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Read the latest articles relevant to your clinical practice, including exclusive insights from Healthed surveys and polls.

By reading selected clinical articles, you earn CPD in the Educational Activities (EA) category whenever you click the “Claim CPD” button and follow the prompts. 

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Dr Vivienne Miller
  • Clinical Articles

Can My Genes Be Making Me Overweight?

Based on an interview with endocrinologist and obesity expert, Professor Joseph Proietto at the Annual Women and Children’s Health Update, Melbourne, March 2018 There are many reasons proposed for our society becoming more overweight than ever before. The commonest explanation is that people are overeating because they have more refined, energy dense foods easily available and requiring little physical effort to access. The other consideration is that people are not moving and exercising as much, due to increased sedentary employment and entertainments that are clearly less effort. Once people become overweight, they feel less like exercising and so the situation worsens. Unfortunately, in our society, food (including alcohol), socialising and entertainment are all strongly associated. Food is easily obtained and is abundant in variety and quantity. Previous generations ate less because of cost, availability and the fact that food generally plainer and perhaps less tasty. This was especially true for the poorer in society, who also tended to have more physically demanding jobs, with less time and money to spend on eating during the day. On a scientific level, genetics and epigenetics are now known to play an important role in the development of obesity. In particular, there are many genes currently being researched in relation to appetite and obesity including leptin (a hormone made mostly by adipose cells that inhibits hunger) and its receptor, and the melanocortin 4 receptor. "For obvious evolutionary reasons, there are no genes (yet) identified that reduce metabolic rate," said Professor Joseph Proietto. So far, all genes that have been found to be associated with obesity have been linked to increased hunger. There are no genes known that reduce metabolism. It is interesting that force-feeding increases energy expenditure while weight loss reduces energy expenditure and, in both cases, it is spontaneous activity that changes, with only minor alteration in basal metabolic rate. This has been demonstrated in overfeeding experiments. Some causes of obesity may be epigenetic. For example, some women who gain excess weight during pregnancy find it more difficult to lose after the pregnancy. This is likely to be due to epigenetic change in the expression of genes connected with obesity. Unfortunately, the offspring of mothers who become overweight before or during pregnancy are likely to inherit these genes, and hence themselves have trouble with weight gain. Certain medical conditions (hypothyroidism, Cushing's syndrome) may induce modest weight gain, but the extreme numbers of people in our society with serious weight problems mean that endocrinological causes are very much in the minority. Hence, we need to look for other causes for obesity in the modern age. One of the biggest problems with healthy lifestyle programmes and extensive community information about diet, weight and exercise in our society is that genetics trump willpower in many cases, especially over the long-term. Following weight loss there are hormonal changes that lead to increased hunger (leptin levels fall and ghrelin levels increase) and in 2011 these changes were shown to be long lasting, so the weight-reduced individual has to fight increased hunger. Given the prolific amount of available food, temptation adds to the problem. In effect, one is then fighting nature.

By Dr Vivienne Miller
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Dr Linda Calabresi
  • Clinical Articles

Get Depressed Patients to Lift Weights

Resistance exercise training significantly reduces depressive symptoms, a new meta-analysis has found. According to international researchers who looked at over 30 randomised clinical trials on the subject, resistance exercise training including activities such as weight lifting reduced depressive symptoms by an average of a third. In fact, the meta-analysis findings suggested that resistance exercise training may be particularly helpful for reducing symptoms in patients with more severe depression. The study results, published in JAMA Psychiatry, concluded that only four people needed to be treated in order to have one to show significant benefit from the intervention. And the improvement inn depressive symptoms occurred regardless of the patient’s overall health status, the volume of resistance training exercise the patient undertook or any improvements in strength the patient experienced. And while the study authors made sure to point out their analysis was not comparing this exercise program with other treatments for depression, reducing symptoms by an average of a third certainly compares with other treatments currently available for this condition. “The available empirical evidence supports [resistance exercise training) as an alternative or adjuvant therapy for depressive symptoms,” the researchers said. What we still don’t know, apparently is exactly what sort of exercise, at what intensity, how frequently and for how long is required until a significant improvement in the depression is achieved. Many of the randomised controlled trials included in the meta-analysis did not measure all these parameters. What the researchers did find was that supervised training programs appeared more effective than non-supervised, which may reflect adherence to the exercise regimen. They also said the most common frequency of resistance exercise training was three times a week. The study authors suggested the limitations of the studies included in this analysis should help direct further research. “Future trials, matching different exercise modes on relevant features of the exercise stimulus, will allow more rigorous and controlled comparisons between exercise modalities, and the examination of interactions between factors such as frequency, intensity, duration and exercise modality,” they said. But regardless of the lack of fine print, the results of this moderate-sized effect of resistance exercise training reported in this study and the complete lack of adverse effects, would seem sufficient to justify recommending it to patients with depression, at least as an adjunctive treatment for one of Australia’s most common mental illnesses. Ref: JAMA Psychiatry doi:10.1001/jamapsychiatry.2018.0572

By Dr Linda Calabresi
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Dr Vivienne Miller
  • Clinical Articles

What Now with Vaginal Mesh for Prolapse?

