CLINICAL INITIATIVES, RESEARCH AND CURRENT UPDATES IN TREATMENT
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Improving Access to Take Home Naloxone in Hospitals and at Risk Populations
Heather Flowers, Hospital Pharmacist, Slade Pharmacy Currumbin
Opioid overdoses remain a significant public health concern in Australia, with opioids implicated in over half of drug-induced deaths.1 Despite this, uptake of Take Home Naloxone (THN) remains suboptimal, particularly in hospital settings where high-risk patients are frequently encountered.2 Since July 2022 naloxone is available free of charge without prescription through the national THN Program, in both nasal and injectable formulations.1,3 This creates a key opportunity for hospital clinicians to improve access prior to discharge. However, evidence suggests this opportunity is often missed, with low prescribed rates even among patients admitted with opioid overdose.2,4 Doctors and nurses can play a critical role by routinely assessing overdose risk and offering
THN. This includes not only patients presenting with overdose, but also those prescribed high-dose opioids for acute or chronic pain. The Faculty of Pain Medicine recommends considering THN for all patients on opioids and specifically for those with oral morphine equivalent daily doses exceeding 40 mg.5 With rising prevalence of potent synthetic opioids, broader THN access is essential.1,6 Hospitals can improve uptake by embedding THN into discharge protocols, educating patients and carers, and partnering with pharmacy teams. Expanding hospital-based supply is a simple intervention to reduce preventable deaths and improve continuity of care.
Dementia Update: Burden, Emerging Therapies, and Modifiable Risk Factors
Darren Wong, Hospital Pharmacist, Slade Pharmacy Richmond
Dementia remains a major contributor to morbidity and mortality in Australia, affecting an estimated 446,500 people and representing the leading cause of death nationally.1 Alzheimer’s disease (AD) is the most common subtype, characterised by amyloid-β (Aβ) plaque deposition and tau-mediated neurodegeneration, leading to progressive cognitive and functional decline.2,3
TGA‑approved disease‑modifying therapies
Lecanemab and donanemab are the first therapies approved by the Therapeutic Goods Administration (TGA) for AD in over two decades.4,5 Both monoclonal antibodies target aggregated Aβ to facilitate plaque clearance, aiming to slow disease progression; they are non-curative.4-7 These treatments are indicated for patients with mild cognitive impairment or mild dementia due to early AD and confirmed amyloid pathology.4,5 In Australia, use is restricted to ApoE ε4 non-carriers or heterozygotes, with genotyping required prior to initiation.4,5
In sponsor-led phase 3 trials, lecanemab and donanemab demonstrated modest slowing of cognitive and functional measures over 18 months in patients with early AD.6,7 In CLARITY-AD, lecanemab slowed decline by 27% on the Clinical Dementia Rating–Sum of Boxes (CDR-SB).6 In TRAILBLAZER-ALZ 2, donanemab slowed decline on the integrated Alzheimer’s Disease Rating Scale (iADRS) by approximately 22% in the overall population and up to 35% in those with low to intermediate tau burden.7 Both agents are associated with amyloid-related imaging abnormalities (ARIA), including ARIA-E (vasogenic oedema/effusions) and ARIA-H (microhaemorrhage or superficial siderosis), representing the principal safety concern; while most ARIA events are asymptomatic, serious events can occur.2.4-7 ARIA risk is higher in ApoE ε4 homozygotes, underpinning current regulatory restrictions.2,4-7 Implementation is constrained by cost, mandatory MRI monitoring, and infusion requirements, and overall benefit–risk remains uncertain, with ongoing evaluation of meaningful clinical impact and cost-effectiveness.2,8
Modifiable risk factors remain central
An estimated 40–45% of dementia cases may be attributable to modifiable risk factors.1,9 Dementia Australia identifies 14 key risks across the life course, including obesity, hearing loss, physical inactivity, hypertension, and depression (see figure 1).9,10 These highlight the central role of vascular, metabolic and psychosocial factors in dementia pathogenesis.10 Consistent with Royal Australian College of General Practitioner’s guidance, optimising cardiometabolic health should be framed as both chronic disease management and a core strategy for dementia prevention and progression slowing.11 While emerging therapies offer promise, addressing modifiable risk factors in general practice remains the most immediate and equitable intervention for Australia’s ageing population.
