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Dermatology

Clinical Articles

Focus on dermatophytes

Once specimens are received in the laboratory, microscopy is performed. An interim report is then released. Specimens are then set up on specialised agar containing antibiotics and cycloheximide to inhibit the growth of bacteria and saprophytic fungi. Cultures are incubated at 28°C for three weeks. If microscopy is positive (M+) and no pathogen (C-) has grown in the interim, specimens are held an extra week. Infrequently, where microscopy and culture of nail scrapings is negative and the diagnosis is still suspected, nails can be examined for fungal elements using special stains.

Results:

Specimen types have been subdivided into three anatomical categories (nails, hair and skin) based broadly on the three clinical presentations of onychomycosis, tinea capitis, and tinea corporis/ cruris/pedis. Onychomycosis refers to fungal infections of the nails and includes tinea unguium caused by dermatophytes but also non-dermatophyte fungi and yeasts, predominantly Candida spp.

Negative laboratory report:

A common reason for negative microscopy and /or culture is an incorrect clinical diagnosis. More than 50% of dystrophic nails do not have a fungal cause, so it is important to establish a correct laboratory diagnosis before treating a patient with an antifungal agent. Other reasons for false negative results include sampling variation associated with an inadequate specimen and/or splitting the sample to perform microscopy and culture; the presence of nonviable hyphae in the distal portion of the nail; uneven colonisation of the nail by fungus; and overgrowth by contaminant saprophytic fungi. Careful re-collection to obtain sufficient material may be necessary to confirm negative results.

Nails:

The analysis of nail specimens from the hands and feet. Fingernails: Of 1202 specimens processed, 59% were negative by both microscopy and culture; 11% had hyphae seen on microscopy but were negative by culture; 27% of all finger and thumbnail cultures grew a yeast, predominantly Candida albicans (88% of all positive nail/hand cultures). Only 3% of all fingernail specimens grew a dermatophyte.

Toenails:

57% of 5097 toenail cultures were negative by both microscopy and culture. 22% were positive by microscopy but culture negative for reasons stated previously. As the literature would suggest, yeast infection of toenails is rare. Dermatophytes (20%) predominate as the main cause of onychomycosis of the lower limbs. Transmission of these dermatophytes is usually via the feet and toe web spaces, which are the major reservoir on the human body. Onychomycosis can be regarded as the end stage of tinea pedis. Desquamated skin scales containing hyphae are shed and survive for months to years on floors and carpets. Infrequently non-dermatophyte moulds are implicated in toenail infections such as Aspergillus. There is some uncertainty as to the significance of these cultures, and repeat culture may be indicated.

Treatment options:

With tinea unguium, topical treatment is successful only with surgical removal of the nail combined with oral therapy. First-line treatment for all types of nail tinea consists of: 1. terbinafine (child < 20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for six weeks for fingernails and 12 weeks for toenails or (if terbinafine is not tolerated) 2. itraconazole 200 mg orally, twice daily for seven days every month for 2-4 months or 3. fluconazole 150 to 450 mg orally, once weekly for 12 to 52 weeks. Successful management of candidiasis of the nail requires removal of risk factors e.g. water immersion.

Tinea capitis:

Of 414 hair samples submitted over this period, 329 (80%) were negative by both microscopy and culture. Dermatophytes isolated include M. canis (46%); T. tonsurans (42%); M. gypseum (5%); T. mentagrophytes (5%) and T. rubrum (2.5%). This condition afflicts predominantly prepubertal children. Clinically it can present as alopecia or a more inflammatory lesion (kerion). It is noteworthy that T. tonsurans, an anthropophilic fungus, is emerging as a common cause of tinea capitis in children and spreads easily from child to child.

Treatment options:

Tinea capitis often requires oral therapy to eradicate the infection. Treatment options include 1. griseofulvin fine particle (child: 20 mg/kg up to) 500 mg orally, daily for 4-8 weeks, or 2. terbinafine (child< 20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for four weeks.

Tinea corporis/cruris/pedis:

Of the 7406 specimens received from skin sites, 73% were both microscopy and culture negative; 5% were positive only by microscopy. Of the 22% culture positive specimens, 19% grew a dermatophyte and 3% a yeast.

Treatment options:

When topical treatments have failed, recommended oral therapy includes: 1. griseofulvin fine particle (child: 10 to 20 mg/kg up to) 500 mg orally, daily for at least four weeks or 2. terbinafine (child <20 kg: 62.5 mg; 20 to 40 kg: 125mg) 250 mg orally, daily for at least two weeks, depending on the response or 3. itraconazole capsules 200 mg orally, twice daily for one week for tinea of the feet or hands or 4. itraconazole capsules 200 mg orally, once daily for one week for tinea elsewhere.

