Bad hearts, poor kidneys cause many an early death

Indigenous people are more than twice as likely as other Australians to report they are in poor health, suffering disproportionately high rates of chronic and life-threatening diseases and impairments that have a significant effect on their quality of life.

In a sobering reminder of just how far there is to go to close the health gap between Indigenous and on-Indigenous Australians, the Australian Institute of Health and Welfare has reported that Aboriginal and Torres Strait Islander people are far more likely to have cardiovascular diseases, breathing problems, mental illness, diabetes, kidney disease, and to have problems with their hearing and sight.

Underlining the scale of the health problems afflicting Indigenous Australians, the Institute estimated that each year the collectively lose 100,000 years of life to premature deaths caused by chronic diseases, disability and injuries.

Cardiovascular disease is the biggest killer, causing a quarter of all Indigenous deaths between 2008 and 2012, followed by cancer (20 per cent of deaths) and injuries and poisonings (15 per cent).

But in some respects the burden of diabetes weighs even more heavily on the Aboriginal and Torres Strait Islander community.

The Institute’s The health and welfare of Australia’s Aboriginal and Torres Strait Islander peoples 2015 report (http://www.aihw.gov.au/publication-detail/?id=60129550168) shows 11 per cent of Indigenous adults had diabetes in 2012-13, while a further 4.7 per cent were at risk of developing the disease.

Related to this, almost 2 per cent had long-term kidney disease – almost four times the rate of the broader community.

This comes at an enormous cost to the community. In 2012-153 alone, Indigenous adults were hospitalised almost 175,000 times because of chronic kidney disease, almost all of them to undergo same-day dialysis. In all, this accounted for almost half of all hospitalisations of Aboriginal and Torres Strait Islanders.

The health disparity between Indigenous Australians and the rest of the community were further underlined by a separate Institute report showing Aboriginal women were twice as likely to die because of complications arising from pregnancy and childbirth.

Between 2008 and 2012, 105 women died from complications of pregnancy and childbirth, a rate of 7.1 deaths per 100,000 women. But among Indigenous women the rate (13.8 per 100,000) was double that among non-Indigenous mothers (6.6 per 100,000).

The results have highlighted calls from the AMA and other health groups for governments around the country to redouble their efforts to the close the health gap.

AMA President Professor Brian Owler said that although there had been some encouraging improvements in child and maternal health, much more needed to be done.

Professor Owler said recently that access to primary health care was especially important in addressing Indigenous disadvantage.

“Achieving equality in health and life expectancy for Aboriginal and Torres Strait Islander peoples is a national priority, but there is still a way to go before we see meaningful and lasting improvements,” the AMA President said. “There is a need for a concerted effort to fund and resource primary health care service providers to detect, treat, and manage chronic health conditions in Aboriginal and Torres Strait Islander communities.”

He said the Federal Government should immediately scrap the Medicare rebate freeze would hit Aboriginal community controlled health services and Aboriginal Medical Services particularly hard, and place enormous pressure on efforts to close the gap.

National Aboriginal Community Controlled Health Organisation Chair Matthew Cooke said that despite some progress in reducing infant mortality, the Institute report highlighted continuing major shortcomings, including for teenagers.

The report found Indigenous children aged between 15 and 18 years were far more likely to be imprisoned than their non-Indigenous counterparts, and were five times more likely to take their own lives.

Adrian Rollins

Deadly hitchhiker threat to young

Researchers have warned of the risk of measles outbreaks among infants, adolescents and young adults because of gaps in the nation’s immunisation coverage against the potentially deadly disease.

While the World Health Organisation has declared Australia measles-free, infectious disease experts have cautioned parents and health authorities that they need to remain vigilant about maintaining high rates of vaccination because of the vulnerability of young people no longer exposed to wild versions of the infection.

A study in the Health Department’s latest Communicable Diseases Intelligence report found the incidence of measles plummeted following the commencement of mass vaccination programs in the 1980s and 1990s, and was now at a level “consistent with elimination of indigenous measles in the country”.

Since the last big outbreak in the early 1990s, when almost 10,000 people caught the disease and four died, the rate of infection has plunged. Between 2000 and 2011, 990 cases were notified but none were fatal.

However, although the disease is no longer considered to be endemic, it is still being brought into the country by people travelling from regions where it is common, raising the risk of infection for vulnerable groups, particularly the very young.

