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Dr Linda Calabresi

Chronic rhinosinusitis is a misery-generating condition – literally. According to a large study just published in The Journal of the American Medical Association, having chronic rhinosinusitis significantly increases your risk of depression and anxiety. And if you also have nasal polyps the risk is higher still. The Korean study was admittedly observational but it did include almost 50,000 individuals from the general population and followed them up for 11 years. Researchers found, over the duration of the study, those people with chronic rhinosinusitis were 54% more likely to develop depression and 57% more likely to develop anxiety than those people who did not suffer this condition. And if nasal polyps accompanied the rhinosinusitis the increase in likelihood for both mental illnesses jumped to the early 60s (61% and 63% respectively). So what are the implications of this study? Well – they are fairly straightforward really. “Physicians should be aware of the potential comorbidities observed in patients with [chronic rhinosinusitis] and provide therapy to reduce the risk of depression and anxiety in these patients,” the study authors helpfully concluded. What we don’t know of course, being simply an observational study without any intervention to test, is whether effectively treating the rhinosinusitis helps the depression or anxiety, and importantly, whether surgically removing the polyps can make a difference to this psychological side-effect. The researchers actually even distance themselves from the conclusion that chronic rhinosinusitis causes depression and anxiety, citing the chicken and egg phenomena. “Whether depression and anxiety amplify the symptoms of [chronic rhinosinusitis] or whether these conditions are the consequence of [chronic rhinosinusitis]is unknown,” they said. But they do say their findings support previous research that has suggested an association between the conditions. They also say their study allowed analysis of the specific phenotype responsible for the chronic rhinosinusitis – whether it be predominantly T1 or T2 response derived. What they found was the association held true regardless of the phenotype – suggesting this was more to do with personality and symptoms than physiology. All in all, what the study authors suggest is that given how common chronic rhinosinusitis is in the population, it is worthwhile keeping a high indexation of suspicion for the development of depression and anxiety not only for the patients’ current quality of life but also because these conditions can affect health outcomes down the line. “[T]hese psychiatric comorbidities may influence not only the diagnosis of [chronic rhinosinusitis] but also its therapeutic and surgical outcomes,” the study authors said.  

Reference:

Kim JY, Ko I, Kim MS, Yu MS, Cho BJ, Kim DK. Association of Chronic Rhinosinusitis With Depression and Anxiety in a Nationwide Insurance Population. JAMA Otolaryngol Head Neck Surg. 2019 Feb 7.  DOI: 10.1001/jamaoto.2018.4103 [Epub ahead of print].
Sullivan Nicolaides Pathology

Allergic disorders result from an inappropriate, usually IgE-mediated, immune response upon exposure to either environmental or food allergens. Common manifestations of allergy include rhinoconjunctivitis, asthma, eczema, acute urticaria and anaphylaxis. Disorders, such as chronic urticaria, hereditary angioedema and T-cell contact dermatitis (metal allergy), while clinically similar in some ways, are not IgE-mediated. Allergic disease manifests in different ways through life and the likely causative agents can also change with age (see Table 1).

Tests used in the diagnosis of IgE-mediated allergy

Total IgE Higher levels of total IgE are often found in patients with allergic conditions. However, normal total IgE does not exclude allergy. Total IgE is also elevated in other conditions including parasitic infections and allergic bronchopulmonary aspergillosis. It is used increasingly in determining anti-IgE therapy in moderate to severe asthmatics. Allergen-specific IgE Allergen-specific IgE can be detected for a large variety of allergens. The presence of a specific IgE to allergen can suggest allergic disease and is detected via a blood test (RAST or radioallergosorbent test) or skin prick test. RAST tests detect many of the different proteins within an individual allergen. Recombinant allergen testing Of the many proteins within a substance, only a few may cause allergic symptoms. Recombinant allergen testing looks for specific characterised protein within an allergen. Interpretation of RAST tests The presence of detectable specific IgE to an allergen does not confirm the patient is allergic to that substance. All results must be interpreted in conjunction with the clinical history of the patient. Low levels of detectable specific IgE can confirm the presence of allergy in the right clinical context. RAST testing aids in the assessment of, and identification of allergic sensitisation, but is not to be used alone as the deciding factor for inclusion or exclusion of allergy. As the level of specific IgE increases, the likelihood of clinical relevance also increases. As shown in Table 2, different allergens have different specific IgE level cutoffs at which serious allergy is >95% likely (positive predictive value or PPV). The range of values is vastly different between allergens and is affected by age and also by geographic region. Table 2 defines levels at which exposure, or a challenge, would be highly hazardous for a patient. Importantly, many patients could have serious reactions at much lower levels.   [table id=1 /]   [table id=2 /]

RAST tests

RAST tests are available for a range of allergens, however Medicare criteria limits rebates based on the number, type and frequency of tests. Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. When ordering RAST tests, it is advisable to include allergens the patient feels are relevant and those likely for the clinical scenario. For common clinical scenarios we recommend the following: Childhood eczema Age <2 years: Milk, Egg, Wheat, Peanut Age >2 years: Milk, Egg, Peanut, Dust mite Additional allergens or an extended RAST combined allergy panel may be ordered. Asthma and allergic rhinoconjunctivitis Dust mite, Grass mix, Animal dander Additional allergens may be ordered or substituted if relevant (e.g. cat dander instead of animal dander). An extended RAST inhalant panel is also available. Default panel if no allergens are specified and no clinical notes are provided Age <5 years: Dust mite, Grass mix, Food Mix Age >5 years: Dust mite, Grass mix, Animal Mix Anaphylaxis Anaphylaxis is a severe life-threatening allergic reaction. It is recommended these patients require specialist assessment by a clinical immunologist or allergist. Initial testing should look for the causative allergen if possible. It is important to note that a negative RAST test does not exclude the allergen tested. RAST testing recommendations ­
  • Test individual likely causative allergen i.e. food, stinging insect. ­
  • Tryptase, if done within 2-6 hours of reaction, can support the occurrence of an allergic reaction. ­
  • Useful as an assessment of mastocytosis (condition with increased numbers of mast cells)

Extended RAST panels

Extended RAST panels have been developed to represent the common allergens encountered clinically in practice. They are particularly relevant in our geographic region and replace the skin prick test panel which is no longer available. Additional allergens may also be requested. All results must be interpreted in conjunction with the patient’s clinical history. Extended RAST Food Panel ­
  • Covers common food-related allergens
  • Almond; Hazelnut; Sesame seed; Banana; Mango; Shrimp (prawn); Cashew; Milk (cow); Soybean; Codfish; Peanut; Walnut; Egg white; Rice; Wheat
Extended RAST Nut Allergy Panel ­
  • Broad collection of commonly consumed nuts, including peanuts ­
  • Individual nut testing with appropriate clinical history is preferred ­
  • Recommend to discuss results with a clinical immunologist or allergist
  • Almond; Macadamia; Pine nut; Brazil; Peanut; Sesame seed; Cashew; Peanut (Ara-h2); Walnut; Hazelnut; Pecan
Extended RAST Combined Allergy Panel ­
  • Combination of common food and environmental allergens ­
  • Replaces the skin prick test panel (no longer available)
  • Almond; Dust mite; Mould mix; Cashew nut; Egg white; Peanut; Cat dander; Grass mix; Shrimp (prawn); Codfish; Hazelnut; Soy; Dog dander; Milk (cow); Wheat
  • * Preferable for children (<12 years) due to low serum volume
Extended RAST Inhalant Panel ­
  • Covers common environmental allergens ­
  • Useful for asthma and allergic rhinitis
  • Acacia (wattle); Blomia tropicalis; Dust mite; Alternaria alternate; Cat dander; Eucalyptus; Aspergillus fumigatus; Cladosporium; Horse dander; Bahia grass; Common ragweed; Johnson grass; Bermuda grass; Dog dander; Perennial rye grass

Recombinant allergens

Omega-5 gliadin ­
  • A component of wheat ­
  • Associated with anaphylaxis ­
  • Often in the context of eating wheat and physical activity within 1-2 hours
Alpha-gal (mammalian meat allergy) ­
  • Associated with anaphylaxis; often delayed following consumption of meat (beef, lamb, pork) ­
  • Related to tick bites
Peanut Allergy Risk Assessment ­
  • Peanuts like all food is made up of many different proteins ­
  • Ara-h2 is associated with anaphylaxis to peanut ­
  • Can assist with risk assessment and should be done in conjunction with a clinical immunologist or allergist ­
  • A negative Ara-h2 in peanut positive patient does not imply there is no risk to anaphylaxis
  • Results of RAST tests can also be of use in monitoring ongoing allergy in patients in conjunction with their treating clinician

How to order allergy tests

RAST tests - standard panels Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. Extended RAST tests (Medicare rebate + $120* per panel)
  • Extended RAST Food
  • Extended RAST Nut
  • Extended RAST Combined
  • Extended RAST Inhalant
Please note, extended RAST panels are not bulk billed. Recombinant allergen tests (Medicare rebate + $60* each)
  • Alpha-gal
  • Omega-5 gliadin
  • Peanut (Ara-h2)
  • Peanut Allergy Risk Assessment
  General Practice Pathology is a regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.
Dr Linda Calabresi

It’s a controversial topic here in Australia. But a new UK study, just published in the New England Journal of Medicine, gives strong support the role of e-cigarettes as a smoking cessation therapy. The randomised controlled trial of almost 900 adult smokers wanting to quit found the one-year abstinence rate was 18% among the e-cigarette users compared to 9.9% among those who were randomised to receive nicotine replacement therapy. Much of the difference could be attributed to adherence to the assigned product. After 12 months, 80% of the e-cigarette group were still using the device whereas only 9% of the alternative group were still taking their nicotine replacement therapy despite being able to choose between the patch, gum, lozenge, nasal spray, inhalator, mouth spray, mouth strip, and microtabs (or any combination of these). Participants in both groups underwent the same multi-session behavioural support as per best practice guidelines. This study provides some of the strongest evidence to date that e-cigarettes are significantly better than nicotine replacement therapy in helping people quit smoking, the study authors suggest. “This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine-replacement products and with 88.1% of participants using combination treatments,” they said. The researchers suggested e-cigarettes had better adherence rate because they were more effective at reducing the symptoms of withdrawal when quitting smoking, because the refillable devices are better at delivering nicotine compared with options such as gum or patches. They also suggest the nicotine dose provided by e-cigarettes was easier to tailor to individual needs than other replacement options. And even though people using the e-cigarettes were more likely to get mouth or throat irritation, this side effect was generally mild and tolerable especially compared to withdrawal symptoms such as constipation, mouth ulcers and weight gain. In general, the researchers claim replacing cigarettes with e-cigarettes is a definite positive in terms of health outcomes and much better than other nicotine replacement options, but they suggest the high rate of adherence in the e-cigarette group may have some negative connotations. “This can be seen as problematic if e-cigarette use for a year signals ongoing long-term use, which may pose as-yet-unknown health risks,” they said. As an accompanying editorial points out, fundamentally nicotine is highly addictive. While electronic cigarettes have been proven to be a great tool in helping people get off normal cigarettes, there may be an issue if non-smokers, especially teenagers take up vaping, making them vulnerable to becoming smokers further down the track. “The cigarette company may well see e-cigarettes as addictive bait that will lead young people toward smoking,” the US editorial authors suggest. They suggest this potential problem could be relatively easily averted by ensuring e-cigarettes aren’t manipulated to enhance their appeal, specifically the authorities should not allow the manufacture of flavoured nicotine products. However, they too acknowledge e-cigarettes have a significant role to play in solving this public health problem – ‘by helping people who are users of combustible tobacco products stop smoking by switching to vaping.’