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

Obstetrics and gynaecology

Clinical Articles

Fatter mothers behind rise in perinatal complications

The increasing BMI of first-time pregnant women is behind a rise in adverse perinatal outcomes over a 25 year time period, a new retrospective Australian study suggests. Analysing data from one major Sydney teaching hospital, researchers found that the prevalence of overweight among women having their first baby increased from 12.7% in 1990-94 to 16.4% in 2010-14, and that of obesity rose from 4.8% to 7.3%. More importantly they found this increase in BMI was associated with a range of adverse perinatal outcomes particularly pre-eclampsia, macrosomia and gestational diabetes. Other complications believed to have increased as a result of the maternal weight gain included caesarean deliveries, post partum haemorrhage, prematurity, admission to the special care nursery and fetal abnormalities. “We found that a substantial proportion of the burden of adverse perinatal outcomes for Australian women is linked to maternal overweight and obesity, and that this proportion has steadily increased over the past 25 years,” the Sydney researchers said. The study involved the analysis of the data recorded on over 42000 singleton births delivered to previously nulliparous women at the Royal Prince Alfred Hospital Sydney between 1990 and 2014. Interestingly over the course of the study period, the mean age for first time mothers rose from 28.7 to 31.6 years, however having adjusted for this as well as other possible confounders such as changing smoking rates, socioeconomic status, and country of birth of the mother the findings confirmed the relative risks of adverse perinatal outcomes had increased in association with rising prevalence of overweight and obesity. Researchers calculated that should overweight or obese women move down one BMI category (for example from obese to overweight) 19% of pre-eclampsia, 15.9% of macrosomia and 14.2% of gestational diabetes could be averted. “Our results indicate that the frequency of adverse perinatal outcomes could be reduced by shifting the distribution of overweight and obesity among first-time mothers by a single BMI class. Investing in obesity prevention strategies that target women prior to their becoming pregnant is likely to provide the greatest benefit,” they concluded. Ref: MJA doi:10.5694/mja17.00344

By Dr Linda Calabresi

Psychiatry

Clinical Articles

Long-term dangers of postnatal depression

There is no debate – postpartum depression can be a devastating disease for a new mother. However, what is probably less well-recognised is the long-term consequences of that illness on the child. The latest findings from an ongoing longitudinal UK study of parents and infants shows that children whose mother was assessed as having moderate to severe depression at both two and eight months after delivery had a substantially increased risk of adverse outcomes across a number of child measures from behaviour and learning to mental health up to 18 years later. The observational study known as the British Avon Longitudinal Study of Parents and Children(ALSPAC) has followed over 9800 women who were pregnant in the early 1990s. In the latest findings, published in JAMA psychiatry, the researchers noted that women who still had moderate to severe depression at eight months postpartum, were likely to still have depression 11 years later. And the children of these women had a four- fold increased risk of behaviour problems as a pre-schooler, twice the risk of being poor at maths in high school and a seven fold increased risk of depression as an adult. Conversely, if the postpartum depression was not persistent at either the moderate or severe level there appeared to be no increased risk of behaviour and learning problems or depression in the offspring, which is reassuring. The study findings published in JAMA psychiatry raise a number of interesting questions. “Having established a highly vulnerable group of mothers still does not answer the question of what to do about interventions, or who, when, or how to treat,” the author of an accompanying editorial says. The design of the study meant the researchers were unable to determine the effects of maternal treatment on reducing postpartum depression and improving child outcomes. As the editorial author also points out, there is also considerable debate whether treatment should focus mainly on the mother and her illness or be directed at the mother-infant relationship. Nonetheless, it is clear that, as a first step at least, these mothers with persistent severe depression need to be identified. Screening for depression which now focuses on pregnancy and the immediate postpartum period needs to be extended to a year after delivery. “Screening both early and late in the first postpartum year will enable the identification of women with persistent [postnatal depression] and thus the offer of appropriate treatment,” the study authors concluded. Ref: JAMA Psychiatry doi:10.1001/jamapsychiatry.2017.4363 doi:10.1001/jamapsychiatry.2017.4265

By Dr Linda Calabresi

Gastroenterology

Clinical Articles

Coeliac disease testing

Coeliac disease is a common disorder affecting the gastrointestinal tract, secondary to an immunologic reaction to gluten. At present it can only be managed by lifelong avoidance of gluten, and thus presents a challenge for patients and their health care professionals.