Children are not eligible for their first measles vaccine until they are 12 months, and national figures for 2000 to 2011 show the incidence of the disease was highest in this age group, reaching a peak of 3.8 per 100,000 in 2011.

Next most vulnerable were children aged between one and four years, followed by adolescents aged 10 to 19 years and young adults aged 20 to 34 years.

The authors of the study, who were from the Health Department, the National Centre for Immunisation Research and Surveillance and the Australian National University, speculated that infants could be particularly vulnerable because of a decline in maternal antibodies in women with vaccine-acquired immunity.

“It has been postulated that because measles is becoming rare, the lack of natural boosting thorough exposure to wild virus in both vaccinated women and women with past infection has consequently resulted in infants becoming more susceptible,” they wrote. “It is therefore important…that timely vaccine uptake among infants occurs at the recommended 12 months of age.”

They also highlighted gaps in coverage caused by the staggered introduction of mass vaccination programs in the 1980s and 1990s.

In particular, they noted that those born between 1968 and 1982 were “particularly susceptible as low vaccine coverage existed when they were infants and circulation of wild virus was becoming less common”. In addition, people in this age group missed out on a second round of vaccinations for adolescents carried out between 1994 and 1998, while a 2001 immunisation campaign aimed at reaching many of them had only limited success.

The researchers said there was a risk of under- or un-vaccinated young adults catching the disease while travelling overseas, and urged greater efforts to assess their immunity before they left the country.

“As most outbreak in Australia begin with an importation of measles from an endemic country, it is essential that measles immunity status be assessed when patients attend clinics to receive vaccinations for international travel,” they said, citing research showing that just 4 per cent of travellers who attended hospital within two years of returning from abroad were vaccinated against measles, mumps and rubella.

“Clearly, age-specific vulnerability of populations exist[s], even though measles is so rare in Australia and, consequently, this may lead to outbreaks in these populations,” the authors said. “Hence, there is an ongoing need to improve vaccine uptake in vulnerable populations.”

Adrian Rollins

Rubella, mumps could soon be history

Rubella has been all-but eliminated and the country may be close to getting rid of mumps amid evidence of an increase in vaccination rates.

Research published by the Commonwealth Health Department in its latest Communicable Diseases Intelligence report suggests that rubella, a mild infection in adults that can nonetheless cause severe congenital abnormalities in unborn babies, is no longer endemic, while the country is close to eliminating mumps despite a recent upsurge in notifications of the disease.

Four years after the Americas were declared rubella-free, researchers from the National Centre for Immunisation Research and Surveillance said it was now so rare in Australia – aside from cases involving infections imported from overseas – that arguably the country met all the criteria for the World Health Organisation to declare it eliminated.

To be declared rubella-free, a country or region must have a low incidence of infection, with only sporadic imported cases with limited spread, high levels of immunity and a robust immunisation program.

Between the mid-1990s and 2005 the average annual notification rate for the disease tumbled from 14.8 per 100,000 to 0.23 per 100,000 by 2005, and there have been just two reported cases of congenital rubella syndrome since 2008. The proportion of imported rubella cases, meanwhile, climbed from 9 to 27 per cent between 2005 and 2012, and the immunisation rate has held above 91 per cent.

The researchers said it only remained to improve surveillance, including genotyping infections to establish their origin, to demonstrate the absence of endemic strains and have Australia declared rubella-free.

Researchers have also held out hope that mumps may soon be eliminated from Australia, if it is not already.

Mumps became a notifiable disease in 2001, and its incidence peaked at 2.8 per 100,000 in 2007 before slipping below 1 per 100,000 by 2012.

As with other countries, there has been an increase in the average age of people with mumps following the introduction of universal child vaccination in 1989. Between 2008 and 2012, it was much more common among 25 to 34-year-olds (1.7 cases per 100,000) than among young children. Those aged one to four years had the lowest incidence, just 0.5 per 100,000.

But researchers admitted that, despite high vaccination coverage against mumps (94 per cent for the first dose of the measles, mumps, rubella vaccine and 90 per cent for the second dose), there was an increasing trend in mumps notifications and the likelihood its incidence was being under-reported.