References:

Hajek P, Phillips-Waller A, Przulj D, Pesola F, Smith KM, Bisal N, et al. A Randomized Trial of E-Cigarettes versus Nicotine-Replacement Therapy.  N Engl J Med. 2019 Jan 30;  DOI: 10.1056/NEJMoa1808779 [Epub ahead of print] Drazen JM, Morrissey S, Campion EW. The Dangerous Flavors of E-Cigarettes. N Engl J Med. 2019 Jan 30. DOI: 10.1056/NEJMe1900484 [Epub ahead of print]
Prof Kristine Macartney

Australia was declared free of measles in 2014. Yet this summer we’ve seen nine cases of measles in New South Wales, and others in Victoria, Western Australia, South Australia and Queensland. High vaccination rates in Australia means the measles virus doesn’t continuously spread, but we still have “wildfire” outbreaks when travellers bring measles into the country, often unknowingly. If you haven’t received two doses of measles vaccine, you are at risk of contracting measles.

How can you catch it?

Measles is a highly contagious virus that spreads by touching or breathing in the same air as an infected person. The virus stays alive in the air or on infected surfaces for up to two hours. An infected person is contagious from the first day of symptoms (fever, cough and runny nose). These general symptoms start about four days before the rash develops, meaning contagious people can spread the virus even before they realise they have measles. If you’re not immune to the virus, through vaccination or past infection, the chance of becoming ill after being near someone with measles is 90%. Being in the same café, waiting in line at the checkout or flying on the same aeroplane as an infected person could be enough to pick up the disease.

Why is it so dangerous?

Measles causes a fever, cough, and a rash that starts around the hairline and then spreads to the whole body. It can also cause middle ear infections (otitis media), chest infections (pneumonia), and diarrhoea. Swelling and inflammation to the brain (encephalitis) occurs in 1 in every 1,000 cases and can lead to permanent brain damage or death. In 2017, 110,000 people died from measles worldwide. Even after surviving the initial illness, measles can cause a devastating and fatal complication known as subacute sclerosing panencephalitis (inflammation of the brain) many years later.

Why are people in their 20s to 50s more at risk?

To protect yourself against measles, you need two doses of measles-mumps-rubella (MMR) vaccine. Children in Australia routinely get this vaccine at 12 and 18 months of age. The second dose is given in combination with the chickenpox vaccine. It’s important to have two doses of MMR vaccine, especially if you haven’t reached your mid-50s. Most people older than this would have been infected with measles before vaccination was routine. People aged in their 20s to early 50s (those born from 1966 and 1994) are most likely to have only had one dose of MMR vaccine. While we’ve had the measles vaccine in Australia since 1968, a two-dose program was only introduced in 1992. A brief school-based catch-up program from 1993 to 1994 offered school children a second dose. Another school-based program provided children with catch-up vaccinations in 1998*. For those who missed out on the school program, catch-up vaccinations were given on an ad-hoc basis via GP clinics. So not everyone in this age group would have received two doses of the measles vaccine. If you are this age, you may not be not fully protected against measles. Checking with a GP or immunisation nurse is the best way to be sure. They will check your records, and may do a blood test if you have no proof of immunisation. Even if you can’t be sure of past vaccinations, it’s still safe to have an extra vaccine. And it’s free for those who need a catch-up dose. If you have a child under 12 months of age and you’re heading to a country with measles, an early additional vaccine dose can be given to protect your baby from measles. This ideally should be done at least a month before you travel, to ensure an immune response has time to develop. The routine scheduled doses at 12 months and 18 months will still need to be given later.

What if you’re not protected?

Unfortunately, there is no treatment for measles. Getting adequately vaccinated is the best form of defence against this serious disease. If you think you’ve been exposed or may be ill from measles, see your GP or call Health Direct or your public health department as soon as possible. If exposed, but not yet ill, it may not be too late to get a protective vaccine and ensure you don’t spread the disease to others. If you are unwell, and suspect measles, call ahead to let the clinic know so they can make provisions to keep you away from other patients in the waiting room. Other, more common, diseases can look like measles, so an urgent specific test (throat swab) must be done to confirm the infection. If measles is proven, public health workers will trace your contacts and your treating doctor will monitor you for complications.

Are we at risk of measles returning in Australia?

Australia currently has all-time high vaccine coverage, with 94.5% of five-year-old children fully immunised at the end of 2017. By keeping vaccine coverage near or above 95%, herd immunity where there are enough people vaccinated helps prevent measles from spreading to others, including those who cannot be vaccinated. But in our interconnected world, we must work together to reduce the threat of measles worldwide by boosting immunisation programs in regions with low coverage, including in the Asia Pacific. Measles have resurfaced in some countries due to falls in vaccine coverage from unfounded safety concerns as well as weak health systems. In the first six months of last year, for instance, Europe had 41,000 cases of measles, nearly double the total number of the previous year. This, among other factors, has prompted the World Health Organisation to list vaccine hesitancy as a top ten threat to global health in 2019. A continued global coordinated effort will be required to maintain elimination and prevent resurgence of this deadly disease in Australia. * Correction: this article has been updated to note a school-based catch-up program also operated in 1998.The Conversation

Kristine Macartney, Professor, Discipline of Paediatrics and Child Health, University of Sydney and Lucy Deng, Staff Specialist Paediatrician, National Centre for Immunisation Research and Surveillance; Clinical Associate Lecturer, Children's Hospital Westmead Clinical School, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.
Dr Linda Calabresi

At first read, the study results seemed disappointing. Yet another promising premise fails to deliver when it comes to actual proof. But the researchers aren’t ready to give up on this hypothesis just yet. In fact, commentators on the study say the results offer ‘great hope’ and represent ‘a major leap forward.’ The SPRINT MIND study, recently published in JAMA was investigating whether intensive blood pressure control (to a systolic less than 120mmHg) worked better than standard blood pressure control (SBP<140mmHg) at reducing the risk of mild cognitive impairment and dementia. This randomised controlled trial was a component of the well-publicised Systolic Blood Pressure Intervention Trial (SPRINT) which looked at the effect of more intensive blood pressure control on cardiovascular and renal outcomes in addition to cognitive function in over 9000 people without a history of diabetes or stroke. Basically, what this study showed was that intensive blood pressure control to a target of less than 120mmHg did not reduce the incidence of probable dementia compared to lowering BP to a target of less than 140mmHg. Depressing, yes? No, say the study authors. Firstly, they say the study demonstrated no ill-effects of intensive BP lowering – which has been an issue of concern for some who have been worried that lowering the BP could decrease cerebral perfusion thereby harming cognitive function. In fact, the study authors showed quite the opposite was true. The intervention actually helped protect cognitive ability. “This is the first trial, to our knowledge, to demonstrate an intervention that significantly reduces the occurrence of [mild cognitive impairment], a well-established risk factor for dementia, as well as the combined occurrence of [mild cognitive impairment] or dementia,” they said. The study authors suggest the lack of benefit in dementia may be due to the fact the SPRINT study was terminated early following the demonstration of benefit of intensive BP control on cardiovascular outcomes and all-cause mortality. Because of this shortened time frame and the fact that there were fewer than expected cases of dementia, they suggest the study may have been ‘underpowered’ to show a result for lowering the risk of dementia. They also say there were fewer cases of dementia among the intensive treatment group compared with the standard treatment group (7.2 vs 8.6 cases per 1000 patient years) even though this wasn’t statistically significant. We cannot know whether this trend would have reached statistical significance had the intervention continued. An accompanying editorial views the study and the results with a good deal of positivity. “For older adults, almost all of who have concern about being diagnosed with Alzheimer Disease and related dementia, [this study] offers great hope,” the US epidemiologist, Dr Kristine Yaffe, said. She points out that this a readily modifiable risk factor, and we should be accelerating our efforts into investigating whether this, along with other vascular health interventions such as physical activity, can indeed prevent dementia, building on the positive results of this study. “The SPRINT MIND study may not be the final approach for prevention of Alzheimer disease or other cognitive impairment but it represents a major leap forward in what has emerged as a marathon journey.”

Reference

Yaffe, K. Prevention of Cognitive Impairment With Intensive Systolic Blood Pressure Control. JAMA [Internet]. 2019 Jan 28. DOI: 10.1001/jama.2019.0008 [Epub ahead of print]
Suzanne Mahady

Bowel cancer mostly affects people over the age of 50, but recent evidence suggests it’s on the rise among younger Australians. Our study, published recently in Cancer Epidemiology, Biomarkers and Prevention, found the incidence of bowel cancer, which includes colon and rectal cancer, has increased by up to 9% in people under 50 from the 1990s until now. Our research examined all recorded cases of bowel cancer from the past 40 years in Australians aged 20 and over. Previous studies assessing bowel cancer incidence in young Australians have also documented an increase in the younger age group. This trend is also being seen internationally. A study from the United States suggests an increase in bowel cancer incidence in people aged 54 and younger. The research shows rectal cancer incidence increased by 3.2% annually from 1974 to 2013 among those aged age 20-29. Bowel cancers are predicted to be the third most commonly diagnosed cancer in Australia this year. In 2018, Australians have a one in 13 chance of being diagnosed with bowel cancer by their 85th birthday. Our study also found bowel cancer incidence is falling in older Australians. This is likely, in part, to reflect the efficacy of the National Bowel Cancer Screening Program, targeted at those aged 50-74. Bowel cancer screening acts to reduce cancer incidence, by detecting and removing precancerous lesions, as well as reducing mortality by detecting existing cancers early. This is important, as bowel cancer has a good cure rate if discovered early. In 2010 to 2014, a person diagnosed with bowel cancer had a nearly 70% chance of surviving the next five years. Survival is more than 90% for people who have bowel cancer detected at an early stage. That is why screening is so effective – and we have previously predicted that if coverage rates in the National Bowel Screening Program can be increased to 60%, around 84,000 lives could be saved by 2040. This would represent an extraordinary success. In fact, bowel screening has potential to be one of the greatest public health successes ever achieved in Australia.

