropathic pain: an overview and literature update’ by Dworkin et al as the primary paper. [16] Unfortunately, as is often the case, evidence specific to our patient was not available.

Determining levels of evidence and strength of recommendation in order to deliver appropriate advice

In order to give valid advice we need to know the strength of the evidence it is based upon, and the size of effect in our population of interest. Various guides exist in order to systemise this process and various methods are commonly used in the literature. The Oxford Centre for Evidence-based Medicine [17] is a well established resource. More recently, The Grading of Recommendations Assessment, Development and Evaluation (GRADE) [18] has been developed with the aim of providing a comprehensive system for grading quality of evidence and strength of recommendations. The resources above provide quality instruction on how to perform the vital step of appraising evidence. Fortunately, this has often already been done for us by others who have summarised the literature, in guidelines or systematic reviews, but it is good to be familiar with the process.

Breaking down the evidence in a real world scenario

Evidence comes from a variety of communities worldwide, and as such, a patient’s specific situation always needs to be taken into account. [22] Various approaches for communicating evidence [23] and mediums for doing so have been evaluated. [24] The way we communicate with patients about risk and effectiveness of treatments can affect their perception and understanding of illness. Communicating with the aid of numerical data, absolute risk (instead of relative risk), both negative and positive perspectives, and with visual aids, all help to improve understanding. [25] Closed loop communication can be used in order to verify understanding. We need to start by translating the evidence into dialogue that would take place between two human beings. This can be helpful in conceptualising the information retrieved. Let’s try…

Doctor: Let’s start by talking about the type of pain you have.

The pain you have is a nerve pain, often called neuropathic pain. This can be due to a lesion or disease. In your case, structures in your lower back are directly irritating nerves. In a simple world you remove the ‘lesion or disease’ and the pain would go away.

Unfortunately, after chronic stimulation the pain message continues to be ‘switched on’ even without a stimulus. This pain can be treated with medications but is often more difficult to manage.

Patient: I totally agree, this pain has been really difficult to manage, and has been getting on top of me for a long time.

Doctor: So your friends have mentioned medications?

Patient: Yes, they have mentioned a few different ones. I’m not sure of the names.

Doctor: There’s a lot of research about medications for the treatment of neuropathic pain, [16] but not a lot have looked at your particular scenario. [26] Of the few medications that have been tested, the evidence suggests only a small amount of benefit. There are some medications that have a lack of efficacy and we should avoid these.

Patient: I am really interested in trying another medication, even if the improvement is only small. Anything that would help me get through the day would be positive.

Doctor: Studies have shown that there are a few main groups of medications that are considered first choice; gabapentin (the one you tried) was one of them. Alternatives include opioids and some antidepressants. We use the antidepressants not because we think you are depressed, but because they have good pain relieving properties for this type of pain. You should know that research found these medications gave meaningful pain relief to around 50 percent of the patients. [23] So, effectively one in two patients. Although this gives us an idea of what to expect, it doesn’t mean it will work for you.

Because of the unclear nature of the evidence, we need to approach the choice of medication carefully, considering your situation. [16]

Patient: So…what are the side effects and how much do these medications cost?

Doctor: Antidepressants, particularly an older group called ‘TCAs’ (tricyclic antidepressants) have been shown to be effective. We don’t fully understand how they work for pain, but do know they provide pain relief in patients who aren’t depressed. [28] On the positive side, they are cheap, are taken once a day and can help with sleep. On the negative side, there are some side effects including dry mouth and constipation. These are not harmful, but annoying, and often resolve with a change in dosage. Rarely, these drugs can cause disturbance to the heart rhythm, and an overdose of these medications is very dangerous to children, so they need to be kept out of reach at all times. Newer antidepressants called SNRIs have shown fewer side effects, but haven’t been studied as thoroughly. [16]

Patient: Besides the heart thing these sound pretty good. I don’t have children at home so that shouldn’t be an issue. Is there anything else on offer?

Doctor: Another group of medications work by slowing down pain impulses; gabapentin is one of these. Although they have proven effectiveness, side effects include dizziness and sedation. As you have mentioned, this is an expensive choice and hasn’t worked for you, so it’s probably not the best option for us at the moment.