Based on an interview with Melbourne urologist, Dr Caroline Dowling conducted in March, 2018 Australia was the first country to ban vaginal mesh products used surgically via transvaginal implantation for the treatment of pelvic organ prolapse. Australia was also a leader in evaluating the complications of these implant, through large scale research.1 On November 28th 2017, the Therapeutic Goods Administration withdrew implants for use in prolapse, stating it “was of the belief that the benefits of using transvaginal mesh products in the treatment of pelvic organ prolapse do not outweigh the risks these products pose to patients”. There are unique risks related to mesh use. These include mesh erosion (up to 14% of cases)1, vaginal and groin pain (up to 3% to 4%)1 and mesh exposure. These complications may be more common and more severe (requiring surgery) if the mesh is used for prolapse repair, as opposed to the treatment of stress incontinence. Reports of complications associated with transvaginal mesh products began over a decade, with the Food and Drug Administration issuing an alert about their use back in 2008. Repeated warnings were then given. In 2013, legal action began in Australia with 300 women registering for a national class action against Johnson & Johnson Medical Australia. So what do GPs tell their patients who have a vaginal mesh in situ, and what alternative managements are there for vaginal prolapse and stress incontinence? Patients who feel they have complications should be reviewed by the surgeon who operated on them, but it worth noting that most women have had no problems with these products and so, in the absence of symptoms may be reassured that they need no further management. “Women who have no problems from their transvaginal mesh implants should be reassured that they do not require them to be removed,” says Melbourne urologist Dr Caroline Dowling There is not an inherent risk with mesh as an implant, it is used widely in general surgery for inguinal hernia and abdominal wound repair. Nonetheless, it would be wise to explain the possible side-effects of the vaginal mesh in case these occur in the future. Alternatives to the vaginal mesh implant are the traditional vaginal prolapse repair using native tissue, and these are effective procedures for most women seeking surgical treatment of their prolapse. There are several alternatives to mesh for the treatment of stress incontinence that has failed conservative therapy, including an autologous fascial sling, bulking agents and Burch colposuspension. In 2015, the Cochrane Incontinence Group concluded that mid-urethral slings were highly effective in the short-term and medium-term and had a good safety profile. The mid-urethral sling remains available in its retropubic and transobturator form, but patients can no longer access mini-slings or single incision slings outside trial settings. This may change once the results of longer term studies become available. Single incisions may have a more favourable side-effect profile than full-length slings. More conservative management includes pelvic floor exercises and silicon pessaries inserted for prolapse and stress incontinence treatment. Pelvic floor exercises may be difficult to do effectively and repeatedly for many women, especially over time. They may also be less effective in cases of significant cystocoele. Silicon pessaries are particularly useful in women who are symptomatic but wish to have further pregnancies, in women who do not want surgery, in the elderly and for those in poor health.3 Patients may need help with the insertion and correct placement, but pessaries work well and may be an underutilised option.
  1. A/Prof. Christopher Maher, Explaining the Vaginal Mesh Controversy. Royal Brisbane and Women's and Wesley Hospitals Brisbane, The University of Queensland. June 17th
https://medicine.uq.edu.au/article/2017/06/explaining-vaginal-mesh-controversy
  1. Ford et al. Mid-urethral sling operations for stress urinary incontinence in women. Cochrane Incontinence Group, July 2015.
http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD006375.pub3/abstract
  1. Jones, K. Harmanli, O. Pessary Use in Pelvic Organ Prolapse and Urinary Incontinence. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876320

By Dr Vivienne Miller
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Dr Linda Calabresi
  • Clinical Articles