Nevertheless, that said it was possible that Australia was among those countries to have achieved, or come close to, eliminating the disease, adding that, “sporadic outbreaks in highly vaccinated populations may be due to the force of infection after virus introduction from an endemic area into high-density, high contact environments”.

They concluded that the trend toward increased notifications required careful monitoring.

The possibility that rubella and mumps may soon be eliminated, if they are not already, has come amid evidence that the nation’s vaccination rate is increasing.

The Federal Government has mounted a crackdown on parents who refuse or fail to ensure their children are vaccinated, threatening to withhold benefits worth thousands of dollars from families and abolishing all but medical exemptions.

But even before these latest measures were announced, figures from the Australian Childhood Immunisation Register show vaccination rates were rising in mid-2014, reaching 91.5 per cent of one-year-olds (up 0.6 of a percentage point), 92.8 per cent of two-year-olds (up 0.2 of a percentage point) and 92.2 per cent of five-year-olds (up 0.3 of a percentage point).

Adrian Rollins

Tinea hidden by a vemurafenib-induced phototoxic reaction in a patient with metastatic melanoma taking dexamethasone

Clinical record

A 41-year-old man with stage IV BRAF-V600E (valine replaced with glutamic acid at amino acid position 600 in the BRAF kinase) metastatic melanoma was started on vemurafenib therapy on a compassionate access program. Before this, he had been on long-term dexamethasone therapy (4 mg daily) for management of brain oedema related to multiple brain metastases. With the exception of his cutaneous melanoma, he had no past history of dermatological conditions, including tinea corporis and photosensitivity.

One week after starting vemurafenib therapy (960 mg twice daily), the patient developed a severe drug-induced photosensitivity reaction, with blistering and erosions on sun-exposed areas of skin. Despite implementing adequate sun avoidance measures and using topical corticosteroids in the acute setting, minimal improvement was seen. As a result, the daily dose of dexamethasone was increased to 8 mg daily for the next 3 weeks and then tapered back down.

Nine months later, the patient was still taking vemurafenib 960 mg twice daily and the dexamethasone dosage had been tapered to 4 mg daily. Although the vemurafenib-induced photosensitivity reaction had ameliorated, persistent blistering, erosions and erythema were noted on the dorsum of both hands (Figure, A). One month later, several new lesions developed on the left forearm, including an annular erythematous plaque with a scaly surface, scattered pustules and ill defined borders. A similar lesion on the left side of the chest was also identified. Skin scrapings were collected and sent for culture. Trichophyton rubrum was identified and the patient was diagnosed with tinea corporis. He was prescribed topical antifungal cream (clotrimazole every 8 hours) for these lesions.

After 7 weeks of clotrimazole therapy, the patient reported a slight reduction in the erythema and scaling of the forearm and chest lesions. However, multiple new pustules had developed on the hands and face in addition to several erythematous nodules over the dorsum of the hands and forearms (Figure, B) suggestive of Majocchi granuloma. A medium-sized inflammatory mass was also identified on the right cheek with multiple pustules, crusts and excoriations and a purulent discharge from follicular orifices (Figure, C), in keeping with facial kerion celsi.

Given the long-term dexamethasone use, previous diagnosis of T. rubrum infection and ongoing progression of the infection despite topical antifungal therapy, the patient was prescribed oral itraconazole, 200 mg daily, for 6 weeks. The kerion celsi was managed with multiple incisions and drainages. Reduced severity of all the skin lesions was subsequently seen over the course of the therapy.

Dermatophytic infections are usually located on the outermost layer of the epidermis.1 However, dermatophytes may affect deeper areas of the skin by invading hair follicles. When this happens, usually through a disruption of the epidermal barrier after the infection of hair follicles,1,2 an inflammatory granulomatous reaction can occur.

Dermatophytic dermal invasion causing inflammatory infiltrates of neutrophils and the development of granulomatous lesions is known as Majocchi granuloma or nodular granulomatous perifolliculitis.2 The dermatophyte that is most commonly involved is T. rubrum;1 the source of the T. rubrum is usually a precedent superficial dermatophytic infection such as the initial tinea corporis in our patient. Clinical examination often shows inflammatory follicular-centred papules, pustules or nodules on hair-bearing skin, which might evolve into larger subcutaneous nodules or abscesses.