Why the increase in young people?

Our study wasn’t designed to identify why bowel cancer is increasing among young people. However, there are some factors that could underpin our findings. The increase in obesity parallels that of bowel cancer, and large population based studies have linked obesity to increased cancer risk. Unhealthy lifestyle behaviours, such as increased intake of highly processed foods (including meats), have also been associated with increased bowel cancer risk. High quality studies are needed to explore this role further. Alcohol is also thought to be a contributor to increasing the risk of bowel cancer. So, should we be lowering the screening age in Australia to people under the age of 50? Evaluating a cancer screening program for the general population requires a careful analysis of the potential benefits, harms, and costs. A recent Australian study modelled the trade-offs of lowering the screening age to 45. It showed more cancers would potentially be detected. But there would also be more colonoscopy-related harms such as perforation (tearing) in an extremely small proportion of people who require further evaluation after screening. A lower screening age would also increase the number of colonoscopies to be performed in the overstretched public health system and therefore could have the unintended consequence of lengthening colonoscopy waiting times for people at high risk.

How to reduce bowel cancer risk

One of the most common symptoms of bowel cancer is rectal bleeding. So if you notice blood when you go to the toilet, see your doctor to have it checked out. A healthy lifestyle including adequate exercise, avoiding smoking, limiting alcohol intake and eating well, remains most important to reducing cancer risk. Aspirin may also lower risk of cancer, but should be discussed with your doctor because of the potential for side effects including major bleeding. Most importantly, we need to ensure eligible Australians participate in the current evidence-based screening program. Only 41% of the population in the target 50-74 age range completed their poo tests in 2015-2016. The test is free, delivered by post and able to be self-administered.The Conversation   This article is republished from The Conversation under a Creative Commons license. Read the original article.
Dr Linda Calabresi

It would be a brave doctor who would ignore the warning ‘allergic to penicillin’ when deciding which antibiotic to prescribe for a patient. But according to a new review published recently in JAMA, despite up to 10% of the population reporting allergies to penicillin, few have clinically significant reactions. “Although many patients report they are allergic to penicillin, clinically significant IgE-mediated or T lymphocyte-mediated penicillin hypersensitivity is uncommon (<5%),” the US review authors said. And the issue is an important one. As the authors point out, not only will patients, labelled as having a penicillin allergy be given alternative antibiotics that are more likely to fail and cause side-effects but the use of these alternatives increase the risk of antimicrobial resistance developing. So for all these reasons, the researchers propose that is worthwhile that all patients labelled as having an allergy to penicillins be re-evaluated. As a starting point, a comprehensive history should be taken. And while the reviewers acknowledge that, to date no allergy questionnaires have been validated in terms of defining risk levels, there are plenty of features in a history that can give a clue as to whether a person could safely be offered skin prick testing or a drug challenge. Broadly speaking, patients with a history of a minor rash, that was not significantly itchy that developed over the course of days into the course of the antibiotic are considered low-risk. This is opposed to people who have a history of developing a very pruritic rash within minutes to hours of taking the drug (which tends to indicate an IgE-mediated reaction) or people who experienced significant blistering and/or skin desquamation after taking penicillin (which generally represents a severe T-cell-mediated reaction). Among those patients whose rash-history suggests they are at low-risk, other factors should be considered before attempting a challenge. “Even in the context of low-risk allergy history, patients with unstable or compromised haemodynamic or respiratory status and pregnant patients should be considered as having at least a moderate-risk history,” they said. However, patients whose penicillin allergy history included non-allergic-type symptoms such gastrointestinal symptoms or patients who only have a family history of penicillin allergy should be considered at low-risk. Once the patient has been assessed as being at low-risk of having an acute allergic reaction, the study authors suggest they be given amoxicillin under medical observation. “For penicillin allergy, administration of 250mg of amoxicillin with one hour of observation demonstrates penicillin tolerance,” they said. Should the patient tolerate this dose of amoxicillin, it can be concluded that all beta-lactams can be administered safely, and the issue of cross-reactivity (between penicillin and cephalosporin which occurs in about 2% of truly penicillin-allergic people) is rendered irrelevant. Patients who are considered at moderate-risk of having an allergic reaction to penicillin, namely those patients with a history of urticaria or mild pruritic rashes but no anaphylaxis should be considered for skin-prick testing. Only those with a negative skin prick test should be considered for an oral drug challenge. People with a history of high-risk reactions – usually anaphylaxis should not be skin-prick tested or challenged. They might be considered for desensitisation programs but only in select circumstances and only under the close supervision of a specialist. All in all, the authors advocate health professionals not simply take the label of ‘allergic to penicillin’ as gospel. “Evaluation of penicillin allergy has substantial benefits for patients by allowing improved antimicrobial choice for treatment and prophylaxis,” they concluded.

Reference

Shenoy ES, Macy E, Rowe T, Blumenthal KT. Evaluation and Management of Penicillin Allergy: A Review. JAMA 2019 Jan 15; 321(2): 188-99. DOI: 10.1001/jama.2018.19283    
Eloise Stephenson

Ross River virus is Australia’s most common mosquito-borne disease. It infects around 4,000 people a year and, despite being named after a river in North Queensland, is found in all states and territories, including Tasmania. While the disease isn’t fatal, it can cause debilitating joint pain, swelling and fatigue lasting weeks or even months. It can leave sufferers unable to work or look after children, and is estimated to cost the economy A$2.7 to A$5.6 million each year. There is no treatment or vaccine for Ross River virus; the only way to prevent is to avoid mosquito bites. Mosquitoes pick up the disease-causing pathogen by feeding on an infected animal. The typical transmission cycle involves mosquitoes moving the virus between native animals but occasionally, an infected mosquito will bite a person. If this occurs, the mosquito can spread Ross River virus to the person.

Animal hosts

Ross River virus has been found in a range of animals, including rats, dogs, horses, possums, flying foxes, bats and birds. But marsupials – kangaroos and wallabies in particular – are generally better than other animals at amplifying the virus under experimental infection and are therefore thought to be “reservoir hosts”. The virus circulates in the blood of kangaroos and wallabies for longer than other animals, and at higher concentrations. It’s then much more likely to be picked up by a blood-feeding mosquito.

Dead-end hosts

When we think of animals and disease we often try to identify which species are good at transmitting the virus to mosquitoes (the reservoir hosts). But more recently, researchers have started to focus on species that get bitten by mosquitoes but don’t transmit the virus. These species, known as dead-end hosts, may be important for reducing transmission of the virus. With Ross River virus, research suggests birds that get Ross River virus from a mosquito cannot transmit the virus to another mosquito. If this is true, having an abundance of birds in and around our urban environments may reduce the transmission of Ross River virus to animals, mosquitoes and humans in cities.

Other reservoir hosts?

Even in areas with a high rates of Ross River virus in humans, we don’t always find an abundance of kangaroos and wallabies. So there must be other factors – or animals yet to be identified as reservoirs or dead-end hosts – playing an important role in transmission. Ross River virus is prevalent in the Pacific Islands, for instance, where there aren’t any kangaroos and wallabies. One study of blood donors in French Polynesia found that 42.4% of people tested had previously been exposed to the virus. The rates are even higher in American Samoa, where 63% of people had been exposed. It’s unclear if the virus has recently started circulating in these islands, or if it’s been circulating there longer, and what animals have been acting as hosts.

What about people?

Mosquitoes can transmit some viruses, such as dengue and Zika between people quite easily. But the chances of a mosquito picking up Ross River virus when biting an infected human is low, though not impossible. The virus circulates in our blood at lower concentrations and for shorter periods of time compared with marsupials. If humans are infected with Ross River virus, around 30% will develop symptoms of joint pain and fatigue (and sometimes a rash) three to 11 days after exposure, while some may not experience any symptoms until three weeks after exposure. To reduce your risk of contracting Ross River virus, take care to cover up when you’re outdoors at sunset and wear repellent when you’re in outdoor environments where mosquitoes and wildlife may be frequently mixing.   This article is republished from The Conversation under a Creative Commons license. Read the original article.
Dr Linda Calabresi

While it appears the message about risky drinking is getting through to younger Australians, baby boomers are as bad as ever. According to a research letter appearing in the latest edition of the MJA, the proportion of 55-70-year-olds who could be classed as high-risk drinkers has risen over the last 15 or so years. The South Australian researchers say this is in ‘stark contrast to the significant decrease in risky drinking among people aged between 12-24 years during the same period.’ And while they do emphasise that by far the majority of older Australians (over 80%) are abstainers or drink at low risk levels, the proportional increase of those now in the high-risk category (from 2.1% in 2004 to 3.1% in 2016) represents an additional 400,000 at-risk individuals – significant in anyone’s language. The findings were based on secondary analyses of data from National drug Strategy Household Surveys conducted in 2004, 2007, 2010, 2013 and 2016. Interestingly the researchers defined the risk categories on the basis of the maximum number of standard alcoholic drinks drunk on a single occasion over the course of a month. So low-risk were those individuals who never consumed more than four drinks in a single session, risky drinkers drank 5-10 drinks in one session at least once a month and high-risk drinkers needed to have drunk 11 or more drinks at least once a month. It’s a slightly different means of assessment to the more common approach of asking about average daily alcohol intake and appears more likely to detect the binge drinker – or your classic ‘social drinker.’ As the letter authors point out, detecting problem drinking in this age group is especially important as this cohort is particularly vulnerable to a range of alcohol-related adverse events from falls to diabetes. Once again, the researchers are looking to GPs to detect those at-risk from drinking among our baby boomer patient population and initiate evidence-based interventions, such as short, opportunistic counselling and information sessions. But they recognise this isn’t always easy. “To facilitate early identification of problem drinking and early intervention, educating health care professionals about patterns and drivers of alcohol consumption by older people should be a priority,” the authors said. Perhaps using the study’s categorisation technique of the maximum number of drinks consumed in a single session might go some way to detecting those at risk.  