Managing the cardiovascular time bomb in patients on antipsychotics

The physical health of mentally ill patients is a "massive problem and we are doing very badly at it,” psychiatrist Dr Matthew Warden told doctors at a recent Healthed evening seminar in Sydney. In particular, the prevalence of high cardiovascular risk among patients with a history of psychosis, means this population was a "ticking time bomb", said Dr Warden, who is the Director of Acute Inpatient Services for Mental Health at St Vincent’s Hospital in Melbourne. Even without antipsychotic medication, a disproportionate number of people with a history of psychosis are overweight or obese, do very little if any physical exercise and smoke. And it is well-known that the metabolic side-effects associated with antipsychotic medications increases this cardiovascular risk enormously. Consequently, there has been growing pressure on psychiatrists to assess, monitor and manage the physical health of their patients with psychosis, but Dr Warden said, realistically this needs to be also done by GPs as they will usually be managing these patients long-term and "they are better at it.” Baseline metabolic measurements need to be taken at first episode of psychosis, including weight, BMI, BP, lipid levels, fasting blood sugar and smoking status. Weight, in particular needs to be monitored carefully following the commencement of antipsychotic medication, as weight gain is extremely common, especially with olanzapine which, Australia-wide is the most commonly prescribed antipsychotic. In answer to a GP’s question following his talk, Dr Ward said it is extremely difficult to avoid or reverse this medication-induced weight gain with diet and exercise alone. In addition, weight loss pharmacotherapy such as phentermine is contraindicated in people with a history of psychosis. Key to managing the weight gain issue was to choose an antipsychotic with the least long-term side effects from the outset. Olanzapine and clozapine are associated with the greatest weight gain while lurasidone and the partial agonists, aripiprazole and ziprasidone have the least effect on weight. Alternatively, for patients who may have been started on olanzapine or similar, swap to a more weight-neutral medication at the first sign they were gaining weight or developing other metabolic side-effects. It is more likely that a person who as gained weight on olanzapine, will lose that weight if switched to another weight-neutral medication early. The longer that patient stays on olanzapine and the weight gain is sustained, the harder it will be to shift even if the medication is changed, Dr Warden said. In addition to managing weight gain in mentally ill patients, Dr Warden also encouraged GPs to offer smoking cessation advice and help. Even though this population were often considered among the most dependent and heaviest smokers, his own research had found a significant number of patients could successfully quit or at the least cut down given the right advice and assistance. While most smoking cessation pharmacotherapy could be used, Dr Warden suggested that varenicline (Champix) was probably best avoided in these patients. At St Vincent’s Hospital in Melbourne, patients receiving antipsychotic therapy have their metabolic markers assessed at admission and at regular intervals after that, including measuring their serum prolactin. “Hyperprolactinaemia is a significant problem and should be monitored every six months if it is elevated or increasing particularly if there are symptoms then either reduce the dose or change antipsychotic or add in low dose aripiprazole which will lower prolactin levels,” Dr Warden explained.   Dr Matthew Warden spoke on the “Management of Metabolic Dysregulation in Patients on Antipsychotics” at the Healthed, Mental Health in General Practice Evening Seminar held in Sydney in June, 2018.

By Dr Linda Calabresi
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Dr Jenny Robson
  • Clinical Articles

Detecting and treating Mycoplasma genitalium

Mycoplasma genitalium (M. genitalium), is thought to affect up to 400,000 Australians. It causes urethritis in men, and in women it can lead to pelvic inflammatory disease, cervicitis and preterm labour. It is also a recognised cause of anorectal proctitis along with other infections including Chlamydia trachomatis (including the LGV strains), gonorrhoea, syphilis, HSV and shigellosis. Asymptomatic infection is also common. Who to test Only test those with symptoms and their contacts. Screening asymptomatic people for M. genitalium is not currently recommended. Diagnosis Females: PCR on endocervical or vaginal swab, first pass urine (FPU), ThinPrep -collected by cervical brush/swab. Males: PCR on urethral swab (in preference to FPU), anorectal swabs. Throat swabs are not recommended as pharyngeal infection is uncommon. Transport: Ambient temperature; if there is any delay from collection to transport to the laboratory, the sample must be refrigerated Current treatment recommendations Preliminary data from the patient populations suggests resistance rates to macrolides may be as high as 64 per cent. The highest rates are likely to be in the men who have sex with men (MSM) population. Although information regarding fluoroquinolone resistance (moxifloxacin) is not available with this test, some studies suggest resistance to fluoroquinolones is present in 10–15% of infections. Doxycycline alone is ineffective in two-thirds of infections but will lower bacterial load in most cases, increasing the likelihood of cure with a subsequent antibiotic. Pretreating M. genitalium infections with doxycycline for one week and then treating susceptible infections with azithromycin and macrolide-resistant infections with a fluoroquinolone eradicates >90% of infections. Current treatment regimens Macrolide sensitive Doxycycline 100mg bd for seven days followed by azithromycin 1g stat then 500mg daily for three days (total 2.5g) OR Doxycycline 100mg bd for seven days followed by azithromycin 1g single dose. It is not known to what extent the improved outcomes resulting from the use of doxycycline followed by 2.5g azithromycin are due to this dose of azithromycin, rather than simply the pre-treatment with doxycycline. The higher dose of azithromycin requires a private prescription. Macrolide resistant Doxycycline 100mg bd for seven days followed by moxifloxacin 400mg daily for seven days. A longer course of moxifloxacin may be required in women with pelvic inflammatory disease. Moxifloxacin requires a private prescription, cannot be used in pregnancy and is expensive. It is associated with diarrhoea, occasional tendinopathy and rare neurological and cardiac events. Treatment failures following appropriate fluoroquinolone treatment may require specialist advice. Additional actions Advise no sex without condoms until tested for cure (14 days after completion of treatment). Advise no sex with untested previous sexual partners. Test of cure Test of cure by PCR should be done at least two weeks after treatment is completed i.e. four weeks after commencing therapy. Contact tracing In heterosexuals, the risk of PID and reproductive complications suggests a greater need to trace, test and treat infected contacts. The time period for contact tracing is unknown. Asymptomatic infection and macrolide resistance are more common in MSM and there is only limited evidence that this is harmful. As moxifloxacin will probably be required for treatment, contact tracing may be best confined to continuing partners of a symptomatic person.   References: Australian STI Management Guidelines for Use in Primary Care http://www.sti.guidelines.org.au/sexually-transmissible-infections/mycoplasma-genitalium#management Australian Contact Tracing Manual contacttracing.ashm.org.au/conditions/when-contact-tracing-is-recommended/mycoplasma-genitalium   General Practice Pathology is a new 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.

