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Introduction: Cholinesterase inhibitors (ChEIs) and memantine are medications used to treat the symptoms of specific types of dementia. Their benefits and harms can change over time, particularly during long term use. Therefore, appropriate use of ChEIs and memantine involves both prescribing these medications to individuals who are likely to benefit, and deprescribing (withdrawing) them from individuals when the risks outweigh the benefits. We recently developed an evidence‐based clinical practice guideline for deprescribing ChEIs and memantine, using robust international guideline development processes.
Main recommendations: Our recommendations aim to assist clinicians to:
Changes in management as a result of the guideline:
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Funding:
The guideline development, publication, dissemination and implementation were funded through an NHMRC‐ARC Dementia Research Development Fellowship awarded to Emily Reeve (APP1105777). The funding body had no involvement in guideline development and, as such, the views and/or interests of the funding body have not influenced the final recommendations.
We thank Lisa Kouladjian O'Donnell, Judith Godin, Caitlin Lees, Emma Squires, Ivanka Hendrix and Robin Parker, who contributed to the systematic review which informed the development of the guideline.
Emily Reeve has received support to attend conferences to present work related to deprescribing by the NHMRC Cognitive Decline Partnership Centre, Canadian Frailty Network, TUTOR‐PHC Program (Western University), University of Sydney Medical School, Ramsay Research and Teaching Fund (Kolling Institute Travel Award, Royal North Shore Hospital Scientific Staff Council), Swiss Society of Internal Medicine and the Pharmacy Association of Nova Scotia; has received prize money from Bupa Health Foundation; and has received grants from the Canadian Frailty Network, CC‐ABHI Knowledge Mobilisation Partnership Program and the US National Institutes of Health for work related to deprescribing. Barbara Farrell has received consultancy fees and grants (including reimbursement for travel for research meetings or education sessions) from the Institute for Healthcare Improvement, College of Psychiatric and Neurologic Pharmacists, European Association of Hospital Pharmacists, Nova Scotia College of Pharmacists, Canadian Society of Hospital Pharmacists, and Ontario Pharmacists Association; and has received research grants from the Canadian Foundation for Pharmacy, Centre for Aging Brain Health and Innovation, Canadian Institute of Health Research, and Ontario Ministry of Health and Long‐Term Care for work related to deprescribing. Wade Thompson received a Master of Science stipend from government of Ontario for work on deprescribing, and speaking fees to present at conferences on deprescribing from the Advanced Learning in Palliative Medicine Conference, Ontario Long‐Term Care Clinicians Conference, and Geriatrics in Primary Care conference (University of Ottawa). Nathan Herrmann has received consultancy fees for dementia drug development from Lilly, Astellas and Merck; grants from Lundbeck and Roche for dementia investigational drug trials; and support from the Canadian Consortium on Neurodegeneration in Aging (CCNA) funded by the Canadian Institute of Health Research and several partners. Ingrid Sketris receives a partial salary stipend from Canadian Institute of Health Research (CIHR) as part of the Canadian Network for Observational Effect Studies and has received grants from CIHR (including funds utilized to present research results) and the Nova Scotia Department of Health and Wellness. Parker Magin has received grants from the Judith Jane Mason & Harold Stannett Williams Memorial Foundation Medical Program Grants, and the Royal Australian College of General Practitioners: Education Research Grant for potentially related work. Sarah Hilmer has received funding from the NHMRC Cognitive Decline Partnership Centre to support work related to deprescribing in people with dementia.
Objectives: To evaluate the performance of the 2013 Pooled Cohort Risk Equation (PCE‐ASCVD) for predicting cardiovascular disease (CVD) in an Australian population; to compare this performance with that of three frequently used Framingham‐based CVD risk prediction models.
Design: Prospective national population‐based cohort study.
Setting: 42 randomly selected urban and non‐urban areas in six Australian states and the Northern Territory.
Participants: 5453 adults aged 40–74 years enrolled in the Australian Diabetes, Obesity and Lifestyle study and followed until November 2011. We excluded participants who had CVD at baseline or for whom data required for risk model calculations were missing.
Main outcome measures: Predicted and observed 10‐year CVD risks (adjusted for treatment drop‐in); performance (calibration and discrimination) of four CVD risk prediction models: 1991 Framingham, 2008 Framingham, 2008 office‐based Framingham, 2013 PCE‐ASCVD.