Patient: Agreed!

Doctor: Finally, the opioid-like medications are an option. However, I would prefer if we could avoid these. Generally, individuals build tolerance to them and they can be addictive.

Patient: I don’t want to have to rely on it all the time, or have to keep using more of the medication. It sounds like the first option, the antidepressants, is the best, particularly if they are going to help me sleep.

Doctor: Yes, assisting with sleep is a great attribute of TCAs, but it takes a while for full effect, so let’s trial a medication called amitriptyline for six weeks and reassess after that. The medication will cost around A$30 a month. I would like to do an ECG to get an idea of your baseline heart rhythm, and for you to complete two questionnaires in order for us to keep track of your progress: the McGill pain questionnaire [29] and the Short form 36. [30]

Please come back and see me sooner if you have any concerns or develop the side effects we talked about. Also, I would like you to consider other ways this pain can be managed. There are many alternative approaches we should explore, most of which do not include medications.

Conclusion

So, that wasn’t too hard, was it? We defined the question, used a top down approach to the evidence pyramid, and accessed a synthesis of the best literature to answer our question. We made an assessment of the quality of the information available, and attempted to translate ‘doctor speak’ into lay terms. Implementation of the evidence will inevitably lead to further questions. The ongoing process of EBP is illustrated as a cycle (Fig. 2).

Gathering evidence based information should no longer be a chore. Using evidence at any level of the pyramid needs thoughtful consideration, requiring close scrutiny of the methods of evidence generation and the method of appraisal. Due to the increasing amount of evidence being published, synthesis and weighing of existing evidence can serve to provide a more comprehensive and relevant source of evidence based recommendations. The streamlined pyramid approach can be skimmed during consultations or scrutinised for assignments.

So the next time a patient (or an examiner!) throws you a curveball, use EBP to find the comprehensive answer they deserve.

Acknowledgements

The authors would like to thank Dr Morris Aziz for his contribution on the topic.

Conflict of interest

None declared.

Correspondence

J Dannaway: jdan9820@uni.sydney.edu.au

References

[1] Dawes M, Summerskill W, Glasziou P, Cartabellotta A, Martin J, Hopayian K, et al. Sicily statement on evidence-based practice. BMC Medical Education. 2005; 5(1):1.

[2] Sackett DL, Rosenberg WMC. On the need for evidence-based medicine. Journal of Public Health. 1995; 17(3):330 –334.

[3] Haynes B, Haines A. Barriers and bridges to evidence based clinical practice. BMJ. 1998 Jul 25;317(7153):273–6.

[4] Hofer AR, Townsend L, Brunetti K. Troublesome Concepts and Information Literacy: Investigating Threshold Concepts for IL Instruction. Portal: Libraries and the Academy. 2012; 12(4):387–405.

[5] Haynes RB. Of studies, syntheses, synopses, and systems: the “4S” evolution of services for finding current best evidence. ACP J. Club. 2001 Apr;134(2):A11–13.

[6] Haynes RB. Of studies, syntheses, synopses, summaries, and systems: the “5S” evolution of information services for evidence-based healthcare decisions. Evidence Based Medicine. 2006; 11(6):162–4.

[7] DiCenso A, Bayley L, Haynes RB. Accessing pre-appraised evidence: fine-tuning the 5S model into a 6S model. Evidence based nursing. 2009; 12(4):99–101.

[8] PrimaryCare Sidebar. [Accessed 2013 Aug 26]. Available from: http://www.racgpoxygen.com.au/products/

[9] Dynamed. [Accessed 2011 Dec 19]. Available from: http://dynamed.ebscohost.com/

[10] BMJ Clinical Evidence. [Accessed 2011 Dec 19]. Available from: http://clinicalevidence.bmj.com/ceweb/index.jsp

[11] Therapeutic Guidelines. [Accessed 2011 Dec 19]. Available from: http://www.tg.org.au/

[12] PubMed. [Accessed 2011 Dec 19]. Available from:http://www.ncbi.nlm.nih.gov/pubmed/

[13] The Cochrane Collaboration. Cochrane Reviews. [Accessed 2011 Dec 19]. Available from: http://www.cochrane.org/cochrane-reviews

[14] Centre for Evidence Based Medicine. Asking focused questions. [Accessed 2011 Dec 19]. Available from: http://www.cebm.net/index.aspx?o=1036

[15] Salisbury J, Glasziou P, Del Mar C, Salisbury J. Evidence-based practice workbook. Oxford: Blackwell; 2007.