By Dr Jenny Robson
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Megan Lee & Joanne Bradbury
  • Clinical Articles

Five Types of Food to Increase Your Psychological Well-Being

We all know eating “healthy” food is good for our physical health and can decrease our risk of developing diabetes, cancer, obesity and heart disease. What is not as well known is that eating healthy food is also good for our mental health and can decrease our risk of depression and anxiety. Mental health disorders are increasing at an alarming rate and therapies and medications cost $US2.5 trillion dollars a year globally. There is now evidence dietary changes can decrease the development of mental health issues and alleviate this growing burden. Australia’s clinical guidelines recommend addressing diet when treating depression. Recently there have been major advances addressing the influence certain foods have on psychological well-being. Increasing these nutrients could not only increase personal well-being but could also decrease the cost of mental health issues all around the world. 1. Complex carbohydrates One way to increase psychological well-being is by fuelling brain cells correctly through the carbohydrates in our food. Complex carbohydrates are sugars made up of large molecules contained within fibre and starch. They are found in fruit, vegetables, and wholegrains and are beneficial for brain health as they release glucose slowly into our system. This helps stabilise our mood. Simple carbohydrates found in sugary snacks and drinks create sugar highs and lows that rapidly increase and decrease feelings of happiness and produce a negative effect on our psychological well-being. We often use these types of sugary foods to comfort us when we’re feeling down. But this can create an addiction-like response in the brain, similar to illicit drugs that increase mood for the short term but have negative long-term effects. Increasing intake of complex carbohydrates and decreasing sugary drinks and snacks could be the first step in increased happiness and well-being. 2. Antioxidants Oxidation is a normal process our cells carry out to function. Oxidation produces energy for our body and brain. Unfortunately, this process also creates oxidative stress and more of this happens in the brain than any other part of the body. Chemicals that promote happiness in the brain such as dopamine and serotonin are reduced due to oxidation and this can contribute to a decrease in mental health. Antioxidants found in brightly coloured foods such as fruit and vegetables act as a defence against oxidative stress and inflammation in the brain and body. Antioxidants also repair oxidative damage and scavenge free radicals that cause cell damage in the brain. Eating more antioxidant-rich foods can increase the feel-good chemicals in our brain and heighten mood. Antioxidants can help restore the happy chemicals in the brain. www.shutterstock.com.au 3. Omega 3 Omega 3 are polyunsaturated fatty acids that are involved in the process of converting food into energy. They are important for the health of the brain and the communication of its feel-good chemicals dopamine, serotonin and norepinephrine. Omega 3 fatty acids are commonly found in oily fish, nuts, seeds, leafy vegetables, eggs, and in grass fed meats. Omega 3 has been found to increase brain functioning, can slow down the progression of dementia and may improve symptoms of depression. Omega 3 are essential nutrients that are not readily produced by the body and can only be found in the foods we eat, so it’s imperative we include more foods high in omega 3 in our everyday diet. 4. B vitamins B vitamins play a large role in the production of our brain’s happiness chemicals serotonin and dopamine and can be found in green vegetables, beans, bananas, and beetroot. High amounts of vitamins B6, B12, and folate in the diet have been known to protect against depression and too low amounts to increase the severity of symptoms. Vitamin B deficiency can result in a reduced production of happiness chemicals in our brain and can lead to the onset of low mood that could lead to mental health issues over a long period. Increasing B vitamins in our diet could increase the production of the feel good chemicals in our brain which promote happiness and well-being. 5. Prebiotics and probiotics The trillions of good and bad bacteria living in our tummies also influence our mood, behaviour and brain health. Chemical messengers produced in our stomach influence our emotions, appetite and our reactions to stressful situations. Prebiotics and probiotics found in yoghurt, cheese and fermented foods such as kombucha, sauerkraut and kimchi work on the same pathways in the brain as antidepressant medications and studies have found they might have similar effects. Prebiotics and Probiotics have been found to suppress immune reactions in the body, reduce inflammation in the brain, decrease depressed and anxious states and elevate happy emotions. Incorporating these foods into our diet will not only increase our physical health but will have beneficial effects on our mental health, including reducing our risk of disorders such as depression and anxiety.   Disclosure Statement Megan Lee receives funding from Southern Cross University and Santos Organics Joanne Bradbury receives funding from the Australian Traditional-Medicinal Society (ATMS), Santos Organics, and Metagenics to support academic research

By Megan Lee & Joanne Bradbury
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Kevin Davies, Jessica Eccles & Neil Harrison
  • Clinical Articles

What Causes Fibromyalgia?