Results: The performance of the 2013 PCE‐ASCVD model was slightly better than 1991 Framingham, and each was better the two 2008 Framingham risk models, both in men and women. However, all four models overestimated 10‐year CVD risk, particularly for patients in higher deciles of predicted risk. The 2013 PCE‐ASCVD (7.5% high risk threshold) identified 46% of men and 18% of women as being at high risk; the 1991 Framingham model (20% threshold) identified 17% of men and 2% of women as being at high risk. Only 16% of men and 11% of women identified as being at high risk by the 2013 PCE‐ASCVD experienced a CV event within 10 years.
Conclusions: The 2013 PCE‐ASCVD or 1991 Framingham should be used as CVD risk models in Australian. However, the CVD high risk threshold for initiating CVD primary preventive therapy requires reconsideration.
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The AusDiab study was coordinated by the Baker Heart and Diabetes Institute, and we gratefully acknowledge the support and assistance of the AusDiab Steering Committee and the study participants. The AusDiab study was funded by the National Health and Medical Research Council (grants 233200 and 1007544), the Australian Government Department of Health and Ageing, the Northern Territory Department of Health and Community Services, the Tasmanian Department of Health and Human Services, the New South Wales, Western Australian, and South Australian Departments of Health, the Victorian Department of Human Services, Queensland Health, City Health Centre Diabetes Service (Canberra), Diabetes Australia, Diabetes Australia Northern Territory, the estate of the late Edward Wilson, the Jack Brockhoff Foundation, Kidney Health Australia, the Marian and FH Flack Trust, the Menzies Research Institute, the Pratt Foundation, Royal Prince Alfred Hospital (Sydney), the Victorian Government OIS Program, Abbott Australasia, Alphapharm, Amgen Australia, AstraZeneca, Bristol‐Myers Squibb, Eli Lilly Australia, GlaxoSmithKline, Janssen‐Cilag, Merck Sharp & Dohme, Novartis Pharmaceuticals, Novo Nordisk Pharmaceuticals, Pfizer, Roche Diagnostics Australia, Sanofi Aventis, and Sanofi‐Synthelabo. Elizabeth Barr is supported by a Heart Foundation post‐doctoral fellowship (101291).
No relevant disclosures.
Victoria's voluntary assisted dying law will soon come into effect; a remaining challenge is effective clinical implementation
The Voluntary Assisted Dying Act 2017 (Vic) (VAD Act) will become operational on 19 June 2019. A designated 18‐month implementation period has seen an Implementation Taskforce appointed, and work is underway on projects including developing clinical guidance, models of care, medication protocols and training for doctors participating in voluntary assisted dying (VAD).1 While some have written on the scope of, and reaction to, the VAD legislation,2,3,4 there has been very little commentary on its implementation. Yet, important choices must be made about translating these laws into clinical practice. These choices have major implications for doctors and other health professionals (including those who choose not to facilitate VAD), patients, hospitals and other health providers. This article considers some key challenges in implementing Victoria's VAD legislation.
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Ben White and Lindy Willmott have been engaged by the Victorian Government to design and provide the legislatively mandated training for doctors involved in voluntary assisted dying. Lindy Willmott is also a member of the board of Palliative Care Australia, but this article only represents her views.
What are the problems in rural health service delivery and what can we do about them?
For decades, the Australian Government has been wrestling with how to “fix the rural health problem”. Long‐standing problems of workforce shortages and maldistribution, difficulties with recruitment and retention, and inadequate access to, and availability of, appropriate services persist.1 These contribute to the poor health status of many non‐metropolitan Australians, especially Aboriginal and Torres Strait Islander populations, despite the fact that governments spend millions of dollars annually on specific rural and remote health programs.2
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John Wakerman receives funding from the Australian Government Department of Health, the Northern Territory Government Department of Health and the Medical Research Future Fund through the Central Australian Academic Health Science Centre.
No relevant disclosures.
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This research was supported by NSW Organ and Tissue Donation Service.
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Objective: To assess the median urine iodine concentration (UIC) of young adults in the Top End of Northern Territory, before and after fortification of bread with iodised salt became mandatory.
Design, setting: Analysis of cross‐sectional data from two longitudinal studies, the Aboriginal Birth Cohort and the non‐Indigenous Top End Cohort, pre‐ (Indigenous participants: 2006–2007; non‐Indigenous participants: 2007–2009) and post‐fortification (2013–15).
Participants: Indigenous and non‐Indigenous Australian young adults (mean age: pre‐fortification, 17.9 years (standard deviation [SD], 1.20 years); post‐fortification, 24.9 years (SD, 1.34 years).
Main outcome measure: Median UIC (spot urine samples analysed by a reference laboratory), by Indigenous status, remoteness of residence, and sex.