Epidemiology

Coeliac disease was first characterised in the late 1940s with diarrhoea and failure to thrive in young children. The wartime shortage of wheat, and adoption of a gluten-free surrogate diet, allowed their symptoms to improve. When wheat was re-introduced into their diets their condition worsened again. Initially thought to be a rare disease of children, we now recognise coeliac disease to be prevalent in adults, including the elderly. Data from the UK reveal that the most common age group diagnosed is between 30 and 45, with more people over 60 than those under 16 years (Coeliac UK: www.coeliac.co.uk). The illness occurs in people of European, Turkish, Middle Eastern, Egyptian and Indian backgrounds. It appears to be rare in sub-Saharan Africa and South-East Asia. There is debate over mass screening in populations such as in the UK and Scandinavia, where the disease incidence approaches 1%. The Gastroenterological Society of Australia (GESA) recommends screening in persons with Type 1 diabetes mellitus, Down syndrome, Turner syndrome, immunoglobulin A (IgA) deficiency, or a family history of coeliac disease, where the condition may be as common as 1 in 10.

Immunopathology

The pathologic understanding of coeliac disease has advanced considerably over the past 10 years, although our understanding is still incomplete. In some individuals, when gluten is digested the peptides cross the intestinal mucosa where they are recognised by the mucosa-associated lymphoid tissue. Those individuals with HLA-DQ2 or -DQ8 are able to process the gluten peptides, resulting in presentation of gliadin/gluten peptides on the surface of antigen-presenting cells. Over 99% of coeliac patients have HLA-DQ2 or -DQ8, and homozygotes for DQ2/8 are more likely than heterozygotes to develop the disease, and more severely. For the peptides to be presented to T cells, they must first be deamidated by a ubiquitous enzyme, tissue transglutaminase (tTG). Tissue transglutaminase alters the gluten-derived peptide so that it remains in the binding site of the HLA molecule, and allows an immune response to occur against the enterocytes that carry the HLADQ2/8-gluten peptide complex. Tissue transglutaminase is present in an active form outside cells; its usual role is to help maintain the extra-cellular matrix. Several isoenzymes of tTG exist throughout the body, tTG2 being present in the GI tract. It is the presence of IgA antibodies to this enzyme— anti-tTG2 antibodies (hereafter ‘tTG antibodies’)—that have become the gold standard serologic marker for coeliac disease. It remains uncertain why antibodies to tTG develop in coeliac patients, although research suggests that tTG can become cross-linked to the gluten peptide and cause specific tTG antibodies to develop, through a process termed ‘epitope spreading’. Tissue transglutaminase antibodies have been shown to pre-date the development of the histologic changes of coeliac disease. It is clear that antibodies to tTG are not pathogenic in most patients, as many cells in the body contain similar tTG. However, in dermatitis herpetiformis, a disease long associated with coeliac disease, these antibodies develop against tTG3 (whereas in coeliac disease they are directed against tTG2). In dermatitis herpetiformis, these tTG3 antibodies may well be pathogenic, leading to classic cutaneous lesions.

Serologic testing

IgA tTG antibodies are now considered the gold standard in the detection of coeliac disease, giving a sensitivity of around 95%, and a specificity of around 90%. IgA tTG antibodies become negative 9–12 months after the introduction of a gluten-free diet. In children less than 2 years of age, IgA production is not mature and may result in false negative IgA tTG. This is especially true for those less than one year of age. At present, all serologic diagnoses should be confirmed by histologic diagnosis, as false positives can occur. Although several studies in children have indicated that very high IgA anti-tTG results may not need to be confirmed by biopsy, Australian guidelines indicate the need for histologic confirmation. IgG tTG antibodies may also be detected in coeliac patients, though they have similar problems to IgG anti-gliadin antibodies (AGA, discussed below), with a poor sensitivity and specificity, despite initial enthusiasm for their utility. Older serologic tests for coeliac disease were based on antibodies directed against gliadin—anti-gliadin antibodies (IgA AGA and IgG AGA). Like all food antibodies, they have relatively poor sensitivity (false negatives) and particularly poor specificity (false positives), especially given that they are a group of antibodies (polyclonal), rather than being directed against a single epitope. The indication for IgA AGA is very limited and should largely be consigned to history. However, these antibodies can be used to monitor early adherence to a gluten-free diet as they become negative 6–9 months after the diet is introduced. IgG AGA, however, remains of use in IgA-deficient patients in whom IgA tTG and IgA AGA are not produced. IgG against deamidated gliadin is of use in IgA-deficient patients in whom IgA tTG and IgA AGA are not produced. This is a modified test, using a gliadin peptide (small piece of protein) that had been altered to more closely resemble the natural peptide found in wheat. IgA deficiency is defined as ‘undetectable or barely detectable’ serum IgA. IgG AGA are also of use in children less than two years of age (and especially children under one), in whom the ability to produce IgA antibodies has not fully developed. All patients with IgA deficiency in whom coeliac disease is suspected should undergo a small bowel biopsy, regardless of the IgG AGA and other testing conducted. It is suggested they be referred to a gastroenterologist, as other diseases such as chronic giardia and autoimmune enteritis may occur. One theory to explain why IgA deficiency is associated with the development of coeliac disease is that IgA is involved in the neutralisation of foreign antigens at mucosal surfaces, and these deficient individuals have greater transmucosal passage of gliadin fragments. Another type of antibody, IgA endomysial antibodies, has also been used to test for the disease in the past. These antibodies were first detected in monkey oesophagus; it is now recognised that the antigen being detected by this method was tTG. These antibodies are highly specific (~ 100%) but have a slightly lower sensitivity (~ 90%) than IgA tTG. Endomysial antibodies are sometimes used in children under two years of age.