[16] Dworkin RH, O’Connor AB, Audette J, Baron R, Gourlay GK, Haanpää ML, et al. Recommendations for the pharmacological management of neuropathic pain: an overview and literature update. Mayo Clinic Proceedings. 2010. p. S3.

[17] CEBM (Centre for Evidence-Based Medicine). [Accessed 2011 Dec 19]. Available from: http://www.cebm.net/index.aspx?o=1001

[18] The grading of recommendations assessment, development and evaluation (GRADE). [Accessed 2012 Dec 19]. Available from: http://www.gradeworkinggroup.org/index.htm

[19] Tran DQH, Duong S, Finlayson RJ. Lumbar spinal stenosis: a brief review of the nonsurgical management. Can J Anaesth. 2010 Jul;57(7):694–703.

[20] Baron R, Freynhagen R, Tölle TR, Cloutier C, Leon T, Murphy TK, et al. The efficacy and safety of pregabalin in the treatment of neuropathic pain associated with chronic lumbosacral radiculopathy. Pain. 2010 Sep;150(3):420–7.

[21] Attal N, Cruccu G, Baron R, Haanpää M, Hansson P, Jensen TS, et al. EFNS guidelines on the pharmacological treatment of neuropathic pain: 2010 revision. European Journal of Neurology. 2010; 17(9):1113–e88.

[22] Centre for Evidence Based Medicine. Making a decision. [Accessed 2011 Dec 19]. Available from: http://www.cebm.net/index.aspx?o=1854

[23] Epstein RM, Alper BS, Quill TE. Communicating evidence for participatory decision making. JAMA: The Journal of the American Medical Association. 2004; 291(19):2359.

[24] Trevena LJ, Barratt A, Butow P, Caldwell P. A systematic review on communicating with patients about evidence. Journal of Evaluation in Clinical Practice. 2006; 12(1):13–23.

[25] Paling J. Strategies to help patients understand risks. BMJ. 2003; 327(7417):745–8.

[26] Attal N, Martinez V. Recent Developments in the Pharmacological Management of Neuropathic Pain. European Neurological Journal. 2010

[27] OʼConnor AB. Neuropathic Pain: Quality-of-Life Impact, Costs and Cost Effectiveness of Therapy. PharmacoEconomics. 2009;27(2):95–112.

[28] Max MB, Culnane M, Schafer SC, Gracely RH, Walther DJ, Smoller B, et al. Amitriptyline relieves diabetic neuropathy pain in patients with normal or depressed mood. Neurology. 1987 Apr;37(4):589–96.

[29] Melzack R, Katz J. The McGill Pain Questionnaire: appraisal and current status. Guilford Press; 2001.

[30] Ware Jr JE. SF-36 health survey update. Spine. 2000;25(24):3130–9.

Categories
Feature Articles Articles

Improving medication adherence amongst Aboriginal and Torres Strait Islander peoples

Introduction

Aboriginal and Torres Strait Islander peoples represent a minority population in Australia, comprising approximately 2.5% of the total Australian population in 2011. [1] There are a number of challenges faced by Aboriginal and Torres Strait Islander peoples, due to social, economic and health differentials as a consequence of the history of marginalisation. [3] Despite improvement in detection and management of chronic disease, Aboriginal and Torres Strait Islander peoples continue to have higher incidences of chronic diseases such as cardiovascular disease and diabetes mellitus. [2,4]

A contributing factor to this gap in health statistics is a low rate of adherence to medication amongst Aboriginal and Torres Strait Islander peoples. [5] While this problem is not unique to this population, there is global evidence that the rates of adherence to medication are lower amongst marginalised groups. [6] In order to help reduce the burden of disease amongst this group, it is important to explore some reasons for non-adherence that are unique to Aboriginal and Torres Strait Islander peoples. In particular, this article will focus on the impact of cultural insensitivity and problems with access to healthcare and medications amongst this population. It will suggest how adherence can be improved through improving cultural sensitivity and access to healthcare, in order to reduce the gap in health statistics between Aboriginal and Torres Strait Islander peoples and non-Aboriginal and Torres Strait Islander peoples.

