Official Journal of the Society of Hospital Pharmacists of Australia

G E R I AT R I C T H E R A P E U T I C S R E V I E W
EDITED BY ROHAN A. ELLIOTT, BPHARM, BPHARMSC (HONS), MCLINPHARM, PHD, BCGP, FSHP

Management of gout in older people

Richard O. Day, AM, MD, FRACP1,2, Wendy Lau, BSc(Med), MBBS, FRACP3,4, Sophie L. Stocker, PhD2,4,
Eindra Aung, PhD2, Mathew J. Coleshill, PhD2,4, Marcel Schulz, MSc2,4, Jacob Bechara, BSc2,4, Jane E.
Carland, PhD2,4, Garry G. Graham, PhD5, Kenneth M. Williams, PhD5, Andrew J. McLachlan, PhD6,7
1 St Vincent’s Hospital Clinical School, UNSW Medicine, Sydney, Australia
2 Department of Clinical Pharmacology and Toxicology, St Vincent’s Hospital, Sydney, Australia
3 Westmead Hospital, Sydney, Australia
4 UNSW Medicine, Sydney, Australia
5 School of Medical Sciences, UNSW Medicine, Sydney, Australia
6 Sydney Pharmacy School, University of Sydney, Sydney, Australia
7 Department of Clinical Pharmacology, St Vincent's Hospital, Sydney, Darlinghurst, Australia

Abstract
Gout is an inflammatory musculoskeletal disorder with a prevalence of 1.6–6.8% in Australia. Gout is characterised by acute attacks
of severe joint pain secondary to raised serum concentrations of uric acid and joint deposits of monosodium urate crystals. Recurrent
attacks can affect quality of life and lead to irreversible joint damage. The prevalence of gout is increased in older people, and age-
related renal impairment, altered drug distribution and increased prevalence of comorbidities have significant consequences for safe
and effective gout pharmacotherapy. For treatment of acute attacks in older people, dose reduction of colchicine may be needed due
to renal impairment, and potential drug interactions require consideration. Use of non-steroidal anti-inflammatory drugs is limited
by peptic ulceration, ischaemic heart disease, hypertension and renal impairment. Short courses of oral glucocorticoids may be
preferable. For long-term urate-lowering therapy, allopurinol, probenecid and febuxostat are available in Australia. Lower starting
doses of allopurinol are recommended in patients with renal impairment, but dose escalation to achieve target urate should follow.
Concerns regarding increased cardiovascular risk with febuxostat are relevant to older patients. Despite the availability of effective
therapy, gout remains undertreated, with maintenance of urate-lowering therapy a major challenge. Education of patients and health
professionals is essential to improve adherence to therapy.

Keywords: gout, uric acid, urate lowering therapy, allopurinol, febuxostat, probenecid, renal impairment, metabolic syndrome.

INTRODUCTION looked by health policy makers, clinicians and society

Gout is an inflammatory musculoskeletal disorder.
Negative connotations about gout abound, but the rela-
tionship with excessive alcohol intake is the most perni-
cious. Although there is some truth in the association, it
is not a universal feature of those with this condition.
The major effect of gout on those who suffer it is well
reflected in Lady Mary Wortley Montagu’s declaration
in the 18th century, ‘People wish their enemies dead – but I
do not; I say give them the gout’.1 Gout has been over-
Address for correspondence: Richard Day, Department of Clinical
Pharmacology and Toxicology, St Vincent’s Hospital, Sydney, New
South Wales 2010, Australia.
E-mail: r.day@unsw.edu.au
generally in favour of conditions where ‘lifestyle’
choices are not considered to have contributed – various
cancers, for example.
WHY FOCUS ON GOUT IN OLDER PEOPLE?
The incidence and prevalence of gout increases with
age. So do comorbidities, notably those that are part of
the metabolic syndrome, namely Type 2 diabetes, hyper-
tension and dyslipidaemia.2,3 Renal function declines
with age, which contributes to the increasing incidence
of gout and has significant consequences for safe and
effective gout pharmacotherapy. Adverse drug reactions
increase with age because of declining efficiency of