Tissue typing

In selected cases, HLA-DQ typing may be of benefit. In patients who are predisposed to the development of coeliac disease, a negative test would essentially rule out the diagnosis. A positive result, on the other hand, would not significantly alter the chance of the person having coeliac disease. In Down syndrome and Turner syndrome patients, this would alleviate the need for life-long screening. Tissue typing may be of value in infants (less than two years), to exclude disease, as serologic markers are less reliable. HLA-DQ typing in relatives of coeliac patients may also be of use, although they are highly likely to have DQ2/8 present, whether or not they also have the disease. As DQ2 is independently associated with IgA deficiency and Type 1 diabetes, tissue typing would be less beneficial in such cases.

By Dr Daman Langguth

Cardiology

Clinical Articles

Omega-3 fatty acids do not prevent heart attacks

Taking fish oil supplements to prevent a heart attack has always been somewhat controversial. However, a new meta-analysis, involving almost 78,000 high risk individuals has provided the best evidence to date that the practice is not worthwhile. (1) The UK researchers analysed the data from 10 trials which had investigated whether taking omega-3 fatty acid supplementation reduced the risk of fatal and non-fatal coronary heart disease as well as other vascular events including stroke. According to the study findings, published in JAMA Cardiology, those individuals randomised to omega-3 fatty acid supplementation for a mean of 4.4 years experienced no significant benefit in terms of preventing adverse vascular outcomes compared with those who did not receive supplementation. “Importantly, this meta-analysis also demonstrated no significant effect on major vascular events in any particular sub-groups, including prior vascular disease, diabetes, lipid levels, or statin use,” the study authors wrote. They suggest that the results of this study provide no support for the recommendations to use approximately 1g/d of omega-3 fatty acids in patients with a history of coronary heart disease to prevent heart attacks or any other vascular disease, which is the current advice from American Heart Association. Our own Australian Heart Foundation guidelines have been a little more circumspect with regard omega-3 fatty acids. While they do suggest supplementation for people whose diet is lacking in fish sources of EPA and DHA, they do say the cardioprotective benefit may be only for some high-risk groups. “There is evidence omega-3 supplements can play a beneficial role in the treatment of patients with high triglyceride levels and patients with existing heart disease, specifically heart failure,” according to their website. (2) Whether this advice is set to change remains to be seen. However, while this latest study might seem like the nail in the coffin for the fish oil business there is an important caveat to consider. The trials included in the meta-analysis involved various doses of omega-3 fatty acid supplementation. All but one trial included combinations of EPA and DHA, with the one exception being a trial of EPA supplementation alone. Daily doses of EPA ranged from 226 to 1800 mg/day and DHA doses varied from 0 to 1700mg/day. Several large randomised controlled trials, involving over 50,000 participants are currently underway investigating whether much higher doses of omega-3 fatty acids will reduce the risk of major cardiovascular events. Even the authors of this latest meta-analysis concede “The results of the ongoing trials are needed to assess if higher doses of omega-3 fatty acids (3-4g/d) may have significant effects on risk of major vascular events.” Ref: 1. JAMA Cardiol. doi: 10.1001/jamacardio.2017.5205 2. https://www.heartfoundation.org.au/images/uploads/main/Programs/Health_Professional_QA_Fish_Omega3_Cardiovascular_Health.pdf