Impact of non-adherence

The World Health Organisation (WHO) estimates that, in developed countries, 50% of patients fail to comply with advice given by medical practitioners, including both medication and lifestyle advice. [6] Non-adherence with medication is a complex problem that is multi-factorial, and can contribute both to the failure of treatment [5] and increased costs to the healthcare system. [7] Often, this lack of adherence is intentional due to side effects, perceived drug effectiveness, and cost. [8] The implications of these barriers to adherence for Aboriginal and Torres Strait Islander peoples will be discussed below, with an emphasis on cultural barriers preventing adherence. [9]

Chronic diseases require adherence to medications and lifestyle modifications, in order to slow disease progression and prevent complications. [10] Therefore, non-adherence to either form of treatment can contribute to the perpetuation of this gap in health statistics. For example, in general, Aboriginal and Torres Strait Islander peoples have higher rates of cardiovascular disease than non-Aboriginal and Torres Strait Islander peoples. [3] Given that medication and lifestyle modifications reduce risk factors of cardiovascular disease and improve mortality, failure to comply with these treatments can result in exacerbation of disease rates. [3] Similarly, diabetes mellitus is a condition that is more prevalent amongst the Aboriginal and Torres Strait Islander population, and its morbidity and mortality are also disproportionately higher amongst this population. [10] Poorly controlled diabetes mellitus, through lack of adequate pharmacological management, can have serious vascular complications. This perpetuation of health inequality would in turn have a negative impact on national health expenditure, leading to increased costs to the health system. [9]

Barriers to adherence

According to the WHO, there are five dimensions that can impair a patient’s adherence with medication. [6] These are the healthcare team or system, socioeconomic factors, the nature of the therapy, the patient and the medical condition. [6] The first four dimensions are especially relevant to Aboriginal and Torres Strait Islander peoples in both rural and urban settings, and will be discussed below.

Socioeconomic factors

First, as stated by the WHO, socioeconomic factors play an important role in the low rates of adherence amongst Aboriginal and Torres Strait Islander peoples. Aboriginal and Torres Strait Islander peoples have a lower income status than non-Aboriginal and Torres Strait Islander peoples, and also have a higher unemployment rate. [11] This may therefore affect adherence to long-term, expensive medical treatment. Geographic location has previously been a barrier to accessing medications for some Aboriginal and Torres Strait Islander communities [3] and is within the WHO’s healthcare system dimension. However, the Australian Government has, in recent years, initiated national programs and legislated to improve access to prescription medications for Aboriginal and Torres Strait Islander peoples. This will be discussed below.

Cultural insensitivity

Of the Aboriginal and Torres Strait Islander peoples who do live in urban centres, many report cultural insensitivity as being the main barrier to receiving care from services that do not specialise in Aboriginal and Torres Strait Islander health. [12] This in turn can influence medication uptake and adherence. In particular, the non-Aboriginal and Torres Strait Islander healthcare system can be seen as unwelcoming. [11] This is a barrier under WHO’s healthcare team dimension. For example, one Aboriginal and Torres Strait Islander patient was unhappy because he was told to go to an Aboriginal and Torres Strait Islander health service, when he presented to a service that does not specialise in Aboriginal and Torres Strait Islander health. [12] This attitude often fosters a poor relationship between the clinician and the individual. [11]

Miscommunication between health practitioner and patient contributes to a lack of adherence to medications. For example, the services outside the Aboriginal and Torres Strait Islander system often do not provide enough support for people who only speak traditional languages within communities. [5] Cass et al. (2002) demonstrated that communication by healthcare service providers to Aboriginal and Torres Strait Islander peoples who preferred to communicate in languages other than English was often poor. [13]