Optimising Osteoporosis: A Medication Management Overview
Sarah Farsi, Hospital Pharmacist, Slade Pharmacy Hollywood
Osteoporosis is a chronic, progressive skeletal disorder characterised by reduced bone mineral density (BMD) and deterioration of bone microarchitecture, leading to increased fragility and fracture risk.1 Fragility fractures commonly occur after minimal trauma, such as a fall from standing height, and are associated with significant morbidity, loss of independence, and increased mortality.2
Osteoporosis remains a major public health issue, affecting 3.4% of Australians,3 with 67% of adults aged 50 years and older having osteoporosis or osteopenia.4 Often asymptomatic until fracture, early identification and treatment are essential to reduce risk and complications.2
Australian guidelines recommend targeted case finding in adults aged ≥50 years.2 This involves using clinical risk factors (e.g. age, female sex, prior fracture, family history, low BMI, smoking, excess alcohol, comorbidities, and use of bone-affecting medications like glucocorticoids), and fracture risk tools such as FRAX, followed by BMD measurement to guide management.2 Patients at very high or imminent fracture risk are prioritised for more intensive therapies, including osteoanabolic agents.2
Management
Antiresorptive Therapy
Antiresorptive therapies remain the cornerstone of osteoporosis management for most patients at increased fracture risk.2 These agents reduce osteoclast-mediated bone resorption, preserving bone mass and improving skeletal strength,1 with established efficacy in reducing vertebral, non-vertebral, and hip fractures.2 Treatment should be guided by overall fracture risk rather than BMD alone.4
Bisphosphates, including alendronate, risedronate, and intravenous zoledronic acid, are first-line therapies for most postmenopausal women and men over 50 years with osteoporosis or a history of fragility fracture.2,4 Treatment duration is individualised with reassessment recommended after 5–10 years; therapy may be paused in lower-risk patients who respond well, but continued in those with persistently low BMD or ongoing fracture risk.2,5
Denosumab inhibits RANK ligand, suppressing osteoclast formation and activity, resulting in rapid increases in BMD and fracture risk reduction.1 It is an effective alternative for patients at high fracture risk, particularly when bisphosphonates are contraindicated or not tolerated. 5,6
Unlike bisphosphonates, denosumab’s effects on bone resorption do not persist after stopping treatment.1 Delays or abrupt discontinuation can cause rapid bone loss and increased vertebral fracture risk1 within months of cessation. 2,6 Transition to a bisphosphonate is recommended when stopping denosumab therapy.2
Medication-related osteonecrosis of the jaw is a rare complication of antiresorptive therapies, preventive measures include pre-emptive dental treatment and maintaining good oral hygiene.5
Osteoanabolic Therapy
Osteoanabolic agents stimulate bone formation and improve bone microarchitecture, offering an alternative strategy for patients at very high risk of future fractures.1,2 To maintain gains in BMD, treatment with osteoanabolic therapies must always be followed by antiresorptive therapy to prevent rapid bone loss after discontinuation.2,7,8
Teriparatide is a recombinant parathyroid hormone analogue that stimulates osteoblast activity and reduces the incidence of vertebral and nonvertebral fractures.1 It is typically reserved for patients at very high fracture risk or those who cannot tolerate or do not respond to other osteoporosis treatments and is given as a daily injection for up to 24 months.1,2
Romosozumab is a monoclonal antibody that inhibits sclerostin, resulting in new bone formation while reducing bone resorption.1 It reduces vertebral and hip fracture risk in postmenopausal women and increases spine and hip BMD in men and women with osteoporosis.1,10 Romosozumab is administered monthly for up to 12 months.1
Clinical trial data indicate that romosozumab is more effective than alendronate in reducing subsequent fractures in high-risk patients10,11 with progressive reduction in new vertebral fractures at 24 months in patients who transitioned to antiresporptive therapies.7 Romosozumab produced greater increases in BMD than teriparatide in patients switching from ineffective bisphosphonate therapy.9
Romosozumab has been associated with an increased risk of serious cardiovascular adverse events compared to other osteoporosis treatments and is not recommended in patients with previous myocardial infarction or stroke.1
Both teriparatide and romosozumab are subsidised on the PBS for patients meeting specific eligibility criteria.2,12
Other Therapies and Prevention Strategies
Menopausal hormone therapy may reduce fracture risk in younger postmenopausal women (within 10 years of menopause), while raloxifene may be considered in selected women at vertebral fracture risk and prior or family history of breast cancer.2,5 Addressing modifiable risk factors remain standard care for all patients.2,5 Adequate calcium and protein intake and vitamin D status are essential to support skeletal health, although supplementation alone is insufficient for fracture prevention.2 Exercise interventions incorporating weight-bearing, resistance, and balance training improve bone strength, muscle function, and reduce falls risk.2 Falls prevention strategies, including medication review, vision assessment, and environmental modification, are essential components of fracture prevention.2,8
Osteoporosis management is increasingly guided by absolute fracture risk, with antiresorptive therapies as first-line and osteoanabolic agents for those at very high risk, supported by comprehensive lifestyle and prevention strategies. Early identification, combined with evidence-based medication use and preventive strategies, is essential to reduce fracture burden and improve patient outcomes.