By Dr Linda Calabresi

Surgery

Clinical Articles

Risk of post-op pneumonia halved

A single 30minute educational session with a physio about post-op breathing exercises prior to elective upper abdo surgery, halves that patient’s risk of respiratory complications compared with usual care, Australian research shows. The randomised study conducted among 441 patients across three hospitals in Australia and New Zealand showed the pre-op intervention reduced the risk of post-operative pulmonary complications from 27% in the control group to 12% in the physio-taught group. In fact, the number need to treat to prevent one such complication was only seven. The effect was greatest in men, those undergoing colorectal surgery, those aged under 65 and those educated by an experienced physiotherapist. So what did this all-important physio session involve? Well, as they say in the classics – it wasn’t rocket science. The physiotherapists had a standard script which included educating the patient about the high likelihood of a pulmonary complication following this type of surgery (10 to 50% according to the literature) and the importance of early ambulation as well as breathing exercises in preventing these. Many patients are unlikely to up and about in the first couple of days following major upper abdominal surgery but at least the breathing exercises can be done from the moment the patient regains consciousness – two sets of 10 slow, deep breaths followed by three coughs, using an abdominal support pillow to reduce pain. And this is to be repeated hourly. This was emphasised in the education session which was conducted at some stage in the six weeks prior to surgery. The physio session also included a practice run through of these exercises. However, interestingly the control group also received pre-op written information about these same facts and exercises, and were reminded of them post-op as part of standard care. What then made the difference? “One explanation for the effectiveness of pre-operative physiotherapy to reduce [post-operative pulmonary complications] is that the preparation, motivation and training of the patient before surgery brings the timing of breathing exercise initiation to immediately after regaining consciousness after surgery,” the study authors suggested. A degree of atelectasis is common with this type of surgery and general anaesthetic. The immediate commencement of these exercises could facilitate the re-inflation of the lungs, and prevent the progression of this atelectasis. The primary end point of this study was the development of one or more of seven respiratory symptoms or signs in the 14 days post op including chest xray evidence of consolidation or collapse, cough with coloured sputum or a respiratory-related high white cell count. One of the secondary endpoints was pneumonia, the relative risk of which was reduced by 52% courtesy of the intervention. In essence, the study showed how the right education and motivation given at the right time can dramatically improve health outcomes with results that are directly applicable to tens of millions of patients awaiting surgery such as this worldwide. “[P]atients reported that pre-operative physiotherapy empowered them to treat themselves and placed high value on its role in improving their post-operative recovery,” the researchers said. Ref: BMJ 2018;360:j5916 doi:10.1136/bmj.j5916

By Dr Linda Calabresi

Psychiatry

Clinical Articles

Ice psychosis: what is it, and why do only some users get it?

There is growing concern about crystal methamphetamine (ice) use in Australia and internationally, in part because of the psychological effects of the drug. Although most people who use ice do not experience psychological problems, about one in three people who use it regularly report experiencing psychosis in their lifetime. Research also suggests that up to 30% of people who experience ice psychosis go on to develop a long-term psychotic illness such as schizophrenia or bipolar disorder. Our new study aimed to find out why some ice users are more likely to experience psychosis than others.
Read more: Ice causes death in many ways, overdose is just one of them

So what is ice psychosis?

Psychosis refers to a range of mental health symptoms, including suspiciousness and paranoia, hallucinations, and unusual or agitated behaviour. Individuals often lose touch with reality, and may not have an understanding of what is happening to them. This can be very distressing for the individual and for their family and friends, and may result in the person having to go to hospital. Psychosis can occur as part of many different mental health disorders, or be triggered by a range of drugs. Amphetamine-type stimulant drugs, such as ice, are particularly known to potentially trigger psychosis. In the 1970s, amphetamines administered in experimental situations were shown to cause psychotic symptoms in healthy people who had never used the drug before. In Australia, ice is the drug that most commonly results in ambulance attendances for psychosis symptoms. And hospital admissions for ice psychosis have increased steeply in the past ten years. These patterns of increasing harms have paralleled the increase in the purity of ice and increasing dependence.

Read more:Weekly Dose: ice and speed, the drugs that kept soldiers awake and a president young

What did the study find?

We know the majority of people who use ice don’t experience psychosis. So we looked at 20 existing studies examining more than 5,000 regular ice users to try to find out what factors made someone more at risk of psychosis. We found the frequency and amount of methamphetamine use, and the severity of dependence, were the factors most commonly associated with the risk of psychosis. Unfortunately, the design of the studies, and the different ways in which they measured the frequency and amount of methamphetamine use, mean we can’t estimate exactly how much an increase in use will result in an increase in risk. Other risk factors included a family history of a psychotic disorder, and current use of other drugs, including cannabis and alcohol. While one study found a link between a history of traumatic experiences in childhood and the experience of ice psychosis, more research needs to be done. Just as important were factors that were not associated with ice psychosis – for example, age, gender, income or employment status. Interestingly, the way in which people used methamphetamine – by smoking versus injecting, for instance – did not appear to affect the likelihood of psychosis.