Results: Among the 368 participants assessed both pre‐ and post‐fortification, the median UIC increased from 58 μg/L (interquartile range [IQR], 35–83 μg/L) pre‐fortification to 101 μg/L (IQR, 66–163 μg/L) post‐fortification (P < 0.001). Urban Indigenous (median IUC, 127 μg/L; IQR, 94–203 μg/L) and non‐Indigenous adults (117 μg/L; IQR, 65–160 μg/L) were both iodine‐replete post‐fortification. The median UIC of remote Indigenous residents increased from 53 μg/L (IQR, 28–75 μg/L) to 94 μg/L (IQR, 63–152 μg/L; p < 0.001); that is, still mildly iodine‐deficient. The pre‐fortification median UIC for 22 pregnant women was 48 μg/L (IQR, 36–67 μg/L), the post‐fortification median UIC for 24 pregnant women 93 μg/L (IQR, 62–171 μg/L); both values were considerably lower than the recommended minimum of 150 μg/L for pregnant women.
Conclusions: The median UIC of young NT adults increased following mandatory fortification of bread with iodised salt. The median UIC of pregnant Indigenous women in remote locations, however, remains low, and targeted interventions are needed to ensure healthy fetal development.
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This investigation was supported by the National Health and Medical Research Council (APP1046391). We acknowledge past and present study teams who traced participants and collected the data, particularly the late Susan Sayers, founder of the ABC study. We thank Victor Uguoma for his statistical advice. We especially thank the young adults in the Aboriginal Birth and Top End Cohorts and their families and communities for their cooperation and support, and all the individuals who helped in urban and rural locations.
Dorothy Mackerras is employed by Food Standards Australia New Zealand, the agency that introduced mandatory iodine fortification.
The importance of packaging, storage, and product design must be reflected by legislation
Electronic nicotine delivery systems (ENDS), including e‐cigarettes, are devices that heat a liquid (e‐liquid) that usually includes propylene glycol or vegetable glycerine, nicotine, and other constituents, such as colourants and flavourings. Nicotine is a naturally occurring toxin in tobacco plants that affects mammalian nervous and cardiovascular systems.1 E‐liquids containing nicotine are a poisoning risk because small amounts of nicotine can induce vomiting, cause seizures, and be lethal, particularly if ingested by young children.2 As Chivers and colleagues3 report in this issue of the MJA, e‐liquids may also contain a range of other toxic and dangerous constituents, including insecticides. In Australia and overseas, ENDS products are subject to regulations similar to those for tobacco products, including minimum age of purchase and restrictions on advertising.4 However, mitigating the risk of poisoning by ENDS products and their e‐liquids has not been the primary object of legislation.
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Biases and assumptions often arise from past experiences and, when unquestioned, can negatively influence the development of effective educational strategies
Knowledge is frequently considered as the panacea for all ills, and its acquisition is often proposed as the solution for ensuring we deliver the best quality health care. For example, training and continuing professional development (CPD) have been proposed as the first steps for medical colleges to address some troubling variations in health care practice in Australia.1 However, while proposing educational strategies to address health outcomes is logical, appropriate and defensible, it is well established that “knowing” something is quite different from “doing” something.2 Nevertheless, CPD curricula are frequently limited to “knowing”.3 While knowledge is a key prerequisite to transforming practice, how do we maximise CPD effectiveness as a strategy to improve care? And is changing individual practice through education all that is needed to change health practices and outcomes?4
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Intersectoral collaboration is needed to engage communities and design effective culturally and age‐appropriate interventions
The gap between the health of Aboriginal and Torres Strait Islander and non‐Indigenous Australians is well documented, with many policies and programs currently working towards improving outcomes. Despite these efforts, life expectancy is 10–11 years less than that of non‐Indigenous Australians,1 and 65% of deaths occur before 65 years of age, compared with 19% in the non‐Indigenous population.1
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We acknowledge other members of the Hot North Diabetes in Youth collaboration (Northern Australia Tropical Disease Collaborative Research Program, NHMRC project grant 1131932): Peter Azzopardi, Elizabeth Barr, Paul Bauert, Gavin Cleland, Christine Connors, James Dowler, Sandra Eades, Keith Forrest, Aveni Haynes, Renae Kirkham, Elizabeth Moore, Vicki O'Donnell, Glenn Pearson, Lydia Scott, Jonathan Shaw, Sally Singleton, Ashim Sinha and Mark Wenitong. Angela Titmuss is supported by an NHMRC Postgraduate Scholarship and RACP Woolcock Scholarship. Alex Brown is supported by an NHMRC Research Fellowship (1137563). Louise Maple‐Brown is supported by an NHMRC Practitioner Fellowship (1078477).
No relevant disclosures.
Summary