Intensive Lipid Lowering in High-Risk Patients: Beyond Statins
Sheridan Klein, Hospital Pharmacist, Slade Pharmacy Richmond
Emerging lipid-lowering therapies are reshaping cardiovascular risk management in Australia, particularly for patients who remain at high risk despite conventional treatment. Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of morbidity and mortality, with aggressive lowdensity lipoprotein cholesterol (LDL-C) reduction recognised as essential to cardiovascular prevention across broad patient populations.1
The 2026 American College of Cardiology/American Heart Association Dyslipidaemia Guideline reinforces statins as firstline pharmacological therapy due to their strong evidence base in reducing cardiovascular events and mortality.2,3 However, many high-risk patients fail to achieve LDL-C targets despite maximally tolerated statin therapy, prompting increasing use of non-statin therapies.2,4 These include ezetimibe and new therapies that target the proprotein convertase subtilisin/ kexin type 9 (PCSK9) pathway.2,4 Currently, Australian and international guidelines increasingly support intensive lipidlowering in secondary prevention when LDL-C remains above 1.8mmol/L despite oral therapy.2-4
PCSK9 binds hepatic LDL receptors and promotes receptor degradation, reducing LDL clearance from circulation.4 Medications that target the PCSK9 pathway are an exciting development in lipid lowering treatment and include evolocumab (Repatha®) and inclisiran (Leqvio®), both of which are listed on the Pharmaceutical Benefits Scheme (PBS) for eligible high-risk patients, and significantly reduce LDL-C and apolipoprotein B.4,5 Evolocumab, a monoclonal antibody, binds circulating PCSK9 and prevents this degradation, whereas inclisiran uses small interfering ribonucleic acid technology to inhibit hepatic PCSK9 synthesis directly.4 Both therapies increase LDL receptor recycling and hepatic LDL uptake, reducing LDL-C by approximately 50-60%.6
PCSK9-targeted therapy is particularly beneficial in patients with familial hypercholesterolaemia, recurrent ASCVD events, persistently elevated LDL-C or statin intolerance.2 Large international trials have demonstrated reductions in myocardial infarction, stroke and cardiovascular mortality with intensive LDL-C lowering using PCSK9 inhibition.6,7 Common adverse effects are generally mild and include injection-site reactions, nasopharyngitis, arthralgia and influenza-like symptoms.4
Dose and frequency of administration is different between therapies. Evolocumab is administered subcutaneously every two or four weeks using a prefilled injection pen, whereas inclisiran is administered by a health professional, repeated
at three months, then every six months thereafter.3,4 Nurses, pharmacists and doctors remain critical in reviewing medication orders, reinforcing adherence, monitoring lipid profiles and adverse effects and supporting patient education regarding injection technique and long-term cardiovascular risk reduction.8
The expansion of PCSK9 inhibitor therapy represents an important advancement in Australian cardiovascular care, offering substantial benefit for high-risk patients who require aggressive lipid lowering beyond traditional therapy.