Journal of Pharmacy Practice and Research (2019) 49, 90–97

© 2019 The Society of Hospital Pharmacists of Australia doi: 10.1002/jppr.1511
Management of gout in older people
clearance mechanisms, changes in drug distribution due
to the relative loss of muscle and increase in fat, and
generally increased end-organ sensitivity.4,5 The multiple
comorbidities common in patients with gout usually
mean multiple medications, increasing the risk of drug–
drug interactions and the hazards that accrue from
polypharmacy.6 The burden of musculoskeletal disor-
ders in the older population, including gout, is pro-
found. This is a major contributor not only to
substantial decrements in quality of life and large finan-
cial cost, but also reduced ability to exercise and control
weight, thereby exacerbating the toll from the metabolic
syndrome.7
WHY PHARMACISTS SHOULD BE
INTERESTED IN GOUT
Gout is most commonly observed in the community set-
ting. Although attacks often happen in hospitals follow-
ing surgery or other stressful presentations, community
pharmacists are often the first port of call for people liv-
ing with gout. Pharmacists can play an important role
in the ongoing management of people with gout, by
supporting adherence to non-pharmacological and phar-
macological strategies to reduce the risk of acute attacks
and avoid preventable medication-related harm.
Although pharmacists have expressed an interest in this
role,8 to date the contribution of community pharmacy
to improving outcomes for people with gout has been
reported to be small.9
ABOUT GOUT
Gout is the most common inflammatory arthritis in
men.10 The prevalence of gout in Australia is 1.6% of
patients attending general practices, and this is increas-
ing, reflecting a world-wide phenomenon in both devel-
oped and developing nations.11–13 In the 2007–08
National Health Survey, 4.7% of working age Aus-
tralians self-reported gout.14 In a 2015 South Australian
population survey, gout prevalence was reported to be
6.8%.15 In Indigenous Australians, the prevalence of
gout is 3.8% overall and 7% in men according to a 2002
survey undertaken in north Queensland,16 but there is
uncertainty about these prevalence rates.17 The condition
is much more common in men than women, with 20%
of men in Sydney (NSW, Australia) over the age of
70 years self-reporting gout when surveyed between
2005 and 2007.18 The condition becomes more prevalent
in women past the menopause, approaching rates seen
in men.
© 2019 The Society of Hospital Pharmacists of Australia
91
Attacks of gout are extremely painful and most com-
monly occur in the base of the great toe, although any
joint is susceptible. An acute attack is a self-limiting con-
dition that, apart from being very painful, substantially
intrudes on the sufferer’s life. If attacks are recurrent,
commonly due to inadequate management, quality of
life is considerably reduced, a fact that is generally
underappreciated.19,20
Gout occurs in people with raised serum concentra-
tions and body loads of urate, the circulating ionised
form of uric acid. This condition is known as hyperuri-
caemia. The definition of hyperuricaemia is contentious,
with different reference ranges for urate concentrations
quoted on pathology reports from different sources.
Urate concentrations in the population are not normally
distributed, but are skewed in the direction of higher
concentrations.21 Urate concentrations tend to increase
with age, renal impairment and after the menopause,22
the latter likely due to the loss of oestrogen, which
enhances urate clearance via the kidneys. The upper
limit of a commonly reported ‘normal range’ for urate is
0.42 mmol/L. This was likely chosen because it is also
the solubility point for urate, above which urate can
precipitate to form monosodium urate crystals.23 How-
ever, many individuals have higher urate concentrations
and never suffer with gout, a condition known as
‘asymptomatic hyperuricaemia’. This is not an indica-
tion for urate-lowering therapy (ULT). Conversely, indi-
viduals with urate concentrations <0.42 mmol/L can
present with gout. We now know that the propensity to
experience gout attacks is affected by an individual’s
innate immunity and ability to trigger the formation of
the ‘inflammasome’ in response to crystals of urate
forming in joints.24,25 One complication in evaluating
suspected gout is that the serum urate concentration
drops during an acute attack, which may divert the clin-