While Majocchi granuloma is sometimes found in healthy individuals, development of the granulomatous reaction depends on the effectiveness of the immune system against the pathogen.3 Glucocorticoids affect cell-mediated immunity, impairing the function of macrophages and neutrophils, and reducing T helper 1-mediated immunity, which plays an important role in the complete resolution of fungal infections.4

BRAF inhibitors, such as vemurafenib, are novel drugs that target an important mutation that is present in about 50% of metastatic melanomas. They have secondary effects on skin, such as development of multiple cutaneous squamous cell carcinomas, verrucal keratoses and a variable degree of photosensitivity.5–8 Since no vemurafenib-related immunosuppressive effects have been reported to date for vemurafenib,9,10 it is unlikely to have played a role in the development of the dermatophytic infection, apart from the severe drug-induced photosensitivity. The immunosuppressive glucocorticoid therapy for the brain metastases and vemurafenib-induced photosensitivity effectively placed the patient at risk of progressive infection from a superficial tinea corporis to a more invasive infection such as Majocchi granuloma. Given the well documented association of vemurafenib and photosensitivity reactions, the diagnosis was initially confounded and further aggravated by the treatment of the ultraviolet A photosensitivity. The introduction of topical antifungals was too late to stop progression of the disease, and the patient eventually developed Majocchi granuloma and a facial kerion for which oral antifungal therapy was needed.

In our patient, multiple cutaneous pathological processes were present concurrently. While the cutaneous secondary effects of vemurafenib are well reported, it is important to consider alternative diagnoses when there is minimal response to therapy. Immunosuppression from corticosteroid therapy (oral or topical) should be taken into consideration in patients taking these medications while also on antineoplastic therapies. Prompt recognition, diagnosis and treatment in this setting could avoid development of more serious complications.

Lessons from practice

While vemurafenib induces ultraviolet A photosensitivity, it is important to consider alternative diagnoses when minimal response to therapy is attained.
Concurrent administration of topical or systemic corticosteroids can alter the presentation of vemurafenib-induced adverse effects.
Trichophyton rubrum can penetrate hair follicles to cause dermal infections that do not respond to topical therapy.

Figure

First report of Lyme neuroborreliosis in a returned Australian traveller

Lyme borreliosis is a tick-borne zoonosis endemic in many parts of the world. We report the first case of Lyme neuroborreliosis in an Australian traveller returning from an endemic area. The diagnosis should be considered in patients with chronic meningoencephalitis and a history of travel to an endemic area.

Clinical record

A 58-year-old woman of European ancestry presented to a rural hospital in New South Wales in May 2014 with an 8-month history of worsening motor instability, confusion and bilateral occipital headaches associated with photophobia, lethargy and somnolence. The patient was from Geraldton in Western Australia and was staying for 2 weeks with her family in NSW. Her symptoms had started 1 month after returning from Lithuania, where she had spent 3 weeks. A tick had bitten her in the pubic hairline during a trip to a pine forest 30 km from Vilnius. One month later, the patient developed two circular non-pruritic rashes on her right thigh (distal to the site of the tick bite) and lower leg, each about 30 mm in diameter; they resolved after 2 weeks without specific intervention. She had experienced continuing headaches, lethargy and a self-limiting episode of diplopia that prompted her to see her general practitioner. Computerised tomography and magnetic resonance imaging of the brain performed before she presented to the hospital showed nothing abnormal.

The patient’s past medical history included hypertension that was well controlled with irbesartan. On presentation, she was afebrile. There were no focal neurological signs or papilloedema. Cardiovascular, respiratory and gastrointestinal parameters were within normal limits. There were no rashes on her extremities, nor evidence of synovitis in her joints.

The results of a full blood examination, urea and electrolyte assessments and liver function tests were within normal limits. The cerebrospinal fluid (CSF) white cell count was 377 × 106/L (reference interval [RI], 0–5 × 106/L), consisting purely of monocytes (ie, no polymorphonuclear leukocytes). No organisms were identified by Gram staining; the results of acid-fast bacilli staining were also negative. CSF biochemical parameters were markedly abnormal, with elevated protein levels (1.93 g/L; RI, 0.15–0.45 g/L) and reduced glucose levels (1.3 mmol/L; RI, 2.8–4.4 mmol/L). Cryptococcal antigen was not detected by lateral flow assay, and polymerase chain reaction (PCR) analysis was negative for herpes simplex viruses 1 and 2, enterovirus, and Mycobacterium tuberculosis. Antibody to syphilis treponema and to HIV was not detected.