Other causes of miscommunication were the health practitioner failing to share control in the consultation with the patient, failing to overcoming language barriers by not using interpreters, and using too much biomedical language during the consultation. [13] When the patient does not feel involved in decision-making, he or she is less motivated to adhere to treatment advice. [5] Furthermore, miscommunication is often unrecognised by the health practitioner, meaning that concepts are never clarified. [13] While most Aboriginal and Torres Strait Islander peoples are fluent in English, such miscommunication can have a negative impact on adherence to treatment for many people, leading in turn to adverse health outcomes. [13]

Furthermore, services that do not specialise in Aboriginal and Torres Strait Islander health sometimes do not accommodate Aboriginal and Torres Strait Islander cultural practices, which may hinder medication adherence. In some Aboriginal and Torres Strait Islander communities, traditional healers can be the first point of call for health problems. [14] Only when the traditional healers are unable to provide a solution does an individual from such a community approach the Western health system. [14] As a consequence, Aboriginal and Torres Strait Islander peoples may be less likely to comply with prescriptions due to unfamiliarity with Western medicine. [13] Furthermore, the concept of prophylactic medication does not exist in some Aboriginal and Torres Strait Islander cultures, so some community members may be reluctant to take medications that are not for the treatment of acute conditions. [15]

The family plays an important role in many Aboriginal and Torres Strait Islander people’s health. [5] Therefore, the family itself can act as a barrier to medication adherence in a number of ways. [5] First, there can be a culture of sharing medications in some communities. [5] This can result in under-treatment of the person who was prescribed the medication. Secondly, some families can influence a person’s decision to adhere to medication, by failing to support the person to adhere to medication, or by encouraging the notion that medication adherence is not cultural.[5] Therefore, educating the community and seeking familial support is important to improve adherence rates to therapies amongst some Aboriginal and Torres Strait Islander peoples. [5]

Healthcare practitioners’ role

There are a number of issues with adherence due to healthcare practitioner behaviours. First, due to cultural differences, a lack of flexibility when prescribing medication has been identified as contributing to non-adherence amongst some groups. [12] For example, health service providers are not always using long-acting medication preparations where possible, nor appropriate combination medications, to reduce the number of tablets that the patient has to take. [15] This falls under the WHO dimension of the nature of the therapy, and is something that health service providers should be aware of when engaging in culturally sensitive medical practice.

Similarly, medical practitioners themselves can be non-adherent to clinical practice guidelines when providing treatment to some Aboriginal and Torres Strait Islander peoples. [16] The study by Fürthauer et al. (2013) showed that medical practitioners may deliberately deviate from a clinical guideline for a particular patient, if they feel that the patient may not adhere to the treatment in the long-term, due to cultural practices or socioeconomic background. [16] This comes under the WHO healthcare team dimension, and is an important cause of non-adherence that needs to be examined closely in the Australian context.

The WHO states that patients should be supported, not blamed, for a lack of adherence. [6] Therefore, practitioners should take an active role to ensure that the healthcare environment supports adherence to medication. [6] For example, practitioners should work with patients to create a therapy regime that fits the patient’s lifestyle. [6] It has been shown that a shift in attitude amongst healthcare practitioners to a more empathetic, collaborative approach with their patients achieves better adherence rates. [6] This includes the practitioner taking the socio-demographic characteristics of the patient into account. [6]

History of marginalisation

In addition, some Aboriginal and Torres Strait Islander peoples feel that health services should recognise the history surrounding racism and discrimination against Aboriginal and Torres Strait Islander peoples, in order to facilitate trust and improve service uptake. [12] This issue is within WHO’s patient-specific dimension, and may eliminate any feelings of ‘cultural shame’ for accessing Western medication due to the history of marginalisation of Aboriginal and Torres Strait Islander peoples. [3] This indicates that more research needs to be undertaken on the psychological impact of marginalisation on Aboriginal and Torres Strait Islander and its link to non-adherence.

Minimising non-adherence

There are a two main ways to improve adherence rates amongst Aboriginal and Torres Strait Islander peoples. One is by improving cultural sensitivity amongst health service providers to provide appropriate services to Aboriginal and Torres Strait Islander peoples, and welcome them to services outside the Aboriginal and Torres Strait Islander system. The other way is by subsidising medications so that Aboriginal and Torres Strait Islander peoples can have better access to treatments.