Read more: Explainer: methamphetamine use and addiction in Australia

Better treatment would make the difference

It’s important to remember almost all of the research on this topic has been cross-sectional. This means measurements of psychotic symptoms and measurements of risk factors have occurred at the same time – so we don’t know which causes the other, only that they’re related. The best way to study risk factors for ice psychosis would be to follow people from before they start using the drug, to when they develop the problem. But this sort of study is very difficult to conduct when it comes to drug use. Differences in the way researchers measure psychosis, or measure methamphetamine use, also affect how we understand the relationship between the two. Taken together, the main finding of our study was that people who used the drug more often and were more dependent on it were more likely to experience psychosis. While this might appear obvious, it does help healthcare workers and treatment services identify people who might be at greatest risk. Similarly, for people who aren’t ready to stop using the drug, changing the frequency or pattern of their use might help them avoid developing psychosis. More broadly, the key message from our research is better treatment of ice use would translate to a reduction in harms from the drug. The challenge remains making sure effective treatment is available when people are ready and willing to access it. Shalini Arunogiri, Addiction Psychiatrist, Lecturer, Monash University This article was originally published on The Conversation. Read the original article.

By Dr Shalini Arunogiri

Sexual health

Pathologists from Sullivan Nicolaides Pathology

Clinical Articles

Syphilis – it’s back

Syphilis

Syphilis, caused by the spirochaete Treponema pallidum is an old disease. Many notable figures throughout history are thought to have suffered from this scourge. It remains exquisitely sensitive to penicillin so, in theory, should be easily treatable. Over the past two years, the number of notified cases of infectious syphilis – syphilis of less than two years' duration — has continued to grow. In the Northern Territory and Queensland, the emerging risk groups are young Aboriginal and Torres Strait Islanders (ATSI), particularly people from the north of the State. In this group, in which young females are infected, there is now a real risk of new cases of congenital syphilis. In other geographical areas, gay and bisexual males form the major risk group. Co-infections with other sexually transmitted infections (STIs) are common and should always be tested for simultaneously. Similarly, all STI screens should include a test for syphilis. At-risk patients require screening for co-existing chlamydia, gonorrhoea and/or and trichomonas if the patient belongs to the ATSI group. Screening for HIV, hepatitis A, B and C should also occur, with hepatitis A and B vaccination in those who are non-immune. The recommended regular screening for asymptomatic gay and bisexual males is outlined in the now renamed STIGMA guidelines (http://stipu.nsw.gov.au/wp-content/uploads/STIGMA_Testing_Guidelines_Final_v5.pdf).

Presentation

Early or infectious syphilis (less than two years' duration) includes primary, secondary and early latent syphilis (Algorithms 1 and 2). • Primary syphilis usually manifests as a chancre (an anogenital or, less commonly, extragenital painless, but also sometimes painful, ulcer with indurated edges). • Progression to secondary syphilis occurs over the following months and presents as an acute systemic illness with rash, which is usually truncal, but also involving palms and soles, condylomata lata (clusters of soft, moist lumps in skin folds of the anogenital area), mucosal lesions, alopecia, lymphadenopathy, hepatitis, or meningitis. • Early latent syphilis is infection of less than two years' duration where the patient is asymptomatic. Late latent syphilis is defined as latent (asymptomatic) syphilis of longer than two years' duration, or of unknown duration. Tertiary syphilis refers to syphilis of longer than two years' duration, or of unknown duration, with cardiovascular, central nervous system or skin and bone (gummatous syphilis) involvement. Risk of transmission of syphilis from a pregnant mother to her fetus depends on the stage of syphilis during pregnancy. Management is clearly outlined in the ASID Management of Perinatal Infections Guidelines (https://www.asid. net.au/documents/item/368)