Referernce:

Roche AM, Kostadinov V. Baby boomers and booze: we should be worried about how older Australians are drinking. Med J Aust. 2019; 210(1): 38-9. DOI: 10.5694/mja2.12025. Available from: https://www.mja.com.au/journal/2019/210/1/baby-boomers-and-booze-we-should-be-worried-about-how-older-australians-are
Martyn Lloyd Jones

For many years experts in the field of drug policy in Australia have known existing policies are failing. Crude messages (calls for total abstinence: “just say no to drugs”) and even cruder enforcement strategies (harsher penalties, criminalisation of drug users) have had no impact on the use of drugs or the extent of their harmful effects on the community. Whether we like it or not, drug use is common in our society, especially among young people. In 2016 43% of people aged 14 and older reported they had used an illicit drug at some point in their lifetime. And 28% of people in their twenties said they had used illicit drugs in the past year. The use of MDMA (the active ingredient in ecstasy) is common and increasing among young people. In the last three months alone five people have died as a result of using illicit drugs at music festivals and many more have been taken to hospital. The rigid and inflexible attitudes of current policy-makers contrast dramatically with the innovative approaches to public health policy for which Australia was once renowned. Since the 1970s many highly successful campaigns have improved road safety, increased immunisation rates in children and helped prevent the spread of blood-borne virus infections. The wearing of seatbelts was made compulsory throughout Australia in the early 1970s. Randomised breath testing and the wearing of helmets by bike riders were introduced in the 1980s. These measures alone have saved many thousands of lives. The introduction of needle exchange and methadone treatment programs in the late 1980s and, more recently, widespread access to effective treatments for hepatitis C have dramatically reduced the health burden from devastating infections such as HIV and the incidence of serious liver disease. Each of these programs had to overcome vigorous and sustained hostility from opponents who argued they would do more harm than good. But in all cases the pessimists were proved wrong. Safety measures on the roads did not cause car drivers and bike riders to behave more recklessly. The availability of clean needles did not increase intravenous drug use. Easier access to condoms did not lead to greater risk taking and more cases of AIDS. We believe — along with many other experts in the field — that as was the case for these earlier programs, the evidence presently available is sufficient to justify the careful introduction of trials of pill testing around Australia. Specifically, we support the availability of facilities to allow young people at venues or events where drug taking is acknowledged to be likely to seek advice about the substances they’re considering ingesting. These facilities should include tests for the presence of known toxins or contaminants to help avert the dangerous effects they may produce. Such a program should be undertaken in addition to, and not instead of, other strategies to discourage or deter young people from taking illicit drugs. Although pill testing has been widely and successfully applied in many European countries over a twenty year period, it has to be admitted the evidence about the degree of its effectiveness remains incomplete. That’s why any program in Australia should be linked to a rigorously designed data collection process to assess its impact and consequences. However, we do know that the argument that pill testing programs will increase drug use and its associated harms is very unlikely to be true. Most people seeking advice about the constituents of their drugs will not take them if they are advised that they contain dangerous contaminants. And it’s easy to avoid false reassurances about safety by careful explanations and detailed information. The opportunity to provide face-to-face advice to young people about the risks of drug taking is one of the great strengths of pill testing programs. Over the last half century we have learnt public health programs have to utilise multiple strategies and provide messages carefully and tailored for different audiences. What works to combat the harms associated with drug-taking in prisons is different from what works for specific cultural groups or for young people attending music festivals. The available evidence suggests pill testing is an effective and useful approach to harm minimisation in this last group. We believe it has the capacity to decrease ambulance calls to festival-goers, help change behaviour and save lives. It has taken until now for pill testing techniques to be developed to a level where they are able to identify the constituents in analysed samples with sufficient precision, reliability and speed. These techniques, and the range of substances for which they can test, will continue to improve over time. On the basis of experience gained in the UK, Europe and Australia it’s clear pill testing is now feasible and practicable. The members of the Australasian Chapter of Addiction Medicine within the Royal Australasian College of Physicians are the main clinical experts in the field of addiction medicine in this country. Together with the Australian Medical Association and many prominent members of the community with experience in this area we feel this is the time for pill testing to be introduced, albeit in careful and controlled circumstances. We believe this position is also supported by peer users, concerned families, and past and present members of police forces across Australia. The fact the “War on Drugs” has failed does not mean we should give up. There are many new weapons available to us, as we have learnt from the successful public health campaigns of the past. Pill testing will not abolish all the harms associated with drug taking, but if handled carefully, carries the likelihood of reducing them significantly. Martyn Lloyd Jones, Honorary Senior Lecturer, University of Melbourne and Paul Komesaroff, Professor of Medicine, Monash University This article is republished from The Conversation under a Creative Commons license. Read the original article.

Dr Linda Calabresi

Finally, we’ve got some robust evidence to answer the question - is ondansetron safe to take for morning sickness. Published in JAMA, a very large retrospective study involving over 1.8 million pregnancies, almost 90,000 of which included exposure to ondansetron in the first trimester has found that taking the drug did not increase the risk of cardiac malformations or congenital malformations overall. However, first trimester ondansetron was associated with a very small increased risk of oral clefts (three additional cases per 10,000 women treated). Interestingly the increased risk for oral clefts was confined to cleft palate, there was no evidence for an increased risk of cleft lip. The information will be eagerly received by the thousands of pregnant women who experience severe nausea and vomiting, and the clinicians who care for them many of whom have been prescribing ondansetron because of its effectiveness, despite the lack of detailed safety data. “Although not formally approved for the treatment of nausea and vomiting during pregnancy, ondansetron, a 5-HT receptor antagonist, has rapidly become the most frequently prescribed drug for nausea and vomiting during pregnancy in the United States because of its perceived superior antiemetic effects and improved adverse effect profile compared with treatment alternatives,” the study authors said. “In 2014, an estimated 22% of pregnant women used ondansetron in the United States,” they said. The major strengths of this study lie in the size of the cohort and the fact that the information on ondansetron exposure was based on filled prescriptions, thereby negating any possible recall bias. Both these factors are particularly important given how rare these abnormalities are and how many possible confounders there could be. As for limitations of the study, of course just because a prescription has been filled doesn’t always mean the medication has been taken, but even if the exposure wasn’t as great as calculated, the risk would be only lessened rather than raised. There is also the possibility that there might have been some other unrecognised factor involved especially since all the women in the study were uninsured and treated under Medicaid insurance and therefore included a higher percentage of women from disadvantaged communities. However, given the detailed information collected on these women and their pregnancies, and the multiple analyses conducted on this data, the likelihood of unmeasured confounders affecting the findings was thought to be low. Overall the results of this study should provide reassurance for clinicians and pregnant women, according to an accompanying editorial, written by a US obstetrician and gynaecologist. “As clinicians and pregnant women engage in informed, shared decision-making surrounding treatment for nausea and vomiting, the current information is important for contextualising risks in light of the potential benefits,” he concluded.

References

Huybrechts KF, Hernández-Díaz S, Straub L, Gray KJ, Zhu Y, Patorno E, et al. Association of Maternal First-Trimester Ondansetron Use With Cardiac Malformations and Oral Clefts in Offspring. JAMA. 2018 Dec 18; 320(23): 2429-37. DOI: [10/1001/jama.2018.18307] Haas DM. Helping Pregnant Women and Clinicians Understand the Risk of Ondansetron for Nausea and Vomiting During Pregnancy. JAMA. 2018 Dec 18; 320(23): 2425-6. DOI: [10.1001/jama.2018.19328]
Daryl Efron and Harriet Hiscock

The rate of medications dispensed for attention-deficit hyperactivity disorder (ADHD) in children aged 17 and under increased by 30% between 2013-14 and 2016-17. The Australian Atlas for Healthcare Variation, released today, shows around 14,000 prescriptions were dispensed per 100,000 children aged 17 and under in 2016-17, compared with around 11,000 in 2013-14. The atlas for 2016-17 also showed some areas had a high dispensing rate of around 34,000 per 100,000 while the area with the lowest rate was around 2,000 per 100,000 – a 17-fold difference. This difference is much lower than in 2013-14, when the highest rate was 75 times the lowest. For decades people have been concerned too many children could be diagnosed with ADHD and treated with medications. We are conducting a study called the Children’s Attention Project, following 500 children recruited through Melbourne schools. So far, we have found only one in four children who met full ADHD criteria were taking medication at age ten. So it looks like, if anything, more children with ADHD should be referred for assessment and consideration of management options.

How many kids are medicated?

ADHD is the most common neurodevelopmental disorder of childhood – the prevalence is around 5% in Australia. Children with ADHD have great difficulty staying focused, are easily distracted and have poor self-control. Many are also physically hyperactive, especially when they are young. To be diagnosed, children need to have major problems from their ADHD symptoms both at home and school. These include learning difficulties, behavioural problems and trouble making friends. Young people with ADHD are more likely to fail school, have lower quality of life, experience substance abuse issues and teenage pregnancy, or end up in prison. Medication can make a big difference to these children’s lives. While there are many ways to help children with ADHD, stimulant medication is the most effective treatment. All international clinical guidelines recommend it for children with significant ADHD that persists after non-medication approaches have been offered. Our previous research found that about 80% of children diagnosed with ADHD by a paediatrician (the main medical specialty that manages ADHD) in Australia are treated with medication. The atlas shows the proportion of children and adolescents who had at least one ADHD medication prescription dispensed was 1.5% in 2013-14 and 1.9% in 2016-7. This is similar to the prevalence of stimulant medication prescription in previous Australian studies in the past 15 years. It sits between the US (high) and Europe (low) and is not excessive given the prevalence of the condition. The Children’s Attention Project found those with the most severe symptoms were more likely to be prescribed medications, as were those from families of lower socioeconomic status. Other Australian studies have found similar results. This is not surprising as ADHD does appear to be more common in children from socioeconomically disadvantaged families. Our research suggests that disadvantaged families in Australia appear to be able to access services for ADHD, at least in metropolitan centres.

Why does it vary between areas?

The atlas finding that there is considerable regional variation in prescribing of stimulant medications in Australia has been identified in previous studies and needs to be better understood. Some variation in health care is normal and good, but too much suggests there may be a problem with the quality of care or access to care. For example, greater prescribing in regional areas may reflect lack of timely access to non-pharmacological services. We do need to keep watching this space, monitoring rates and regional variation of medication use. A landmark study in the US, published in 1999, compared medication with intensive parent and teacher behaviour training. The children who received medication had a much greater reduction in ADHD symptoms. But medication is only one consideration in ADHD. Other supports are also important. Behavioural therapies can help reduce anxiety and behaviour problems in children with ADHD and improve relationships with parents and teachers. However, accessing psychologists can be hard for many families. While Medicare rebates are available for up to ten sessions per year, costs can still be a barrier. In our research, Victorian parents reported out-of-pocket costs of up to A$200 per session with a psychologist. ADHD is not considered a disability under the National Disability Insurance Scheme, so families are not eligible for funding packages. Further research is needed to better understand the factors influencing access to care for Australian children with ADHD, and why there is such variation in rates of prescribing between regions. We also need to ensure children across Australia get equitable access to non-medication management. We need evidence-based clinical guidelines relevant to the Australian healthcare system, which is quite different from places such as the UK and US. This work must include adult ADHD, which is an emerging area with a raft of clinical and service system complexities.The Conversation This article is republished from The Conversation under a Creative Commons license. Read the original article.