Given the clinical presentation and the history of travel to an area where Lyme disease is endemic, serological testing for Borrelia in both serum and CSF was requested, and treatment with ceftriaxone (4 g daily) was commenced, with a presumptive diagnosis of Lyme neuroborreliosis.

Serological screening was performed at the Institute of Clinical Pathology and Medical Research, Westmead (Sydney), with an enzyme immunoassay (EIA) for IgG against recombinant antigens from Borrelia burgdorferi sensu stricto strain B31, B. afzelii and B. garinii (NovaLisa Borrelia burgdorferi IgG, NovaTec Immundiagnostica GmbH, Germany). The signal to cut-off ratio in this assay was 6.83 for serum and 5.57 for CSF (ratios less than 0.9 are considered negative).

To confirm these results, western immunoblotting was undertaken using a modification of the polyacrylamide gel electrophoresis (PAGE) method described by Dressler and colleagues.1 Sonicated B. burgdorferi strain 297 (at 0.5 mg/mL) and B. afzelli ATCC 51567 (at 1.0 mg/mL) were separately applied to precast SDS-PAGE gels (ExcelGel SDS Homogeneous 12.5, GE Healthcare Life Sciences, Sweden). The serum of our patient showed IgG responses to two B. burgdorferi antigens (molecular weights: 41, 58 kDa) and five B. afzelii antigens (22, 39, 41, 58, 83 kDa). IgG to the same antigens, as well as to a sixth B. afzelii antigen (45 kDa), was detected in her CSF. The criteria of the United States Centers for Disease Control and Prevention (CDC) stipulate that five or more specific IgG bands are required for a positive serological result.2

The patient returned to Geraldton, where she completed two weeks of treatment with intravenous ceftriaxone (4 g daily). The cellular and biochemical parameters of CSF collected 3 weeks after completion of treatment had improved: the white cell count was 45 × 106/L, the protein levels were 0.7 g/L and the glucose concentration was 2.3 mmol/L. Five months later, her CSF parameters were completely normal, with a normal biochemical profile and no pleocytosis. The patient continues to see her GP and has made a good clinical recovery; her headaches, lethargy and neurological symptoms have all resolved.

Discussion

Our case highlights the importance of obtaining a thorough travel history in a patient presenting with chronic meningoencephalitis. Our review of the literature indicated that this was the first case of Lyme neuroborreliosis imported into Australia from overseas. Clinicians should consider neuroborreliosis in patients with a history of travel to an endemic area who present with persistent neurological symptoms. Other causes of chronic meningitis include cryptococcal meningitis, which is endemic in Australia, but had been excluded in our patient. Mycobacterium tuberculosis infection and tick-borne encephalitis are further diagnoses to consider in travellers with meningoencephalitis who have returned from Eastern Europe.

Lyme disease is a multisystem infectious disorder transmitted by ticks of the Ixodes complex.3 Three B. burgdorferi sensu lato species, namely B. burgdorferi sensu stricto, B. garinii, and B. afzelii, are pathogenic to humans in Europe. In contrast, B. burgdorferi sensu stricto is the only species known to cause human infection in the United States.3 The disease has protean manifestations, depending on the clinical stage at presentation. Stage I disease usually presents with a typical rash, erythema migrans, 7–14 mm from the site of the tick bite. Constitutional symptoms, including headache, myalgia, arthralgia and fever, may accompany the erythema migrans. Stage II disease is characterised by dissemination to other skin areas, the nervous system, joints or heart, and may include a wide variety of symptoms. Stage III, or late Lyme disease, occurs months to years after a tick bite, and usually causes large joint arthritis or neurological symptoms.3 In our patient, the presence of an erythema migrans rash at more than one site, presented together with neurological symptoms, indicated stage II disease.