ician from consideration of the diagnosis. A definitive
diagnosis is made by demonstrating needle-shaped, neg-
atively birefringent crystals in aspirated joint fluid.
Unsurprisingly, the higher an individual’s urate concen-
tration, the more likely a gout attack is to occur. If urate
concentrations are maintained below 0.36 mmol/L, gout
attacks will cease and accumulated deposits of urate
crystals in the joints, subcutaneous tissue and organs
such as the kidney will dissipate, the latter even faster if
urate concentrations are maintained below 0.3 mmol/
L.26,27
Urate is the end-product of the metabolism of purines
that are released when cells die and nucleic acids from
DNA and RNA are released. Rarely, the metabolic path-
way forming urate is overactive due to genetic variants
in some of the enzymes involved, leading to hyperuri-
caemia. More commonly, the kidneys of people with
Journal of Pharmacy Practice and Research (2019) 49, 90–97
92
hyperuricaemia are less efficient at clearing urate from
the blood via renal tubular transport systems than those
without hyperuricaemia, resulting in elevated urate con-
centrations. This reduced renal clearance has been attrib-
uted to genetic variation in the drug transporters
responsible for movement of urate across the renal
tubule.28,29 Renal impairment also contributes to raised
urate.
Recurrent acute attacks, apart from being distressing
and disruptive, signal possible joint and organ damage,
especially kidney damage. This is the signal for the suf-
ferer and clinician to contemplate pharmacotherapy to
prevent recurrence and damage from continued deposi-
tion of crystals in joints and organs. Effective therapies
are available to reduce urate plasma concentration to
levels at which recurrent attacks will settle (<0.36 mmol/
L) and excess deposits of monosodium urate will dissi-
pate (<0.30 mmol/L recommended).
Of all the rheumatic disorders, gout is the only one
where a patient can be guaranteed that there will be no
further attacks of gout so long as their plasma urate is
controlled by taking their ULT. Yet, the prevalence of
this condition continues to increase. There are two
explanations: (1) most importantly, adherence to therapy
is essential to guarantee elimination of attacks; and (2)
the dose of ULT needs to be sufficient to achieve the
aforementioned plasma urate concentrations.
ABOUT GOUT MANAGEMENT:
PHARMACOTHERAPY AND ISSUES IN OLDER
PEOPLE
Attention to lifestyle, including diet and exercise, and
attending to comorbidities and risk factors for acceler-
ated cardiovascular disorders is a critical component of
the management and education of people with gout,
although most of the benefit from these measures
derives from reduction of cardiovascular risk.30–33 The
focus upon pharmacotherapy in this paper should not
be construed as undervaluing the contribution of non-
pharmacological interventions to the long-term health of
people with gout.
Acute Gout
Acute attacks of gout can be treated with colchicine,
non-steroidal anti-inflammatory drugs (NSAIDs) or cor-
ticosteroids. Some people use adrenocorticotrophin
(ACTH) injections, but the advantage of this approach
relative to glucocorticosteroids is not established.34
Rarely, colchicine, NSAIDs and oral and injectable glu-
cocorticosteroids are contraindicated and, in the absence
Journal of Pharmacy Practice and Research (2019) 49, 90–97
R. O. Day et al.
of infection, rheumatologists may prescribe parenterally
administered drugs that block the cytokine interleukin-
1, such as canakinumab and anakinra.33
Colchicine
A revision to the long-held guidance to dose colchicine
until abdominal pain and diarrhoea occur has been an
important advance. In an acute attack of gout, the cor-
rect regimen is to take two colchicine 0.5-mg tablets (to-
tal dose 1 mg), followed by one 0.5-mg tablet 1 h later
and then withhold the drug for at least 24 h. This
approach is effective and substantially safer.35 Because
the drug is partially cleared by the kidneys (~40–60%),
the dose should be reduced if the patient’s creatinine
clearance is reduced (e.g. <30 mL/min).36,37 Colchicine is
also metabolised in the liver by cytochrome P450 3A4/5
and subject to transport from the systemic circulation to
the gut via P-glycoprotein. These clearance mechanisms
put patients on colchicine at risk of serious drug interac-
tions, notably by drugs that inhibit cytochrome P450
3A4/5 and P-glycoprotein, such as clarithromycin and