Chronic rhinosinusitis is a misery-generating condition – literally. According to a large study just published in The Journal of the American Medical Association, having chronic rhinosinusitis significantly increases your risk of depression and anxiety. And if you also have nasal polyps the risk is higher still. The Korean study was admittedly observational but it did include almost 50,000 individuals from the general population and followed them up for 11 years. Researchers found, over the duration of the study, those people with chronic rhinosinusitis were 54% more likely to develop depression and 57% more likely to develop anxiety than those people who did not suffer this condition. And if nasal polyps accompanied the rhinosinusitis the increase in likelihood for both mental illnesses jumped to the early 60s (61% and 63% respectively). So what are the implications of this study? Well – they are fairly straightforward really. “Physicians should be aware of the potential comorbidities observed in patients with [chronic rhinosinusitis] and provide therapy to reduce the risk of depression and anxiety in these patients,” the study authors helpfully concluded. What we don’t know of course, being simply an observational study without any intervention to test, is whether effectively treating the rhinosinusitis helps the depression or anxiety, and importantly, whether surgically removing the polyps can make a difference to this psychological side-effect. The researchers actually even distance themselves from the conclusion that chronic rhinosinusitis causes depression and anxiety, citing the chicken and egg phenomena. “Whether depression and anxiety amplify the symptoms of [chronic rhinosinusitis] or whether these conditions are the consequence of [chronic rhinosinusitis]is unknown,” they said. But they do say their findings support previous research that has suggested an association between the conditions. They also say their study allowed analysis of the specific phenotype responsible for the chronic rhinosinusitis – whether it be predominantly T1 or T2 response derived. What they found was the association held true regardless of the phenotype – suggesting this was more to do with personality and symptoms than physiology. All in all, what the study authors suggest is that given how common chronic rhinosinusitis is in the population, it is worthwhile keeping a high indexation of suspicion for the development of depression and anxiety not only for the patients’ current quality of life but also because these conditions can affect health outcomes down the line. “[T]hese psychiatric comorbidities may influence not only the diagnosis of [chronic rhinosinusitis] but also its therapeutic and surgical outcomes,” the study authors said.  

Reference:

Kim JY, Ko I, Kim MS, Yu MS, Cho BJ, Kim DK. Association of Chronic Rhinosinusitis With Depression and Anxiety in a Nationwide Insurance Population. JAMA Otolaryngol Head Neck Surg. 2019 Feb 7.  DOI: 10.1001/jamaoto.2018.4103 [Epub ahead of print].
Clinical Articles iconClinical Articles

Allergic disorders result from an inappropriate, usually IgE-mediated, immune response upon exposure to either environmental or food allergens. Common manifestations of allergy include rhinoconjunctivitis, asthma, eczema, acute urticaria and anaphylaxis. Disorders, such as chronic urticaria, hereditary angioedema and T-cell contact dermatitis (metal allergy), while clinically similar in some ways, are not IgE-mediated. Allergic disease manifests in different ways through life and the likely causative agents can also change with age (see Table 1).

Tests used in the diagnosis of IgE-mediated allergy

Total IgE Higher levels of total IgE are often found in patients with allergic conditions. However, normal total IgE does not exclude allergy. Total IgE is also elevated in other conditions including parasitic infections and allergic bronchopulmonary aspergillosis. It is used increasingly in determining anti-IgE therapy in moderate to severe asthmatics. Allergen-specific IgE Allergen-specific IgE can be detected for a large variety of allergens. The presence of a specific IgE to allergen can suggest allergic disease and is detected via a blood test (RAST or radioallergosorbent test) or skin prick test. RAST tests detect many of the different proteins within an individual allergen. Recombinant allergen testing Of the many proteins within a substance, only a few may cause allergic symptoms. Recombinant allergen testing looks for specific characterised protein within an allergen. Interpretation of RAST tests The presence of detectable specific IgE to an allergen does not confirm the patient is allergic to that substance. All results must be interpreted in conjunction with the clinical history of the patient. Low levels of detectable specific IgE can confirm the presence of allergy in the right clinical context. RAST testing aids in the assessment of, and identification of allergic sensitisation, but is not to be used alone as the deciding factor for inclusion or exclusion of allergy. As the level of specific IgE increases, the likelihood of clinical relevance also increases. As shown in Table 2, different allergens have different specific IgE level cutoffs at which serious allergy is >95% likely (positive predictive value or PPV). The range of values is vastly different between allergens and is affected by age and also by geographic region. Table 2 defines levels at which exposure, or a challenge, would be highly hazardous for a patient. Importantly, many patients could have serious reactions at much lower levels.   [table id=1 /]   [table id=2 /]

RAST tests

RAST tests are available for a range of allergens, however Medicare criteria limits rebates based on the number, type and frequency of tests. Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. When ordering RAST tests, it is advisable to include allergens the patient feels are relevant and those likely for the clinical scenario. For common clinical scenarios we recommend the following: Childhood eczema Age <2 years: Milk, Egg, Wheat, Peanut Age >2 years: Milk, Egg, Peanut, Dust mite Additional allergens or an extended RAST combined allergy panel may be ordered. Asthma and allergic rhinoconjunctivitis Dust mite, Grass mix, Animal dander Additional allergens may be ordered or substituted if relevant (e.g. cat dander instead of animal dander). An extended RAST inhalant panel is also available. Default panel if no allergens are specified and no clinical notes are provided Age <5 years: Dust mite, Grass mix, Food Mix Age >5 years: Dust mite, Grass mix, Animal Mix Anaphylaxis Anaphylaxis is a severe life-threatening allergic reaction. It is recommended these patients require specialist assessment by a clinical immunologist or allergist. Initial testing should look for the causative allergen if possible. It is important to note that a negative RAST test does not exclude the allergen tested. RAST testing recommendations ­
  • Test individual likely causative allergen i.e. food, stinging insect. ­
  • Tryptase, if done within 2-6 hours of reaction, can support the occurrence of an allergic reaction. ­
  • Useful as an assessment of mastocytosis (condition with increased numbers of mast cells)

Extended RAST panels

Extended RAST panels have been developed to represent the common allergens encountered clinically in practice. They are particularly relevant in our geographic region and replace the skin prick test panel which is no longer available. Additional allergens may also be requested. All results must be interpreted in conjunction with the patient’s clinical history. Extended RAST Food Panel ­
  • Covers common food-related allergens
  • Almond; Hazelnut; Sesame seed; Banana; Mango; Shrimp (prawn); Cashew; Milk (cow); Soybean; Codfish; Peanut; Walnut; Egg white; Rice; Wheat
Extended RAST Nut Allergy Panel ­
  • Broad collection of commonly consumed nuts, including peanuts ­
  • Individual nut testing with appropriate clinical history is preferred ­
  • Recommend to discuss results with a clinical immunologist or allergist
  • Almond; Macadamia; Pine nut; Brazil; Peanut; Sesame seed; Cashew; Peanut (Ara-h2); Walnut; Hazelnut; Pecan
Extended RAST Combined Allergy Panel ­
  • Combination of common food and environmental allergens ­
  • Replaces the skin prick test panel (no longer available)
  • Almond; Dust mite; Mould mix; Cashew nut; Egg white; Peanut; Cat dander; Grass mix; Shrimp (prawn); Codfish; Hazelnut; Soy; Dog dander; Milk (cow); Wheat
  • * Preferable for children (<12 years) due to low serum volume
Extended RAST Inhalant Panel ­
  • Covers common environmental allergens ­
  • Useful for asthma and allergic rhinitis
  • Acacia (wattle); Blomia tropicalis; Dust mite; Alternaria alternate; Cat dander; Eucalyptus; Aspergillus fumigatus; Cladosporium; Horse dander; Bahia grass; Common ragweed; Johnson grass; Bermuda grass; Dog dander; Perennial rye grass

Recombinant allergens

Omega-5 gliadin ­
  • A component of wheat ­
  • Associated with anaphylaxis ­
  • Often in the context of eating wheat and physical activity within 1-2 hours
Alpha-gal (mammalian meat allergy) ­
  • Associated with anaphylaxis; often delayed following consumption of meat (beef, lamb, pork) ­
  • Related to tick bites
Peanut Allergy Risk Assessment ­
  • Peanuts like all food is made up of many different proteins ­
  • Ara-h2 is associated with anaphylaxis to peanut ­
  • Can assist with risk assessment and should be done in conjunction with a clinical immunologist or allergist ­
  • A negative Ara-h2 in peanut positive patient does not imply there is no risk to anaphylaxis
  • Results of RAST tests can also be of use in monitoring ongoing allergy in patients in conjunction with their treating clinician

How to order allergy tests

RAST tests - standard panels Medicare Australia limits rebates for RAST tests to a maximum of four specific allergens and/or mixes per pathology request and a maximum of four RAST test episodes per year. Extended RAST tests (Medicare rebate + $120* per panel)
  • Extended RAST Food
  • Extended RAST Nut
  • Extended RAST Combined
  • Extended RAST Inhalant
Please note, extended RAST panels are not bulk billed. Recombinant allergen tests (Medicare rebate + $60* each)
  • Alpha-gal
  • Omega-5 gliadin
  • Peanut (Ara-h2)
  • Peanut Allergy Risk Assessment
  General Practice Pathology is a regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.
Clinical Articles iconClinical Articles

It’s a controversial topic here in Australia. But a new UK study, just published in the New England Journal of Medicine, gives strong support the role of e-cigarettes as a smoking cessation therapy. The randomised controlled trial of almost 900 adult smokers wanting to quit found the one-year abstinence rate was 18% among the e-cigarette users compared to 9.9% among those who were randomised to receive nicotine replacement therapy. Much of the difference could be attributed to adherence to the assigned product. After 12 months, 80% of the e-cigarette group were still using the device whereas only 9% of the alternative group were still taking their nicotine replacement therapy despite being able to choose between the patch, gum, lozenge, nasal spray, inhalator, mouth spray, mouth strip, and microtabs (or any combination of these). Participants in both groups underwent the same multi-session behavioural support as per best practice guidelines. This study provides some of the strongest evidence to date that e-cigarettes are significantly better than nicotine replacement therapy in helping people quit smoking, the study authors suggest. “This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine-replacement products and with 88.1% of participants using combination treatments,” they said. The researchers suggested e-cigarettes had better adherence rate because they were more effective at reducing the symptoms of withdrawal when quitting smoking, because the refillable devices are better at delivering nicotine compared with options such as gum or patches. They also suggest the nicotine dose provided by e-cigarettes was easier to tailor to individual needs than other replacement options. And even though people using the e-cigarettes were more likely to get mouth or throat irritation, this side effect was generally mild and tolerable especially compared to withdrawal symptoms such as constipation, mouth ulcers and weight gain. In general, the researchers claim replacing cigarettes with e-cigarettes is a definite positive in terms of health outcomes and much better than other nicotine replacement options, but they suggest the high rate of adherence in the e-cigarette group may have some negative connotations. “This can be seen as problematic if e-cigarette use for a year signals ongoing long-term use, which may pose as-yet-unknown health risks,” they said. As an accompanying editorial points out, fundamentally nicotine is highly addictive. While electronic cigarettes have been proven to be a great tool in helping people get off normal cigarettes, there may be an issue if non-smokers, especially teenagers take up vaping, making them vulnerable to becoming smokers further down the track. “The cigarette company may well see e-cigarettes as addictive bait that will lead young people toward smoking,” the US editorial authors suggest. They suggest this potential problem could be relatively easily averted by ensuring e-cigarettes aren’t manipulated to enhance their appeal, specifically the authorities should not allow the manufacture of flavoured nicotine products. However, they too acknowledge e-cigarettes have a significant role to play in solving this public health problem – ‘by helping people who are users of combustible tobacco products stop smoking by switching to vaping.’