Two-tier serological assessment — a screening EIA followed by confirmatory immunoblotting — remains the mainstay of diagnosis for Lyme borreliosis, although molecular methods and culturing clinical specimens are also possible.2The diagnostic sensitivity of culturing Borrelia species is poor, so that it is rarely undertaken in clinical practice, its use being largely limited to research settings.4 Molecular methods have a higher diagnostic sensitivity when using skin biopsies from an erythema migrans or synovial fluid than when testing blood or CSF.4,5 Molecular methods have not been standardised across laboratories and false-positive results are possible.4

On the other hand, the recombinant EIA for anti-Borrelia IgG has high sensitivity and specificity after the first few weeks of infection. The results of testing the serum and CSF of our patient for anti-Borrelia IgG were highly positive. Confirmation by immunoblotting greatly increases the positive predictive value of EIA, but this technique may be less sensitive, although it is very specific when using the CDC criteria for IgG immunoblotting in Lyme disease. In our case, only the IgG blotting results for B. afzelii antigens met the CDC criteria for a positive finding.

The European Federation of Neurological Sciences guidelines require two of the following criteria to be fulfilled for a possible diagnosis of Lyme neuroborreliosis, and that all three be met for a definite diagnosis:

neurological symptoms;
CSF pleocytosis; and
detection of intrathecal antibodies or, if symptoms began in the past 6 weeks, identification of the pathogen in the CSF by PCR or culture.6

Our patient met all three criteria, making this a definite diagnosis of Lyme neuroborreliosis.

The clinical presentation of Lyme neuroborreliosis differs according to the Borrelia species involved. B. garinii is the most common cause of Lyme neuroborreliosis in Europe, followed by B. afzelii. B. garinii infection often manifests as typical early neuroborreliosis, characterised by painful meningoradiculitis (Bannwarth syndrome) and meningeal irritation, whereas the clinical features of central nervous involvement in B. afzelii infection, as in our patient, are often non-specific and difficult to diagnose.5 In contrast to infection with B. garinii, CSF parameters in patients with Lyme neuroborreliosis caused by B. afzelii can be atypical, with a normal biochemical profile and without pleocytosis.5 In our patient, the presence of persistent non-specific neurological and constitutional symptoms, together with positive CSF and serum IgG immunoreactivity to B. afzelii antigens, provided enough evidence to attribute this infection to B. afzelii.

Oral administration of amoxicillin or doxycycline is usually the treatment of choice for early stage Lyme borreliosis. Patients with neurological or cardiac manifestations are typically treated for 2–4 weeks with intravenous ceftriaxone.3 Longer-term parenteral treatment is not recommended, because it does not provide any additional improvement in patients with persisting neurological or constitutional symptoms; it is also associated with adverse events.7 Improvement in both clinical and CSF markers after 2 weeks of intravenous ceftriaxone in our patient was reassuring, and suggests that a shorter duration of treatment is possible even in patients with neurological symptoms.

The existence of Lyme disease in Australia has been debated for decades,8 and in recent years there has been growing public interest. In February 2014, the Royal College of Pathologists of Australasia released a position statement on diagnostic laboratory testing for Lyme disease in Australia and New Zealand.9 Ticks of the genus Ixodes are present in Australia, but species known to transmit Borrelia species have not been found.10Earlier research,10 as well as the most recent study of ticks in areas around the northern beaches of Sydney and other parts of Australia (Associate Professor Peter Irwin, Murdoch University, WA, personal communication, November 2014) have not found Borrelia species in Australian ticks.

Lyme disease can present as non-specific symptoms that persist for weeks to months after infection. A careful travel history is therefore an important part of the assessment of any patient with clinical features suggesting the disease.

[Department of Error] Department of Error

Ong ACM, Devuyst O, Knebelmann B, Walz G, on behalf of the ERA-EDTA Working Group for Inherited Kidney Diseases. Autosomal dominant polycystic kidney disease: the changing face of clinical management. Lancet 2015; 385: 1993–2002—In figure 3, panel C, of this Review (May 16), the baseline mean estimated glomerular filtration rate of the placebo group in the sirolimus study should be 92 mL/min/1·73 m2 and the mean age 32 years. This correction has been made to the online version as of June 26, 2015.