diltiazem.38 Safe storage of colchicine is important
because it is lethal in overdose because it inhibits cell
division by inhibiting microtubule assembly during cell
replication.28 Unfortunately, the drug is without an anti-
dote. Children are at serious risk if they can access this
drug.
Non-steroidal Anti-inflammatory Drugs
There is no good reason to pick one NSAID over
another. Although indomethacin has a historical position
as the NSAID of choice, this is no longer appropriate
because it also has more of the adverse effects shared by
all NSAIDs, including gastrointestinal intolerance with
indigestion and ulceration, exacerbation of hypertension,
cardiac failure, renal impairment and the risk of throm-
bosis, particularly myocardial infarction. Ibuprofen,
meloxicam or naproxen are reasonable choices, the key
being to limit duration of therapy to the 5–7 days of an
attack and to protect the upper gastrointestinal tract
with a proton pump inhibitor.39–41 Older patients with
past peptic ulceration, ischaemic heart disease, hyperten-
sion or renal impairment are at greater risk for exacerba-
tions of these conditions, so avoidance of NSAIDs in
this age group is preferred.
Glucocorticoids
Glucocorticosteroids are powerful anti-inflammatory
medicines and a better option in older patients than
NSAIDs for acute gout attacks. A common regimen is
oral prednisolone 25 mg for 2 days, reducing to zero
over the next 3–4 days. Sleep disturbances, psychologi-
cal symptoms and exacerbations of hypertension or
© 2019 The Society of Hospital Pharmacists of Australia
Management of gout in older people
cardiac failure are hazards, but short exposures can gen-
erally be managed. There is also the option of injecting
a synthetic glucocorticoid into affected joint(s), which is
highly effective but more realistic for larger joints such
as the knee.28
Recurrent and Persistent Gout
Urate-Lowering Therapy
The major challenge for ULT is maintaining adherence
and persistence with therapy. Rates of persisting with
ULT are low, ranging from 40% to 70%, with most stud-
ies reporting rates below 50% at 1 year.42–44 Older peo-
ple are more likely to be taking multiple medicines for
comorbid health conditions and, as such, may have
more problems with adherence. An important disincen-
tive to maintaining adherence is the occurrence of acute
attacks of gout in the first 6 months after commencing
ULT. This phenomenon is more common if the serum
urate concentration is lowered rapidly. Not surprisingly,
patients not expecting this after commencing a therapy
to prevent gout are likely to lose confidence in ULT. The
likelihood of acute attacks during the induction of ULT
has led to the mantra ‘start low, go slow’ to describe the
approach to establishing ULT over the first 6 months, to
reduce the risk of acute attacks.45 The other strategy is
to coprescribe prophylactic therapy against acute attacks
for these initial 6 months.46 Any of the three options
described earlier (colchicine, NSAIDs or corticosteroids)
can be used, but colchicine has emerged as the most
appropriate, especially for older patients. NSAIDs or
prednisolone therapy for 6 months in this age group,
especially with cardiovascular comorbidities, is inadvis-
able. Colchicine dosing should be reduced from a stan-
dard 0.5 mg twice a day to once a day in those with
renal impairment (e.g. creatinine clearance <30 mL/min).
Dosing also needs to be reduced if loose bowels are an
issue. It is important that patients are educated to recog-
nise the adverse effects of colchicine so that early dose
adjustment or discontinuation occurs.
Allopurinol
Allopurinol inhibits urate synthesis by xanthine oxidore-
ductase, also known as xanthine oxidase.23 There has
been an important shift in how we use this highly effec-
tive medicine. Concern regarding Stevens–Johnson syn-
drome (SJS), a severe cutaneous and mucosal
consequence of allopurinol hypersensitivity, and the
now contested relationship to dose and renal impair-
ment,47 led to dosing advice that achieved neither
enhanced safety nor control of gout.48 The active
metabolite of allopurinol, oxypurinol, is cleared exclu-
sively by the kidneys and is retained in renal
© 2019 The Society of Hospital Pharmacists of Australia
93
impairment.23 Hence, guidelines had recommended
dose reduction in keeping with renal function.28 As a
result, older people, with their higher rates of renal
impairment, were systematically underdosed because of