Fibromyalgia is something of a mystery. It can’t be detected with scans or blood tests, yet it causes lifelong pain for millions of people. The disease mainly affects women (about 75-90% of cases), causing pain all over the body. Because not all healthcare professionals are adept at identifying and diagnosing fibromyalgia, reported rates of the condition vary greatly from country to country. In China, it affects only 0.8% of people, in France around 1.5%, in Canada 3.3%, and in Turkey 8.8%. Estimates in the US range from 2.2% to 6.4%, and in Russia, about 2% of the population is affected. People with the condition are often diagnosed if they have longstanding muscle pain, bone or joint pain and fatigue. Fibromyalgia can also cause insomnia, “brain fog”, some symptoms of depression or anxiety, as well as a range of other complaints, including irritable bowel syndrome and headache. Many patients are also hypermobile (“double-jointed”), and there is some overlap with chronic fatigue syndrome (also known as ME). Guidelines from the American College of Rheumatology make it clear that the diagnosis should be made using defined criteria based on the “widespread pain index” (which scores the number of painful regions out of 19) coupled with a symptom severity scale. The diagnosis also takes fatigue, generalised pain, unrefreshing sleep and cognitive symptoms into account. It doesn’t matter if the patient has another rheumatic disease, they can still be diagnosed with fibromyalgia. The scoring system, recommended by the American College of Rheumatology, is often used in clinical trials, but in the clinic, most doctors rely on detecting tender points in specific places and on excluding other medical conditions, including rheumatic conditions. Unlike say, rheumatoid arthritis or lupus, the tests do not show clear evidence of inflammation or autoimmunity (when the body’s immune system attacks itself) and scans are normal. The lack of inflammation or structural abnormality in muscles or joints – aside from making diagnosis difficult – is the main reason there are no widely accepted or effective treatments. In rheumatic diseases, where we understand the mechanisms that underlie the condition, we have the most effective treatments. In rheumatoid arthritis, for example, we know that much of the inflammation is caused by a cell-signalling protein (cytokine) called tumour necrosis factor and that blocking the activity of this protein switches off the disease in most patients. A number of possible mechanisms have been proposed in fibromyalgia, including abnormal muscle metabolism, reduced levels of steroid hormones such as cortisol, or abnormal small nerve fibres. But these abnormalities aren’t found in all patients with the condition. As such, they can’t be used as part of a diagnostic test, nor can they help develop treatments. Some experts have suggested that fibromyalgia may be related to abnormalities in the autonomic nervous system – the part of the nervous system that controls bodily functions, such as heart rate and blood pressure – and how the brain responds to pain signals and reacts to external stressors (such as infections). But there is currently no hard evidence to back up this theory. Looking for clues To fill in some of the gaps in our knowledge about this devastating condition, our research team at Brighton and Sussex Medical School is investigating the potential role of the autonomic nervous system and inflammation in fibromyalgia and chronic fatigue syndrome. For our study, we have two groups of patients: one with pain as the main symptom and the other with fatigue as the main symptom. We also have matched controls – people without the disease, but otherwise similar characteristics – to make meaningful comparisons. The study is in two parts. First, we will test the patients’ autonomic nervous system using a tilt-table. This involves tilting the person head downwards to see how well their body adapts to this change in posture by changing heart rate and blood pressure (both of which are monitored during the test).Second, we will stimulate patients’ immune systems with a typhoid vaccine (the normal type used in travellers) and perform magnetic resonance brain scans to look for changes in blood flow and also measure the levels of “inflammatory mediators” (the chemicals the body produces in response to stimuli of this type), to see whether these are higher in the fibromyalgia patients. Our study should, for the first time, help us to address the question of whether there really is an abnormal brain response to inflammation or infection in these patient groups and enable us to explore the relationship between the abnormal functioning of the autonomic nervous system and fibromyalgia and chronic fatigue syndrome. Fibromyalgia rarely goes away and treatment options are limited. Only by developing a proper understanding of the disease processes underlying this condition will doctors be able to make a clear, positive diagnosis, and most importantly, offer effective therapy.   Disclosure Statement Kevin Davies receives funding from AR-UK. Jessica Eccles receives funding from Academy of Medical Sciences, National Institute of Health Research, MQ Neil Harrison receives funding from the Wellcome Trust, Medical Research Council (MRC), Arthritis Research UK, and Janssen Pharmaceuticals.