Improving cultural sensitivity

In order to minimise non-adherence, it is imperative that the health system be more culturally sensitive towards Aboriginal and Torres Strait Islander peoples. [3] Service providers outside the Aboriginal and Torres Strait Islander health system need to be trained in the cultural values and healthcare beliefs of Aboriginal and Torres Strait Islander communities, in order to provide culturally sensitive advice and treatment. [3] Service providers should also be trained in communicating concepts to non-English speaking patients. [4] This involves the use of interpreters, which has been found to be beneficial in improving communication between Aboriginal and Torres Strait Islander peoples and health practitioners. [4] If required, these individuals can also be educated about medications through the use of pictures and anatomical models. [14] Similarly, medical practitioners should be encouraged to adhere to clinical guidelines when prescribing medications and to treat this group as they would any other group of patients. [16]

Another way of creating a culturally sensitive environment in healthcare centres is to better engage Aboriginal and Torres Strait Islander peoples in this process. [5] While interpreter services clearly fulfil this objective, [3] their role can be supplemented with other culturally sensitive practices. For example, Aboriginal and Torres Strait Islander peoples may feel more welcome if they see members of their communities in brochures. [5] It has been suggested that pharmacies displaying Aboriginal and Torres Strait Islander paintings and employing more Aboriginal and Torres Strait Islander staff will make Aboriginal and Torres Strait Islander peoples more likely to seek information and participate in screening programs. [5]

Increased engagement of Aboriginal and Torres Strait Islander peoples with health workers can be achieved by employing more Aboriginal and Torres Strait Islander Health Workers (AHWs), who have often lived in the region where they work. [17] AHWs act in a variety of capacities to better liaise with Aboriginal and Torres Strait Islander peoples in healthcare settings and facilitate a more positive experience. [5] They undertake clinical work, such as providing health checks and administering vaccinations, or conduct research and implement community development projects. [17] One study found that AHWs, together with pharmacists, have the potential to improve adherence with appropriate funding and education. [5] However more research needs to be undertaken to further evaluate the role of AHWs, specifically in reducing non-adherence.

A difficulty, however, in building culturally-sensitive practices, is that there are many Aboriginal and Torres Strait Islander cultures in Australia, not simply one unified culture. Therefore, a strategy that works for one group may not necessarily work for another. [5] Aboriginal and Torres Strait Islander peoples should therefore be involved in the formulation of policy strategies with health services to increase adherence. [3]

Subsidising medications

It is also necessary to consider the fiscal situation of individuals in Aboriginal and Torres Strait Islander communities. Aboriginal and Torres Strait Islander peoples have a lower median weekly household income than non-Aboriginal and Torres Strait Islander peoples. [1] Therefore, access to subsidised medication may be a way to improve adherence to medication. There are a number of initiatives funded by the Australian Government to try to improve adherence to medications.

As part of the Australian National Medicines Policy, a Quality of Use of Medicines (QUM) strategy was introduced in Australia in 1992. [18] This strategy included evaluating and improving Aboriginal and Torres Strait Islander health in remote areas through a number of ways, including the development of guidelines for culturally appropriate pharmaceutical services and evaluating medication use. [18] On the whole, it appears that the program achieved a number of its objectives, including improving Aboriginal and Torres Strait Islander health. [19] It was intended to complement a legislative change made around the same time to the National Health Act 1953.

This legislative change was made by the Australian Government to improve Aboriginal and Torres Strait Islander peoples’ access to the Pharmaceutical Benefits Scheme (PBS). Section 100 of the National Health Act 1953 gives the Minister for Health the power to make special arrangements for the supply of pharmaceutical benefits to people who are living in isolated areas, are receiving treatment for which pharmaceutical benefits are inadequate, or for whom pharmaceutical benefits can be more conveniently supplied. [20] If the Minister exercises this power, pharmacies can supply remote Aboriginal and Torres Strait Islander primary healthcare services with PBS-listed drugs in bulk, and Aboriginal and Torres Strait Islander patients can access prescription medication free of charge. [20]