References:

Hajek P, Phillips-Waller A, Przulj D, Pesola F, Smith KM, Bisal N, et al. A Randomized Trial of E-Cigarettes versus Nicotine-Replacement Therapy.  N Engl J Med. 2019 Jan 30;  DOI: 10.1056/NEJMoa1808779 [Epub ahead of print] Drazen JM, Morrissey S, Campion EW. The Dangerous Flavors of E-Cigarettes. N Engl J Med. 2019 Jan 30. DOI: 10.1056/NEJMe1900484 [Epub ahead of print]
Clinical Articles iconClinical Articles

Australia was declared free of measles in 2014. Yet this summer we’ve seen nine cases of measles in New South Wales, and others in Victoria, Western Australia, South Australia and Queensland. High vaccination rates in Australia means the measles virus doesn’t continuously spread, but we still have “wildfire” outbreaks when travellers bring measles into the country, often unknowingly. If you haven’t received two doses of measles vaccine, you are at risk of contracting measles.

How can you catch it?

Measles is a highly contagious virus that spreads by touching or breathing in the same air as an infected person. The virus stays alive in the air or on infected surfaces for up to two hours. An infected person is contagious from the first day of symptoms (fever, cough and runny nose). These general symptoms start about four days before the rash develops, meaning contagious people can spread the virus even before they realise they have measles. If you’re not immune to the virus, through vaccination or past infection, the chance of becoming ill after being near someone with measles is 90%. Being in the same café, waiting in line at the checkout or flying on the same aeroplane as an infected person could be enough to pick up the disease.

Why is it so dangerous?

Measles causes a fever, cough, and a rash that starts around the hairline and then spreads to the whole body. It can also cause middle ear infections (otitis media), chest infections (pneumonia), and diarrhoea. Swelling and inflammation to the brain (encephalitis) occurs in 1 in every 1,000 cases and can lead to permanent brain damage or death. In 2017, 110,000 people died from measles worldwide. Even after surviving the initial illness, measles can cause a devastating and fatal complication known as subacute sclerosing panencephalitis (inflammation of the brain) many years later.

Why are people in their 20s to 50s more at risk?

To protect yourself against measles, you need two doses of measles-mumps-rubella (MMR) vaccine. Children in Australia routinely get this vaccine at 12 and 18 months of age. The second dose is given in combination with the chickenpox vaccine. It’s important to have two doses of MMR vaccine, especially if you haven’t reached your mid-50s. Most people older than this would have been infected with measles before vaccination was routine. People aged in their 20s to early 50s (those born from 1966 and 1994) are most likely to have only had one dose of MMR vaccine. While we’ve had the measles vaccine in Australia since 1968, a two-dose program was only introduced in 1992. A brief school-based catch-up program from 1993 to 1994 offered school children a second dose. Another school-based program provided children with catch-up vaccinations in 1998*. For those who missed out on the school program, catch-up vaccinations were given on an ad-hoc basis via GP clinics. So not everyone in this age group would have received two doses of the measles vaccine. If you are this age, you may not be not fully protected against measles. Checking with a GP or immunisation nurse is the best way to be sure. They will check your records, and may do a blood test if you have no proof of immunisation. Even if you can’t be sure of past vaccinations, it’s still safe to have an extra vaccine. And it’s free for those who need a catch-up dose. If you have a child under 12 months of age and you’re heading to a country with measles, an early additional vaccine dose can be given to protect your baby from measles. This ideally should be done at least a month before you travel, to ensure an immune response has time to develop. The routine scheduled doses at 12 months and 18 months will still need to be given later.

What if you’re not protected?

Unfortunately, there is no treatment for measles. Getting adequately vaccinated is the best form of defence against this serious disease. If you think you’ve been exposed or may be ill from measles, see your GP or call Health Direct or your public health department as soon as possible. If exposed, but not yet ill, it may not be too late to get a protective vaccine and ensure you don’t spread the disease to others. If you are unwell, and suspect measles, call ahead to let the clinic know so they can make provisions to keep you away from other patients in the waiting room. Other, more common, diseases can look like measles, so an urgent specific test (throat swab) must be done to confirm the infection. If measles is proven, public health workers will trace your contacts and your treating doctor will monitor you for complications.

Are we at risk of measles returning in Australia?

Australia currently has all-time high vaccine coverage, with 94.5% of five-year-old children fully immunised at the end of 2017. By keeping vaccine coverage near or above 95%, herd immunity where there are enough people vaccinated helps prevent measles from spreading to others, including those who cannot be vaccinated. But in our interconnected world, we must work together to reduce the threat of measles worldwide by boosting immunisation programs in regions with low coverage, including in the Asia Pacific. Measles have resurfaced in some countries due to falls in vaccine coverage from unfounded safety concerns as well as weak health systems. In the first six months of last year, for instance, Europe had 41,000 cases of measles, nearly double the total number of the previous year. This, among other factors, has prompted the World Health Organisation to list vaccine hesitancy as a top ten threat to global health in 2019. A continued global coordinated effort will be required to maintain elimination and prevent resurgence of this deadly disease in Australia. * Correction: this article has been updated to note a school-based catch-up program also operated in 1998.The Conversation

Kristine Macartney, Professor, Discipline of Paediatrics and Child Health, University of Sydney and Lucy Deng, Staff Specialist Paediatrician, National Centre for Immunisation Research and Surveillance; Clinical Associate Lecturer, Children's Hospital Westmead Clinical School, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.
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At first read, the study results seemed disappointing. Yet another promising premise fails to deliver when it comes to actual proof. But the researchers aren’t ready to give up on this hypothesis just yet. In fact, commentators on the study say the results offer ‘great hope’ and represent ‘a major leap forward.’ The SPRINT MIND study, recently published in JAMA was investigating whether intensive blood pressure control (to a systolic less than 120mmHg) worked better than standard blood pressure control (SBP<140mmHg) at reducing the risk of mild cognitive impairment and dementia. This randomised controlled trial was a component of the well-publicised Systolic Blood Pressure Intervention Trial (SPRINT) which looked at the effect of more intensive blood pressure control on cardiovascular and renal outcomes in addition to cognitive function in over 9000 people without a history of diabetes or stroke. Basically, what this study showed was that intensive blood pressure control to a target of less than 120mmHg did not reduce the incidence of probable dementia compared to lowering BP to a target of less than 140mmHg. Depressing, yes? No, say the study authors. Firstly, they say the study demonstrated no ill-effects of intensive BP lowering – which has been an issue of concern for some who have been worried that lowering the BP could decrease cerebral perfusion thereby harming cognitive function. In fact, the study authors showed quite the opposite was true. The intervention actually helped protect cognitive ability. “This is the first trial, to our knowledge, to demonstrate an intervention that significantly reduces the occurrence of [mild cognitive impairment], a well-established risk factor for dementia, as well as the combined occurrence of [mild cognitive impairment] or dementia,” they said. The study authors suggest the lack of benefit in dementia may be due to the fact the SPRINT study was terminated early following the demonstration of benefit of intensive BP control on cardiovascular outcomes and all-cause mortality. Because of this shortened time frame and the fact that there were fewer than expected cases of dementia, they suggest the study may have been ‘underpowered’ to show a result for lowering the risk of dementia. They also say there were fewer cases of dementia among the intensive treatment group compared with the standard treatment group (7.2 vs 8.6 cases per 1000 patient years) even though this wasn’t statistically significant. We cannot know whether this trend would have reached statistical significance had the intervention continued. An accompanying editorial views the study and the results with a good deal of positivity. “For older adults, almost all of who have concern about being diagnosed with Alzheimer Disease and related dementia, [this study] offers great hope,” the US epidemiologist, Dr Kristine Yaffe, said. She points out that this a readily modifiable risk factor, and we should be accelerating our efforts into investigating whether this, along with other vascular health interventions such as physical activity, can indeed prevent dementia, building on the positive results of this study. “The SPRINT MIND study may not be the final approach for prevention of Alzheimer disease or other cognitive impairment but it represents a major leap forward in what has emerged as a marathon journey.”

Reference

Yaffe, K. Prevention of Cognitive Impairment With Intensive Systolic Blood Pressure Control. JAMA [Internet]. 2019 Jan 28. DOI: 10.1001/jama.2019.0008 [Epub ahead of print]
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Bowel cancer mostly affects people over the age of 50, but recent evidence suggests it’s on the rise among younger Australians. Our study, published recently in Cancer Epidemiology, Biomarkers and Prevention, found the incidence of bowel cancer, which includes colon and rectal cancer, has increased by up to 9% in people under 50 from the 1990s until now. Our research examined all recorded cases of bowel cancer from the past 40 years in Australians aged 20 and over. Previous studies assessing bowel cancer incidence in young Australians have also documented an increase in the younger age group. This trend is also being seen internationally. A study from the United States suggests an increase in bowel cancer incidence in people aged 54 and younger. The research shows rectal cancer incidence increased by 3.2% annually from 1974 to 2013 among those aged age 20-29. Bowel cancers are predicted to be the third most commonly diagnosed cancer in Australia this year. In 2018, Australians have a one in 13 chance of being diagnosed with bowel cancer by their 85th birthday. Our study also found bowel cancer incidence is falling in older Australians. This is likely, in part, to reflect the efficacy of the National Bowel Cancer Screening Program, targeted at those aged 50-74. Bowel cancer screening acts to reduce cancer incidence, by detecting and removing precancerous lesions, as well as reducing mortality by detecting existing cancers early. This is important, as bowel cancer has a good cure rate if discovered early. In 2010 to 2014, a person diagnosed with bowel cancer had a nearly 70% chance of surviving the next five years. Survival is more than 90% for people who have bowel cancer detected at an early stage. That is why screening is so effective – and we have previously predicted that if coverage rates in the National Bowel Screening Program can be increased to 60%, around 84,000 lives could be saved by 2040. This would represent an extraordinary success. In fact, bowel screening has potential to be one of the greatest public health successes ever achieved in Australia.