By Kevin Davies, Jessica Eccles & Neil Harrison
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Dr Linda Calabresi
  • Clinical Articles

Vaccinating the Immunosuppressed – Who, What and When

Vaccination in immunosuppressed adult patients has many facets and can be challenging for GPs who don’t deal with these cases regularly. But there are a few key considerations that can help guide clinicians, says Associate Professor Michael Woodward, Melbourne-based geriatrician, writer, researcher and passionate advocate for health promotion. Firstly, not all immunosuppression is equal. It is important to ascertain the degree of immunosuppression, as some people may be being unnecessarily denied vaccines because they are taking medication that can suppress the immune system but only at higher doses or in different formulations. “For instance, someone who is on inhaled corticosteroids for their asthma or on low dose (less than 20mg) prednisolone daily for just a few weeks is not significantly immunosuppressed and can be vaccinated in the same way as other people,” said Professor Woodward in an interview following his presentation at Healthed’s recent Annual Women's and Children’s Health Update in Perth. However, those on higher doses of steroids or on steroids more long-term, as well as those people who have conditions associated with immunosuppression such as haematological malignancy do need special consideration when it comes to vaccination. Most importantly, live vaccines are not to be given to this group. This includes the new herpes zoster vaccine (Zostavax), which absolutely contraindicated in severely immunocompromised patients. The consequences of inadvertently administering this vaccine to an immunosuppressed patient hit the headlines some months ago, highlighting the importance of this guideline. The other question often asked is whether patients who are known to be immunosuppressed, and therefore at greater risk of significant infections actually need more or stronger doses of the vaccines they are able to have. In some cases that is a very real and worthwhile consideration if you want to achieve the objective of immunoprotection, Professor Woodward said. For example, you might consider giving an immunosuppressed patient the pneumococcal vaccine (Prevenar 13) as opposed to the polysaccharide pneumococcal vaccine (Pneumovax 23). “The conjugate vaccine is generally slightly more likely to produce an immune response [than the polysaccharide vaccine],” he said. The other scenario where GPs might need to be considering vaccination in association with immunosuppression, is in patients who are scheduled for an elective splenectomy. The lack of a spleen is known to be associated with a reduction of the body’s ability to respond to a vaccine, so it is currently recommended that people who are about to undergo a splenectomy have the influenza, pneumococcal and the newer zoster vaccine. In addition, they should be vaccinated against H. influenza B and receive the two meningococcal vaccines currently available. All these are detailed as part of the pre-splenectomy recommendations on the spleen.org.au website, with the exception of the zoster vaccine, as the guidelines have yet to be updated. However, Professor Woodward says most health professionals in this area are advocating the inclusion of the zoster vaccine. Some of these vaccinations may also be given shortly after the removal of the spleen in cases where the splenectomy has been urgent, but this is generally not the remit of the GP. In general, the question of vaccination in the immunosuppressed patient can be complicated. It is a highly specialised area and Professor Woodward suggested, if in doubt GPs might want to seek input from a specialist in this area such as an immunologist or a rheumatologist.

By Dr Linda Calabresi
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Dr Linda Calabresi
  • Clinical Articles

Stillbirth a Higher Risk for New Australians

It appears we might still be failing some of our poorer migrant women, with new study finding that they have higher rates of stillbirth compared to Australian-born mothers. Analysing data from stillbirths that occurred in Western Australia over the period 2005 to 2013, researchers found that while stillbirth rates overall were low and often much lower than in these migrant women’s country of birth, they were higher in non-Australian born women, especially in those women who were born in Africa. Published recently in The Medical Journal of Australia, the study also took note of whether the deaths occurred in the antepartum period (between 20 weeks gestation up to before labour commences) or the intrapartum period (which is the period after labour has started), in an attempt to determine when and in whom intervention might be warranted. Researchers found the key factor was the woman’s country of birth rather than her ethnic origin, as there appeared no difference in stillbirth rates among white and non-white Australian-born women. However, women born in Africa were twice as likely to have a stillbirth in the weeks before going into labour compared with Australian-born women. And Indian-born women were 70% more likely. Migrant women born in other countries collectively had an increased risk of about 40% of an antepartum stillbirth. And frighteningly, it appeared the rates of stillbirth occurring once labour had started were also much higher than that which occurs in Australian born women. Almost twice the risk for most migrant women, and more than double that again for African-born women. “That the rate intrapartum stillbirth was twice as high among African women is especially worrying, as intrapartum stillbirth is regarded as preventable and indicative of inadequate quality of care,” the study authors wrote. So why is this happening, the researchers asked. Why is it, that, despite access to the same standard of healthcare as the rest of the Australian population, these women are more at risk of losing their babies, especially African-born women and especially so late in the pregnancy? The study authors suggest cultural issues may play a major role. They point to statistics that show African-born women are more likely to have pregnancies lasting 42 weeks or more, a well-recognised risk factor for stillbirth. Qualitative studies have also determined there is often, particularly among African-born women, a deeply-held suspicion of interventions in pregnancy believing them to interfere with the natural process of childbirth and possibly having long-term repercussions. Consequently, there is not only a poorer attention to antenatal care but also a resistance to procedures such as induction of labour and caesarean section. “More in-depth investigation of the patterns of health service use, pregnancy, and labour care for migrant women, particularly African migrants, is warranted,” the researchers said. They suggest education is the most likely solution, but the changing of what is likely to be long-held and culturally-associated attitudes will need both sensitivity and intelligence. “Culturally appropriate antenatal engagement and educational programs about the risk of stillbirth and the indications for and the safety of induction and related interventions may be useful preventive strategies,” they concluded.  