The impact of this scheme on access to medications for Aboriginal and Torres Strait Islander peoples in remote areas has been evaluated. [21] It has been found that access to subsidised medications has significantly improved due to the S100. [21] However, it has been recommended that non-PBS medications commonly used by Aboriginal and Torres Strait Islander peoples should be included under S100, in order to further improve access. [21] In addition, there are limitations for people who live just outside the geographic boundaries and are not able to access the medications. [21] Therefore, it has been recommended that the section’s scope be broadened. [21]

More recently, the Australian Government Department of Health and Ageing began funding the Quality Use of Medicines Maximised for Aboriginal and Torres Strait Islander People Program (QUMAX) in 2008. [22] The aim of this program is to improve adherence with, and access to, medication amongst non-remote Aboriginal and Torres Strait Islander populations specifically. [23] This is achieved by providing financial assistance to Aboriginal and Torres Strait Islander health services to purchase medications, as well as providing patients directly with co-payments. [23] In addition, the Closing the Gap – Copayment Measure Program was introduced in 2010 to improve access to PBS medications for all Aboriginal and Torres Strait Islander peoples who are living with a chronic disease and required treatment. [24] Eligible patients are entitled to receive a waiver on the co-payment for medications under the PBS. [24]

In 2011, the Australian Government undertook an evaluation of the QUMAX and found that there was a 14% increase in PBS utilisation by Aboriginal and Torres Strait Islander peoples, especially for anti-hypertensive, lipid-lowering and asthma medications. [23] Furthermore, there was an 18% increase in utilisation among patients who were not entitled to concessional medications. [23] Some health services combined the QUMAX initiative with Aboriginal and Torres Strait Islander health assessments and care plans, which further incentivised patients to take up subsidised medications. [23]

QUMAX has arguably shown efficacy in reducing the cost barrier to accessing and complying with medications. [23] However, it is not clear whether it has eradicated inequities in PBS expenditure between Aboriginal and Torres Strait Islander and non-Aboriginal and Torres Strait Islander populations. [23] Therefore, it should continue, taking into account the recommendations set out in the evaluation. In particular, measures to address geographical barriers by providing transport for the delivery and the collection of medications should be implemented. [23] Furthermore, the recommendation to improve cultural training amongst pharmacists should be given special attention. [23]

Conclusion

Non-adherence with medication is a significant problem. It leads to negative health outcomes for the individual, and can result in the public health system incurring high costs. Given that the rates of non-adherence and chronic disease are greater amongst the Aboriginal and Torres Strait Islander population, specific measures need to be taken in order to minimise non-adherence. Healthcare workers should be trained to be more culturally sensitive and to provide clear, unambiguous treatment advice. They should also take care when prescribing medications to provide treatments with the lowest number of tablets appropriate. Healthcare services should be made more welcoming to Aboriginal and Torres Strait Islander peoples by including Aboriginal and Torres Strait Islander artwork, employing more Aboriginal and Torres Strait Islander staff, and involving Aboriginal and Torres Strait Islander communities in the policy-making process. Policy-makers need to be aware that there are many distinct Aboriginal and Torres Strait Islander cultures, not just a single homogenous one. Finally, medications should continue to be subsidised to Aboriginal and Torres Strait Islander peoples, to ensure that those most vulnerable to chronic illness are able to access treatment.

Conflict of interest

None declared.

Correspondence

S Kumble: skum24@student.monash.edu

References

[1] Australian Bureau of Statistics. 2011 Census QuickStats [Internet]. 2011 [cited 2013 August 4]. Available from: http://www.censusdata.abs.gov.au/census_services/getproduct/census/2011/quickstat/0

[2] Healey, J, editor. The Health of Indigenous Australians. Balmain: SpinneyPress; 2010.

[3] Davidson P, Abbott P, Davison J, DiGiacomo M. Improving Medication Uptake in Aboriginal and Torres Strait Islander Peoples. Heart Lung Circ. 2010; 19(5-6):372-7.

[4] Roe Y, Zeitz C, Fredericks B. Study Protocol: establishing good relationships between patients and health care providers while providing cardiac care. Exploring how patient-clinician engagement contributes to health disparities between Indigenous and non-Indigenous Australians in South Australia. BMC Health Serv. Res. 2012; 12:397-407.