Why the increase in young people?

Our study wasn’t designed to identify why bowel cancer is increasing among young people. However, there are some factors that could underpin our findings. The increase in obesity parallels that of bowel cancer, and large population based studies have linked obesity to increased cancer risk. Unhealthy lifestyle behaviours, such as increased intake of highly processed foods (including meats), have also been associated with increased bowel cancer risk. High quality studies are needed to explore this role further. Alcohol is also thought to be a contributor to increasing the risk of bowel cancer. So, should we be lowering the screening age in Australia to people under the age of 50? Evaluating a cancer screening program for the general population requires a careful analysis of the potential benefits, harms, and costs. A recent Australian study modelled the trade-offs of lowering the screening age to 45. It showed more cancers would potentially be detected. But there would also be more colonoscopy-related harms such as perforation (tearing) in an extremely small proportion of people who require further evaluation after screening. A lower screening age would also increase the number of colonoscopies to be performed in the overstretched public health system and therefore could have the unintended consequence of lengthening colonoscopy waiting times for people at high risk.

How to reduce bowel cancer risk

One of the most common symptoms of bowel cancer is rectal bleeding. So if you notice blood when you go to the toilet, see your doctor to have it checked out. A healthy lifestyle including adequate exercise, avoiding smoking, limiting alcohol intake and eating well, remains most important to reducing cancer risk. Aspirin may also lower risk of cancer, but should be discussed with your doctor because of the potential for side effects including major bleeding. Most importantly, we need to ensure eligible Australians participate in the current evidence-based screening program. Only 41% of the population in the target 50-74 age range completed their poo tests in 2015-2016. The test is free, delivered by post and able to be self-administered.The Conversation   This article is republished from The Conversation under a Creative Commons license. Read the original article.
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It would be a brave doctor who would ignore the warning ‘allergic to penicillin’ when deciding which antibiotic to prescribe for a patient. But according to a new review published recently in JAMA, despite up to 10% of the population reporting allergies to penicillin, few have clinically significant reactions. “Although many patients report they are allergic to penicillin, clinically significant IgE-mediated or T lymphocyte-mediated penicillin hypersensitivity is uncommon (<5%),” the US review authors said. And the issue is an important one. As the authors point out, not only will patients, labelled as having a penicillin allergy be given alternative antibiotics that are more likely to fail and cause side-effects but the use of these alternatives increase the risk of antimicrobial resistance developing. So for all these reasons, the researchers propose that is worthwhile that all patients labelled as having an allergy to penicillins be re-evaluated. As a starting point, a comprehensive history should be taken. And while the reviewers acknowledge that, to date no allergy questionnaires have been validated in terms of defining risk levels, there are plenty of features in a history that can give a clue as to whether a person could safely be offered skin prick testing or a drug challenge. Broadly speaking, patients with a history of a minor rash, that was not significantly itchy that developed over the course of days into the course of the antibiotic are considered low-risk. This is opposed to people who have a history of developing a very pruritic rash within minutes to hours of taking the drug (which tends to indicate an IgE-mediated reaction) or people who experienced significant blistering and/or skin desquamation after taking penicillin (which generally represents a severe T-cell-mediated reaction). Among those patients whose rash-history suggests they are at low-risk, other factors should be considered before attempting a challenge. “Even in the context of low-risk allergy history, patients with unstable or compromised haemodynamic or respiratory status and pregnant patients should be considered as having at least a moderate-risk history,” they said. However, patients whose penicillin allergy history included non-allergic-type symptoms such gastrointestinal symptoms or patients who only have a family history of penicillin allergy should be considered at low-risk. Once the patient has been assessed as being at low-risk of having an acute allergic reaction, the study authors suggest they be given amoxicillin under medical observation. “For penicillin allergy, administration of 250mg of amoxicillin with one hour of observation demonstrates penicillin tolerance,” they said. Should the patient tolerate this dose of amoxicillin, it can be concluded that all beta-lactams can be administered safely, and the issue of cross-reactivity (between penicillin and cephalosporin which occurs in about 2% of truly penicillin-allergic people) is rendered irrelevant. Patients who are considered at moderate-risk of having an allergic reaction to penicillin, namely those patients with a history of urticaria or mild pruritic rashes but no anaphylaxis should be considered for skin-prick testing. Only those with a negative skin prick test should be considered for an oral drug challenge. People with a history of high-risk reactions – usually anaphylaxis should not be skin-prick tested or challenged. They might be considered for desensitisation programs but only in select circumstances and only under the close supervision of a specialist. All in all, the authors advocate health professionals not simply take the label of ‘allergic to penicillin’ as gospel. “Evaluation of penicillin allergy has substantial benefits for patients by allowing improved antimicrobial choice for treatment and prophylaxis,” they concluded.

Reference

Shenoy ES, Macy E, Rowe T, Blumenthal KT. Evaluation and Management of Penicillin Allergy: A Review. JAMA 2019 Jan 15; 321(2): 188-99. DOI: 10.1001/jama.2018.19283    
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Ross River virus is Australia’s most common mosquito-borne disease. It infects around 4,000 people a year and, despite being named after a river in North Queensland, is found in all states and territories, including Tasmania. While the disease isn’t fatal, it can cause debilitating joint pain, swelling and fatigue lasting weeks or even months. It can leave sufferers unable to work or look after children, and is estimated to cost the economy A$2.7 to A$5.6 million each year. There is no treatment or vaccine for Ross River virus; the only way to prevent is to avoid mosquito bites. Mosquitoes pick up the disease-causing pathogen by feeding on an infected animal. The typical transmission cycle involves mosquitoes moving the virus between native animals but occasionally, an infected mosquito will bite a person. If this occurs, the mosquito can spread Ross River virus to the person.

Animal hosts

Ross River virus has been found in a range of animals, including rats, dogs, horses, possums, flying foxes, bats and birds. But marsupials – kangaroos and wallabies in particular – are generally better than other animals at amplifying the virus under experimental infection and are therefore thought to be “reservoir hosts”. The virus circulates in the blood of kangaroos and wallabies for longer than other animals, and at higher concentrations. It’s then much more likely to be picked up by a blood-feeding mosquito.

Dead-end hosts

When we think of animals and disease we often try to identify which species are good at transmitting the virus to mosquitoes (the reservoir hosts). But more recently, researchers have started to focus on species that get bitten by mosquitoes but don’t transmit the virus. These species, known as dead-end hosts, may be important for reducing transmission of the virus. With Ross River virus, research suggests birds that get Ross River virus from a mosquito cannot transmit the virus to another mosquito. If this is true, having an abundance of birds in and around our urban environments may reduce the transmission of Ross River virus to animals, mosquitoes and humans in cities.

Other reservoir hosts?

Even in areas with a high rates of Ross River virus in humans, we don’t always find an abundance of kangaroos and wallabies. So there must be other factors – or animals yet to be identified as reservoirs or dead-end hosts – playing an important role in transmission. Ross River virus is prevalent in the Pacific Islands, for instance, where there aren’t any kangaroos and wallabies. One study of blood donors in French Polynesia found that 42.4% of people tested had previously been exposed to the virus. The rates are even higher in American Samoa, where 63% of people had been exposed. It’s unclear if the virus has recently started circulating in these islands, or if it’s been circulating there longer, and what animals have been acting as hosts.

What about people?

Mosquitoes can transmit some viruses, such as dengue and Zika between people quite easily. But the chances of a mosquito picking up Ross River virus when biting an infected human is low, though not impossible. The virus circulates in our blood at lower concentrations and for shorter periods of time compared with marsupials. If humans are infected with Ross River virus, around 30% will develop symptoms of joint pain and fatigue (and sometimes a rash) three to 11 days after exposure, while some may not experience any symptoms until three weeks after exposure. To reduce your risk of contracting Ross River virus, take care to cover up when you’re outdoors at sunset and wear repellent when you’re in outdoor environments where mosquitoes and wildlife may be frequently mixing.   This article is republished from The Conversation under a Creative Commons license. Read the original article.
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While it appears the message about risky drinking is getting through to younger Australians, baby boomers are as bad as ever. According to a research letter appearing in the latest edition of the MJA, the proportion of 55-70-year-olds who could be classed as high-risk drinkers has risen over the last 15 or so years. The South Australian researchers say this is in ‘stark contrast to the significant decrease in risky drinking among people aged between 12-24 years during the same period.’ And while they do emphasise that by far the majority of older Australians (over 80%) are abstainers or drink at low risk levels, the proportional increase of those now in the high-risk category (from 2.1% in 2004 to 3.1% in 2016) represents an additional 400,000 at-risk individuals – significant in anyone’s language. The findings were based on secondary analyses of data from National drug Strategy Household Surveys conducted in 2004, 2007, 2010, 2013 and 2016. Interestingly the researchers defined the risk categories on the basis of the maximum number of standard alcoholic drinks drunk on a single occasion over the course of a month. So low-risk were those individuals who never consumed more than four drinks in a single session, risky drinkers drank 5-10 drinks in one session at least once a month and high-risk drinkers needed to have drunk 11 or more drinks at least once a month. It’s a slightly different means of assessment to the more common approach of asking about average daily alcohol intake and appears more likely to detect the binge drinker – or your classic ‘social drinker.’ As the letter authors point out, detecting problem drinking in this age group is especially important as this cohort is particularly vulnerable to a range of alcohol-related adverse events from falls to diabetes. Once again, the researchers are looking to GPs to detect those at-risk from drinking among our baby boomer patient population and initiate evidence-based interventions, such as short, opportunistic counselling and information sessions. But they recognise this isn’t always easy. “To facilitate early identification of problem drinking and early intervention, educating health care professionals about patterns and drivers of alcohol consumption by older people should be a priority,” the authors said. Perhaps using the study’s categorisation technique of the maximum number of drinks consumed in a single session might go some way to detecting those at risk.  