Reference

Mozooni M, Preen DB, Pennell CE. Stillbirth in Western Australia, 2005–2013: the influence of maternal migration and ethnic origin. Med J Aust. 2018; 209(9): 394-400. DOI 10.5694/mja18.00362
By Dr Linda Calabresi
pregnancy
Dr Julia Marcello
  • Clinical Articles

Antidepressants in Pregnancy

“Be patient with yourself… nothing in Nature blooms all year.” One of my favourite quotes regarding perinatal depression and anxiety which affects 10-16% of all new parents. The importance of perinatal mental health cannot be overstated. Research has shown that an untreated perinatal mental health condition can lead to substance misuse, poor antenatal attendance as well as poor self-care. There is also a risk of poor attachment to the infant, and a long-term risk of poor child development outcomes through neglect. Suicide is the final risk. The government have recently supported our concerns regarding this important topic by changing the MBS item numbers (16590, 16591, 16407) to include a mental health assessment. We have a duty of care to our patients to know what is safe to prescribe or continue to use in pregnancy- remembering that pregnancy is not protective against mental illness. Did you know that more than half of all women abruptly discontinue antidepressant medication upon confirming a pregnancy? Almost 70% of these women suffer a relapse of depression. Currently the recommendations for a woman on an antidepressant who has been euthymic for at least 12 months include cease the medication in pregnancy, continue the current medication, change to an alternative, safer medication or cease the medication and then reintroduce it if a relapse occurs. Antidepressant medications can cross the placenta, meaning the fetus is exposed. There are also potential pregnancy complications, but the risks to the fetus and the pregnancy are very low. Congenital malformation may occur from exposure to some antidepressants in the first trimester. Growth restriction and neurobehavioural problems may result from exposure in the second trimester. And congenital cardiac defects have been associated with paroxetine use in pregnancy. Postpartum haemorrhage is the only significant potential obstetric complication associated with SSRI and SNRI use. There is also a small increased risk of persistent pulmonary hypertension of the newborn associated with SSRI, SNRI and TCA use in late pregnancy. Antidepressants taken in late pregnancy, may also cause poor neonatal adaptation syndrome (PNAS). This manifests as hypotonia, respiratory distress, hypoglycaemia, seizures and most commonly ‘jittery-ness’ in the infant. Paroxetine has the highest risk of PNAS. Despite this, it is NOT recommended that the dose of medication be reduced in late pregnancy. Because the fetus may not clear the medication in the same way the mother does, lowering the dose might simply risk a relapse of depression in the mother while gaining little or no benefit to the infant. RANZCOG states that SSRIs are generally considered low risk and safe to prescribe in pregnancy and breastfeeding. It is important to know that sertraline has the lowest placental exposure and the lowest excretion into breastmilk. Other medications are listed in the table below as a quick reference guide:

Table 1. ANTIDEPRESSANT CATEGORIES FOR PREGNANCY AND BREASTFEEDING:

Medication Pregnancy Category Breastfeeding
TCAs * avoid doxepin during breastfeeding C Compatible
Citalopram C Compatible
Escitalopram *preferred to citalopram in breastfeeding C Compatible
Fluoxetine C Compatible
Mirtazapine C Compatible
Paroxetine *can cause cardiac defects with high dose first trimester but safest for breastfeeding along with sertraline D Compatible
Sertraline B Compatible
Venlafaxine C Compatible
Compatible- an acceptably low relative infant dose or no significant plasma concentrations or no adverse effects in breastfed infants. When managing perinatal depression is it important to consider potential risk against the known benefits of the medications and the potential detrimental effects of mental illness on the development of the infant and other children in the home.