[Correspondence] Nepali earthquakes and the risk of an epidemic of hepatitis E

The recent earthquakes in Nepal killed thousands, displaced tens of thousands, and destroyed much of the country’s infrastructure. Thousands of Nepalis are living in makeshift camps, with limited or no access to clean drinking water. There is now considerable risk of infectious diseases in affected areas.1,2

[Comment] Eliminating acute kidney injury by 2025: an achievable goal

Writing in our first Series on Global Kidney Disease in 2013, Giuseppe Remuzzi and colleagues observed that, “Although in some parts of the world acute and chronic kidney diseases are preventable or treatable disorders, in many other regions these diseases are left without any care. The nephrology community needs to commit itself to reduction of this divide between high-income and low-income regions”.1 Their warning and call to action were propitious. The burden of chronic kidney disease continues to increase.

[Comment] Japan’s vision for health care in 2035

Over the past half century Japan has made remarkable achievements in good population health at low cost, with increased equity.1 However, a demographic shift towards rapid ageing, the growth of non-communicable diseases (NCDs), and advances in medical technology have led to great changes in health-care needs. In the Lancet 2011 Series on Japan: Universal Health Care at 50 Years, three major challenges to Japan’s health system were identified: sustainability, governance, and responsiveness.2 In that Series, several reforms were proposed to assure the sustainability and equity of Japan’s health accomplishments: implementation of human-security, value-based reforms; redefinition of the roles of central and local governments; improvements in the quality of health care; and a commitment to global health.

Tackling climate biggest ‘global health opportunity in 100 years’

The effects of climate change are already being felt and it presents a “potentially catastrophic” threat to human health unless urgent action is taken to rein in carbon dioxide emissions, according to a report by the respected Lancet Commission on Health and Climate Change.

In findings that reinforce AMA warnings about the need for governments to prepare for the inevitable health effects of climate change and extreme weather events, the Lancet Commission said that the world was at risk of undoing half a century of gains in global health and development.

The Commission’s report, Health and climate change: policy responses to protect public health, warned that unless there was a change of course, the world was on track to exceed 2900 billion tonnes of carbon dioxide emissions within the next 15 to 30 years, forcing global average temperatures up by between 2.6 and 4.8 degrees Celsius by the end of the century.

But the Commission said that, rather than being viewed as a burden, addressing climate change should be seen as “the greatest global health opportunity of this century”.

“Many mitigation and adaptation responses to climate change are ‘no regret’ options which lead to direct reductions in the burden of ill health, enhance community resilience, alleviate poverty, and address global inequity,” the report said.

AMA President Professor Brian Owler said the Lancet report, prepared by a collaboration of European and Chinese climate scientists, geographers, social and environmental scientists, engineers, health professionals, energy policy experts and political scientists, provided further evidence on the need for global action to combat and mitigate the effects of climate change on human health.

“It is the AMA’s view that climate change is a significant worldwide threat to human health that requires urgent action, and we recognise that human activity has contributed to climate change,” Professor Owler said. “There is considerable evidence to encourage governments around the world to plan for the major impacts of climate change, which include extreme weather events, the spread of diseases, disrupted supplies of food and water, and threats to livelihoods and security.”

Earlier this year, Professor Owler helped launch an Australian Academy of Science report, Climate change challenges to health: Risks and opportunities, that detailed the likely health effects of climate change, including increasingly deadly heatwaves, the spread of food and water borne illnesses and diseases like malaria, and the death and damage caused by more frequent and extreme storms, droughts and floods.

Governments around the world are preparing to attend the United Nations’ Paris Climate Change Conference in November, and the AMA President said there was an urgent need for action.

“The evidence is clear – we cannot sit back and do nothing,” Professor Owler said. “Governments must prepare for the inevitable health and social effects of climate change and extreme weather events.”

The Lancet Commission has called for the framework for an international carbon pricing mechanism to be established in the next five years, along with a rapid expansion in the use of renewables and the speedy phase out of coal-fired power.

In a rallying call for the medical community, the Commission said that until now health effects had been largely ignored in the international debate over climate change, but doctors needed to help lead a change in focus that would bring the consequences of rising global temperatures into sharp relief.

“Health professionals have worked to protect against health threats such as tobacco, HIV/AIDS and polio, and have often confronted powerful entrenched interests in doing so,” it said. “Likewise, they must be leaders in responding to the health threat of climate change. A public health perspective has the potential to unite all actors behind a common cause – the health and wellbeing of our families, communities and countries.”

Professor Owler said the Abbott Government should use the Lancet Commission report and the Australian Academy of Science study as key references in the development of the action plan it takes to the Paris Climate Change Conference.

Adrian Rollins