By Pathologists from Sullivan Nicolaides Pathology

Oncology

Clinical Articles

Surviving breast cancer not the end of the story

Breast cancer survival has improved dramatically over the last few decades. Courtesy of earlier diagnosis and better treatments, five year survival has increased from 70% in the 1980s to 90%, says Melbourne medical oncologist, Dr Jacqueline Chirgwin in the latest issue of the MJA. It is little wonder then that there is now increased focus on the ongoing general health in this ever-growing population of breast cancer survivors. “Although breast cancer is worldwide the most common cancer in women, many, perhaps most patients die from other causes,” she says. Dr Chirgwin’s comments are in relation to an Australian study, published in the same issue of the journal which showed comorbid conditions are more likely to develop in women who have been diagnosed with hormone-dependent breast cancer than in women without cancer. The South Australian researchers reached this conclusion after analysing a random sample of PBS data from a cohort of women who commenced endocrine therapy at some time in the eight years from 2004 and compared that with age and sex matched controls who weren’t taking anti-cancer treatment. Conditions significantly more likely to develop in the breast cancer women included depression, pain or pain-inflammation, osteoporosis, diabetes, cardiovascular disorders and gastric acid disorders. As the study authors point out there are a number of very logical reasons why these conditions are more likely in this particular group of women. For example it is hardly surprising that someone given a diagnosis of breast cancer might subsequently develop depression and be prescribed antidepressants. Similarly a number of the cancer medications may contribute to comorbidities such as cardiovascular disease, osteoporosis and musculoskeletal pain, in addition menopausal hormone therapy is contraindicated. In addition some risk factors for breast cancer are the same risk factors for other chronic conditions such as heart disease and diabetes, namely excessive alcohol consumption, obesity and physical inactivity. And while the findings might not be all that surprising, the researchers suggest that we are missing a major opportunity to target this at-risk group in a manner which will ultimately improve their health outcome, independent of the breast cancer. “As most women diagnosed with breast cancer in Australia can now be cured, the burden of non-cancer comorbidities is becoming a major health concern for these patients, but this is still largely unrecognised. Future breast cancer research should focus on strategies that effectively respond to the burden imposed by these comorbidities,” they concluded. Ref: MJA doi:10.5694/mja17.00006 doi:10.5694/mja17.00938

By Dr Linda Calabresi

Neurology

Clinical Articles

Neuroscience in pictures: the best images of the year

To understand how the healthy brain works and what occurs in brain disease, neuroscientists use many microscopy techniques, ranging from whole-brain human MRIs to imaging within a single neuron (brain cell), creating stunning images in the process.

By Dr Wei Luan, Dr Merja Joensuu, Ravi Kiran Kasula

Public health

Clinical Articles

Depressing news for smokers

Using prescription drugs or over-the-counter products like gums, mints or patches won’t increase your chances of quitting smoking a year later, according to a new study. The US researchers followed two groups of people 2002/03 and 2010/11 and found at the end of the 12-month period, those using varenicline (sold in Australia as Champix), bupropion (Zyban), or nicotine-replacement therapy (gums, mints or patches) were no more likely to have quit smoking for 30 days or more than those who didn’t use these drugs.
Read more – Weekly Dose: Champix’s effectiveness is questionable and safety record is concerning

Evidence based smoking cessation?

We’re told the best way to quit smoking is to use an “evidence-based” method: a strategy supported by high-quality research evidence. And for the last 30 or so years, this has been nicotine-replacement therapy, bupropion (Zyban) and varenicline (Champix), which claim to increase (and sometimes double) your chance of success. In the hierarchy of evidence, the lowest form is anecdote or case studies (“I smoked for 20 years, then an alternative therapist sprinkled magic powder on me, and the next day I stopped smoking!”). These cannot withstand the most elementary critical appraisal, starting with the basic question of how many similar smokers sprinkled with the powder kept smoking and how many who went nowhere it also stopped smoking. Far higher up the evidence pyramid is the double-blinded, randomised controlled trial (RCTs). In these, both the person taking the treatment and those delivering it are unware of who is taking the active drug and who is taking the comparison placebo or comparison drug. All enrolled in RCTs are randomly allocated to the active or placebo/comparison groups. The numbers of participants are sufficiently large enough to allow for an outcome to be declared statistically significant (or not) above a chance finding.

Read more – Randomised control trials: what makes them the gold standard in medical research?

Some have tried to dismiss earlier findings about the poor performance of nicotine-replacement therapy by emphasising “indication bias”. In the real world, those who opt to use medications to try to quit are likely to be more intractable smokers, more highly addicted to nicotine, and with histories of failure at quitting unaided. No one should therefore be surprised if they fail more often than those who try to quit on their own. In this new study, this issue was anticipated and all smokers were assessed by what the study authors called a “propensity to quit” score. This score accounts for factors such as smoking intensity, nicotine dependence, their quitting history, self-efficacy to quit, and whether they lived in a smoke-free home where quitting would likely be more supported. In the analysis, those who tried to quit with drugs and those who didn’t were matched on this propensity score, so “like with like” could be compared in the analysis. The findings held even when these “propensity” to quit factors were taken into account.