[5] Hamrosi K, Taylor S J, Aslani P. Issues with prescribed medications in Aboriginal communities: Aboriginal Health Workers’ perspectives. Rural Remote Health. 2006; 6(2):557-569.

[6] World Health Organisation. Adherence to Long-Term Therapies Evidence for Action. Switzerland: World Health Organisation; 2003.

[7] Roller, L. Medication adherence in tribal Aboriginal children in urban situations. Curr Ther. 2002; 43(11):64-5.

[8] Laba T-L, Brien J-A, Jan S. Understanding rational non-adherence to medications. A discrete choice experiment in a community sample in Australia. BMC Fam Pract. 2012; 13(61).

[9] Donato R and Segal L. Does Australia have the appropriate health reform agenda to close the gap in Indigenous health? Aust Health Rev. 2013; 37:232-238.

[10] Bailie R, Si D, Dowden M, O’Donoghue L, Connors C, Robinson G, Cunningham J, Weeramanthri T. Improving organisational systems for diabetes care in Australian Indigenous communities. BMC Health Serv. Res. 2007; 7:67-78.

[11] Altman J. The Economic and Social Context of Indigenous Health. In: Thomson  N, editor. The Health of Indigenous Australians. Perth: Oxford University Press; 2003.

[12] Lau P, Pyett P, Burchill M, Furler J, Tynan M, Kelaher M et al. Factors influencing access to Urban General Practices and Primary Health Care by Aboriginal Australians—A qualitative study. AltNat. 2012; 8(1):66-84.

[13] Cass A, Lowell A, Christie M, Snelling PL, Flack M, Marrnganyin B et al. Sharing the true stories: improving communication between Aboriginal patients and health care workers. Med J Aust 2002; 176(10):466-470.

[14] McGrath, P. The biggest worry..’: research findings on pain management for Aboriginal and Torres Strait Islander  peoples in Northern Territory, Australia. Rural Remote Health. 2006; 6(3):549-562.

[15] Larkin C, Murray R. Assisting Aboriginal and Torres Strait Islander  patients with medication management. Aust Prescr. 2005; 28(5):123-125.

[16] Fürthauer J, Flamm M, Sönnichsen A. Patient and physician related factors of adherence

to evidence based guidelines in diabetes mellitus type 2, cardiovascular disease and prevention: a cross sectional study. BMC Fam Pract. 2013; 14(47).

[17] Mitchell M, Hussey L. The Aboriginal and Torres Strait Islander Health Worker. Med J Aust. 2006; 184(10):529-530.

[18] Emerson L, Bell K, Manning R. Quality Medication Use in Aboriginal Communities. Paper presented at: The 5th National Rural Health Conference; 1999 March 14-17; Adelaide, South Australia.

[19] Smith, A. Quality use of medicines – are we nearly there yet? Aust Prescr. 2012; 35:174-5.

[20] National Health Act 1953 [Cth] s 100.

[21] Kelaher M, Taylor-Thomson D, Harrison N, O’Donoghue L, Dunt D, Barnes T et al. Evaluation of PBS Medicine Supply Arrangements for Remote Area Aboriginal Health Services Under S100 of the National Health Act. Co-operative Research Centre for Aboriginal Health and Program Evaluation Unit, University of Melbourne. Melbourne; 2004. Report No.: RFT:102/0203.

[22] Couzos S, Sheedy V, Thiele DD. Improving Aboriginal and Torres Strait Islander  and Torres Strait Islander people’s access to medicines – the QUMAX program. Med J Aust. 2011; 195(2):62-63.

[23] Wallace A, Lopata T, Benton M, Keevy N, Jones L, Rees A et al. Evaluation of the Quality Use of Medicines Maximised for Aboriginal and Torres Strait Islander  and Torres Strait Islander Peoples (QUMAX) Program. Australia: Urbis; 2011.

[24] Medicare. Closing the Gap—PBS Co-payment Measure [Internet]. 2010 [updated 1 July 2010, cited 2013 August 5]. Available from: http://www.medicareaustralia.gov.au/provider/pbs/prescriber/closing-the-gap.jsp