Key References:

  1. The Royal Australian and New Zealand College of Obstetricians and Gynaecologists.  Perinatal Depression and Anxiety: C-Obs 48. East Melbourne (AU): RANZCOG; Mar 2015. 16 p. RANZCOG Cat. No.: C-Obs 48. Available from: https://www.ranzcog.edu.au/RANZCOG_SITE/media/RANZCOG-MEDIA/Women%27s%20Health/Statement%20and%20guidelines/Clinical-Obstetrics/Mental-health-care-in-the-perinatal-period-(C-Obs-48).pdf?ext=.pdf
  2. White L. Antidepressants in Pregnancy. O&G Magazine. 2018; 20(3): 24-25. Available from: https://www.ogmagazine.org.au/20/3-20/antidepressants-in-pregnancy/
  3. Galbally M, Lewis AJ, Snellen M. Introduction Pharmacological management of major depression in pregnancy. In: Gabally M, Snellen M, Lewis AJ, editors. Psychopharmacology and Pregnancy. Berlin: Springer; 2014. p. 67-85.
  Dr Julia Marcello works at Bentley Maternity Unit which provides maternity services to low risk women in WA. The unit is staffed by GP obstetricians, specialist obstetricians and gynaecologists and midwives and offers the option of private care within a public setting. The midwife service is available to low risk women and includes antenatal care, birthing services and postnatal care through the visiting midwifery service and lactation consultant support.  GP shared care services are also available. The Unit also provides a gynaecology service led by Dr Aseel Alkiaat and specialists from King Edward Hospital.  For further information go to www.bhs.health.wa.gov.auFor-health-professionals
By Dr Julia Marcello
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Dr Linda Calabresi
  • Clinical Articles

Probiotics Don’t Help in Kids’ Gastro

Giving children with acute gastroenteritis probiotics will not help them recover more quickly, according to two large randomised controlled trials. At least if the probiotic includes Lactobacillus rhamnosus. The research, published in the New England Journal of Medicine, provides solid evidence against the adjunctive treatment, which, as the study authors point out, has been recommended by many health professionals and authoritative bodies. “Many experts consider acute infectious diarrhoea to be the main indication for probiotic use,” they said. However, the two studies, both conducted on children aged three months to four years with a less than 72-hour history of acute vomiting and diarrhoea, failed to show any benefit of taking a five-day course of the probiotics. One of the studies conducted across six tertiary paediatric centres in Canada, involved almost 900 children with acute gastroenteritis randomly assigned to receive either a combination probiotic (L. rhamnosus and L. helveticus) or placebo. The other very similar study, this one involving US centres, included 970 children with gastroenteritis and tested the effectiveness of giving the single probiotic Lactobacillus rhamnosus against placebo. The results of the two trials, using almost identical outcome measures were the same – the probiotics did not make a difference. “Neither trial showed a significant difference in the duration of diarrhoea and vomiting, the number of unscheduled visits to a health provider or the duration of day-care absenteeism,” an accompanying editorial concluded. The role of probiotics in the management of gastroenteritis in children has been an area of controversy and contradiction not only among individual specialists but also among different expert bodies, with guideline recommendations varying from “not recommended” by the Centers of Disease Control and Prevention to “strongly recommended” by the European Society for Pediatric Gastroenterology, Hepatology and Nutrition. But now, it appears this grey area has now become very black and white. “Taken together, neither of these large, well-done trials provides support for the use of probiotics containing L. rhamnosus to treat moderate-severe gastroenteritis in children,” the editorial stated. The caveat, of course, is that this evidence while robust only applies to this particular probiotic. There might still be probiotics out there that do make a difference. The editorial author referred to a recent large randomised-controlled trial conducted in rural India that found giving healthy newborns the probiotic, L. planatarum in the first few days of life was associated with a significantly lower risk of sepsis and lower respiratory tract infection in the subsequent two months. So while these studies might appear to be the nail in the coffin for L. rhamnosus -containing probiotics, it is still a case of ‘watch this space’ with regard the role of probiotics more generally.

Reference

Schnadower D, Tarr PI, Casper TC, Gorelick MH, Dean JM, O'Connell KJ, et al. Lactobacillus rhamnosus GG versus Placebo for Acute Gastroenteritis in Children. N Engl J Med. 2018 Nov 22; 379(21): 2002-2014. DOI: 10.1056/NEJMoa1802598 Freedman SB, Williamson-Urquhart S, Farion KJ, Gouin S, Willan AR, Poonai N, et al. Multicenter Trial of a Combination Probiotic for Children with Gastroenteritis. N Engl J Med. 2018 Nov 22; 379(21): 2015-26. DOI: 10.1056/NEJMoa1802597 LaMont JT. Probiotics for Children with Gastroenteritis. N Engl J Med 2018 Noc 22; 379(21): 2076-77. DOI: 10.1056/NEJMe1814089
By Dr Linda Calabresi
pregnancy
Dr Linda Calabresi
  • Clinical Articles

Safety Data on Ondansetron in Pregnancy

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]
By Dr Linda Calabresi

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