Referernce:

Roche AM, Kostadinov V. Baby boomers and booze: we should be worried about how older Australians are drinking. Med J Aust. 2019; 210(1): 38-9. DOI: 10.5694/mja2.12025. Available from: https://www.mja.com.au/journal/2019/210/1/baby-boomers-and-booze-we-should-be-worried-about-how-older-australians-are
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For many years experts in the field of drug policy in Australia have known existing policies are failing. Crude messages (calls for total abstinence: “just say no to drugs”) and even cruder enforcement strategies (harsher penalties, criminalisation of drug users) have had no impact on the use of drugs or the extent of their harmful effects on the community. Whether we like it or not, drug use is common in our society, especially among young people. In 2016 43% of people aged 14 and older reported they had used an illicit drug at some point in their lifetime. And 28% of people in their twenties said they had used illicit drugs in the past year. The use of MDMA (the active ingredient in ecstasy) is common and increasing among young people. In the last three months alone five people have died as a result of using illicit drugs at music festivals and many more have been taken to hospital. The rigid and inflexible attitudes of current policy-makers contrast dramatically with the innovative approaches to public health policy for which Australia was once renowned. Since the 1970s many highly successful campaigns have improved road safety, increased immunisation rates in children and helped prevent the spread of blood-borne virus infections. The wearing of seatbelts was made compulsory throughout Australia in the early 1970s. Randomised breath testing and the wearing of helmets by bike riders were introduced in the 1980s. These measures alone have saved many thousands of lives. The introduction of needle exchange and methadone treatment programs in the late 1980s and, more recently, widespread access to effective treatments for hepatitis C have dramatically reduced the health burden from devastating infections such as HIV and the incidence of serious liver disease. Each of these programs had to overcome vigorous and sustained hostility from opponents who argued they would do more harm than good. But in all cases the pessimists were proved wrong. Safety measures on the roads did not cause car drivers and bike riders to behave more recklessly. The availability of clean needles did not increase intravenous drug use. Easier access to condoms did not lead to greater risk taking and more cases of AIDS. We believe — along with many other experts in the field — that as was the case for these earlier programs, the evidence presently available is sufficient to justify the careful introduction of trials of pill testing around Australia. Specifically, we support the availability of facilities to allow young people at venues or events where drug taking is acknowledged to be likely to seek advice about the substances they’re considering ingesting. These facilities should include tests for the presence of known toxins or contaminants to help avert the dangerous effects they may produce. Such a program should be undertaken in addition to, and not instead of, other strategies to discourage or deter young people from taking illicit drugs. Although pill testing has been widely and successfully applied in many European countries over a twenty year period, it has to be admitted the evidence about the degree of its effectiveness remains incomplete. That’s why any program in Australia should be linked to a rigorously designed data collection process to assess its impact and consequences. However, we do know that the argument that pill testing programs will increase drug use and its associated harms is very unlikely to be true. Most people seeking advice about the constituents of their drugs will not take them if they are advised that they contain dangerous contaminants. And it’s easy to avoid false reassurances about safety by careful explanations and detailed information. The opportunity to provide face-to-face advice to young people about the risks of drug taking is one of the great strengths of pill testing programs. Over the last half century we have learnt public health programs have to utilise multiple strategies and provide messages carefully and tailored for different audiences. What works to combat the harms associated with drug-taking in prisons is different from what works for specific cultural groups or for young people attending music festivals. The available evidence suggests pill testing is an effective and useful approach to harm minimisation in this last group. We believe it has the capacity to decrease ambulance calls to festival-goers, help change behaviour and save lives. It has taken until now for pill testing techniques to be developed to a level where they are able to identify the constituents in analysed samples with sufficient precision, reliability and speed. These techniques, and the range of substances for which they can test, will continue to improve over time. On the basis of experience gained in the UK, Europe and Australia it’s clear pill testing is now feasible and practicable. The members of the Australasian Chapter of Addiction Medicine within the Royal Australasian College of Physicians are the main clinical experts in the field of addiction medicine in this country. Together with the Australian Medical Association and many prominent members of the community with experience in this area we feel this is the time for pill testing to be introduced, albeit in careful and controlled circumstances. We believe this position is also supported by peer users, concerned families, and past and present members of police forces across Australia. The fact the “War on Drugs” has failed does not mean we should give up. There are many new weapons available to us, as we have learnt from the successful public health campaigns of the past. Pill testing will not abolish all the harms associated with drug taking, but if handled carefully, carries the likelihood of reducing them significantly. Martyn Lloyd Jones, Honorary Senior Lecturer, University of Melbourne and Paul Komesaroff, Professor of Medicine, Monash University This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Finally, we’ve got some robust evidence to answer the question - is ondansetron safe to take for morning sickness. Published in JAMA, a very large retrospective study involving over 1.8 million pregnancies, almost 90,000 of which included exposure to ondansetron in the first trimester has found that taking the drug did not increase the risk of cardiac malformations or congenital malformations overall. However, first trimester ondansetron was associated with a very small increased risk of oral clefts (three additional cases per 10,000 women treated). Interestingly the increased risk for oral clefts was confined to cleft palate, there was no evidence for an increased risk of cleft lip. The information will be eagerly received by the thousands of pregnant women who experience severe nausea and vomiting, and the clinicians who care for them many of whom have been prescribing ondansetron because of its effectiveness, despite the lack of detailed safety data. “Although not formally approved for the treatment of nausea and vomiting during pregnancy, ondansetron, a 5-HT receptor antagonist, has rapidly become the most frequently prescribed drug for nausea and vomiting during pregnancy in the United States because of its perceived superior antiemetic effects and improved adverse effect profile compared with treatment alternatives,” the study authors said. “In 2014, an estimated 22% of pregnant women used ondansetron in the United States,” they said. The major strengths of this study lie in the size of the cohort and the fact that the information on ondansetron exposure was based on filled prescriptions, thereby negating any possible recall bias. Both these factors are particularly important given how rare these abnormalities are and how many possible confounders there could be. As for limitations of the study, of course just because a prescription has been filled doesn’t always mean the medication has been taken, but even if the exposure wasn’t as great as calculated, the risk would be only lessened rather than raised. There is also the possibility that there might have been some other unrecognised factor involved especially since all the women in the study were uninsured and treated under Medicaid insurance and therefore included a higher percentage of women from disadvantaged communities. However, given the detailed information collected on these women and their pregnancies, and the multiple analyses conducted on this data, the likelihood of unmeasured confounders affecting the findings was thought to be low. Overall the results of this study should provide reassurance for clinicians and pregnant women, according to an accompanying editorial, written by a US obstetrician and gynaecologist. “As clinicians and pregnant women engage in informed, shared decision-making surrounding treatment for nausea and vomiting, the current information is important for contextualising risks in light of the potential benefits,” he concluded.

References

Huybrechts KF, Hernández-Díaz S, Straub L, Gray KJ, Zhu Y, Patorno E, et al. Association of Maternal First-Trimester Ondansetron Use With Cardiac Malformations and Oral Clefts in Offspring. JAMA. 2018 Dec 18; 320(23): 2429-37. DOI: [10/1001/jama.2018.18307] Haas DM. Helping Pregnant Women and Clinicians Understand the Risk of Ondansetron for Nausea and Vomiting During Pregnancy. JAMA. 2018 Dec 18; 320(23): 2425-6. DOI: [10.1001/jama.2018.19328]
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The rate of medications dispensed for attention-deficit hyperactivity disorder (ADHD) in children aged 17 and under increased by 30% between 2013-14 and 2016-17. The Australian Atlas for Healthcare Variation, released today, shows around 14,000 prescriptions were dispensed per 100,000 children aged 17 and under in 2016-17, compared with around 11,000 in 2013-14. The atlas for 2016-17 also showed some areas had a high dispensing rate of around 34,000 per 100,000 while the area with the lowest rate was around 2,000 per 100,000 – a 17-fold difference. This difference is much lower than in 2013-14, when the highest rate was 75 times the lowest. For decades people have been concerned too many children could be diagnosed with ADHD and treated with medications. We are conducting a study called the Children’s Attention Project, following 500 children recruited through Melbourne schools. So far, we have found only one in four children who met full ADHD criteria were taking medication at age ten. So it looks like, if anything, more children with ADHD should be referred for assessment and consideration of management options.

How many kids are medicated?

ADHD is the most common neurodevelopmental disorder of childhood – the prevalence is around 5% in Australia. Children with ADHD have great difficulty staying focused, are easily distracted and have poor self-control. Many are also physically hyperactive, especially when they are young. To be diagnosed, children need to have major problems from their ADHD symptoms both at home and school. These include learning difficulties, behavioural problems and trouble making friends. Young people with ADHD are more likely to fail school, have lower quality of life, experience substance abuse issues and teenage pregnancy, or end up in prison. Medication can make a big difference to these children’s lives. While there are many ways to help children with ADHD, stimulant medication is the most effective treatment. All international clinical guidelines recommend it for children with significant ADHD that persists after non-medication approaches have been offered. Our previous research found that about 80% of children diagnosed with ADHD by a paediatrician (the main medical specialty that manages ADHD) in Australia are treated with medication. The atlas shows the proportion of children and adolescents who had at least one ADHD medication prescription dispensed was 1.5% in 2013-14 and 1.9% in 2016-7. This is similar to the prevalence of stimulant medication prescription in previous Australian studies in the past 15 years. It sits between the US (high) and Europe (low) and is not excessive given the prevalence of the condition. The Children’s Attention Project found those with the most severe symptoms were more likely to be prescribed medications, as were those from families of lower socioeconomic status. Other Australian studies have found similar results. This is not surprising as ADHD does appear to be more common in children from socioeconomically disadvantaged families. Our research suggests that disadvantaged families in Australia appear to be able to access services for ADHD, at least in metropolitan centres.

Why does it vary between areas?

The atlas finding that there is considerable regional variation in prescribing of stimulant medications in Australia has been identified in previous studies and needs to be better understood. Some variation in health care is normal and good, but too much suggests there may be a problem with the quality of care or access to care. For example, greater prescribing in regional areas may reflect lack of timely access to non-pharmacological services. We do need to keep watching this space, monitoring rates and regional variation of medication use. A landmark study in the US, published in 1999, compared medication with intensive parent and teacher behaviour training. The children who received medication had a much greater reduction in ADHD symptoms. But medication is only one consideration in ADHD. Other supports are also important. Behavioural therapies can help reduce anxiety and behaviour problems in children with ADHD and improve relationships with parents and teachers. However, accessing psychologists can be hard for many families. While Medicare rebates are available for up to ten sessions per year, costs can still be a barrier. In our research, Victorian parents reported out-of-pocket costs of up to A$200 per session with a psychologist. ADHD is not considered a disability under the National Disability Insurance Scheme, so families are not eligible for funding packages. Further research is needed to better understand the factors influencing access to care for Australian children with ADHD, and why there is such variation in rates of prescribing between regions. We also need to ensure children across Australia get equitable access to non-medication management. We need evidence-based clinical guidelines relevant to the Australian healthcare system, which is quite different from places such as the UK and US. This work must include adult ADHD, which is an emerging area with a raft of clinical and service system complexities.The Conversation This article is republished from The Conversation under a Creative Commons license. Read the original article.
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