RCTs are very different to real world use

Critics have long pointed out that RCTs have many features which make them a pale shadow of how drugs are used in the real world. RCTs often exclude people with mental illness, poor English, and no fixed address. Excluding hard-to-reach and treat participants is likely to produce more flattering results. In the real world, people are not paid or otherwise incentivised to keep taking the drugs across the full period of the trial, so compliance is almost always far lower. In the real world, people do not get reminder calls, texts or visits from researchers highly motivated to minimise trial drop-out. There is no “Hawthorne effect”: when trial involvement and the attention paid to participants alters the outcomes. Nicotine-addicted people generally know very quickly if they have been allocated to the placebo arm in NRT trials because their brains feel deprived of nicotine. They invariably experience unpleasant symptoms. Knowing they have been allocated to the placebo undermines the integrity of the trial because it is important participants believe the drug might be effective. Large, real world studies like the one just published, which assess long-term success, not just end-of-treatment or short-term results, are therefore of most importance in assessing effectiveness. These new data ought to cause such rhetoric to cool right down. As for the evidence on e-cigarettes in quitting, neither the US Preventive Health Services Task Force, nor the UK’s National Institute for Health and Care Excellence or Australia’s National Health and Medical Research Council, have endorsed e-cigarettes as an effective way of quitting smoking.

Read more: Want to quit smoking? Switching to e-cigarettes no advantage

Quitting smoking is the single most important thing anyone can do to reduce the likelihood they will get heart or lung disease, and a whole string of cancers. It has been in the clear interests of the pharmaceutical and, more recently, the vaping (e-cigarette) industries, to promote the notion that anyone who tries to quit alone is the equivalent of someone with pneumonia refusing antibiotics. Hundreds of millions around the world have quit smoking without using any pharmaceutical intervention. Before nicotine-replacement therapies became available in the 1980s, many millions of smokers successfully quit smoking without using any drug or nicotine substitute. The same still happens today: most ex-smokers quit by going cold turkey. The problem is, in recent years, the government has moth-balled the national quit campaign, the megaphone for promoting this very positive message. Commercial interests are now commodifying something millions have always done for themselves. Simon Chapman, Emeritus Professor in Public Health, University of Sydney This article was originally published on The Conversation. Read the original article.

By Emeritus Prof Simon Chapman AO

Psychiatry

Clinical Articles

Menopausal hormonal therapy prevents depression

Sometimes evidence proves what was long-suspected to be true. A new study, just published in JAMA Psychiatry shows women who took hormone replacement therapy early in the menopausal transition had almost half the risk of developing clinically significant depressive symptoms compared to women who took a placebo. The study also confirmed that women of this age and stage are at high risk of significant depression, with almost one third of women in the placebo group developing symptoms and signs of the condition over the 12 month study period. Previous research had suggested that hormone therapy could help manage existing depression in menopausal women, however according to the Canadian researchers, this study, conducted among initially euthymic women was the first to show hormone therapy’s role in preventing the affective disorder. More than 170 perimenopausal and early post-menopausal women were randomly assigned to receive transdermal oestradiol (0.1mg/day) and intermittent oral micronized progesterone or placebo patches and tablets for 12 months. They were assessed regularly for depression using a validated depression scale (CES-D). Women on placebo were more likely to record a score that equated with significant depression at least once over the study period (32.3%) compared with women taking the hormone therapy (17.3%). Interestingly, women who had had what the researchers called ‘stressful life events’ in the six months prior to enrolment in the trial actually had greater benefit from the hormone therapy. Whereas other possible confounders such as baseline vasomotor symptoms, a history of depression, and baseline oestradiol levels did not appear to affect the protective benefit of the therapy. The progesterone was given for 12 days every three months, to induce vaginal bleeding so the finding that this adverse effect was more common in the hormone therapy group was hardly surprising but of note the two groups did not differ in other adverse effects including headaches, bloating, breast tenderness, weight gain and GI symptoms. An accompanying editorial sounded a few warnings about the study including the fact that the oestrogen dose was higher than currently recommended for treating women with hot flushes and the progestin dose was less than that recommended to protect the endometrium. The two editorial authors, including Dr Martha Hickey, from the University of Melbourne also cautioned that using hormone therapy to prevent depression might result in prolonged hormone exposure with the known risks associated with this, and is not currently recommended for this indication. However, the study authors were cautiously enthusiastic about their findings saying, “If confirmed in a larger sample of early perimenopausal women, the findings of this study…suggest that hormone therapy may also be indicated for the prevention and/or treatment of depressive symptoms appearing in the early menopause transition, regardless of whether menopausal symptoms are present.” Ref: JAMA Psychiatry. doi:10.1001/jamapsychiatry.2017.3998

By Dr Linda Calabresi

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Evidence based smoking cessation?

RCTs are very different to real world use

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