fear of allopurinol hypersensitivity such that the target
urate concentration was not commonly achieved and
gout was often uncontrolled. The advice to limit the
dose in people with renal impairment has been super-
seded, and most contemporary guidelines recommend
dose increases until urate target concentrations are
reached; this often means that allopurinol doses exceed
300 mg/day.27
A further important insight has been the revelation
that the daily dose of allopurinol, or indeed any ULT,
required to reach target concentrations correlates with
the pretreatment serum urate concentration.49,50 Exami-
nation of plasma concentrations of oxypurinol has indi-
cated that they are not better correlated with urate
concentrations than dose, such that measuring oxypuri-
nol can be reserved for cases where a lack of response is
not understood, often non-adherence being suspected.50
Regardless of the approach, the risk of allopurinol
hypersensitivity remains. However, it is known to be
much more likely to occur in patients who have one or
two HLA-B*58:01 antigens indicating the autoimmune
pathogenesis of this devastating adverse reaction.51 It is
recommended that this human leucocyte antigen (HLA),
which has a prevalence of approximately 15% in Han
Chinese, a little less in Koreans and Thai people but
much less in Caucasians, is tested for in higher-risk
patients if allopurinol is being considered, the test being
100% specific for SJS, although not very sensitive.52–54
Guidelines now recommend a starting dose of allopuri-
nol based on renal function, with the dose then increased
at 2- to 5-weekly intervals until the target urate serum con-
centration is reached.55 The manufacturer’s product infor-
mation (https://www.mimsonline.com.au.acs.hcn.com.au/
Search/FullPI.aspx?ModuleName=Product%20Info&searc
hKeyword=allopurinol&PreviousPage=~/Search/QuickSea
rch.aspx&SearchType=&ID=124000001_2) notes that the
upper limit for dosing is 900 mg/day, so there is plenty of
room to move.
Uricosuric Medicines: Probenecid, Lesinurad, Verinurad
and Benzbromarone
Members of this class of medicines inhibit the uptake of
urate from the proximal renal tubule by inhibiting the
uric acid transporter URAT1 on the renal tubule mem-
brane.56 Experience indicates that the efficacy of urico-
suric medications is not substantively different from that
of allopurinol if doses of allopurinol are adjusted
according to serum urate, but well-conducted head-to-
head studies are lacking. Moderate renal function at
Journal of Pharmacy Practice and Research (2019) 49, 90–97
94
least is required for efficacy, but there is variation across
the class in this regard. A hazard with commencing this
class of ULT, in addition to the risk of precipitating an
attack of gout, is precipitation of urate in the renal
tubules leading to acute obstructive uropathy. This is
countered by maintaining hydration through this risk
period and following the ‘start low, go slow’ dosing
maxim. Combinations of allopurinol and uricosuric
medicines are rational and highly effective if doses of
either alone are insufficient to reach target urate concen-
trations.57–60 Probenecid is available in Australia; lesinu-
rad is registered in Europe and the US, but not
Australia;61 verinurad, a molecule related to lesinurad,
is in an advanced stage of clinical development and is
claimed to have a lower renal impairment signal than
its forebear and is likely to reach the market soon;62 and
benzbromarone was withdrawn from the Australian
market because of serious hepatotoxicity in a small
number of patients and is now only accessible via the
Special Access Scheme, reserved for patients where
other ULT options are not tolerated.63 Benzbromarone is
a potent uricosuric and remains active at lower crea-
tinine clearance levels than probenecid.
Febuxostat
Febuxostat is an alternative xanthine oxidoreductase inhi-
bitor available on the Australian Pharmaceutical Benefits
Scheme as an Authority Required medicine for chronic or
tophaceous gout in patients with a medical contraindica-
tion to allopurinol, a documented history of allopurinol
hypersensitivity syndrome or intolerance of allopurinol
(http://www.pbs.gov.au/medicine/item/10445R). Febux-
ostat is a useful addition to the armamentarium for ULT,
but ‘leakage’ beyond these criteria is likely, and the devel-
opment of this and other ULT medicines at great expense
to individuals and the community has been critiqued.64
There were concerns at registration that there was a car-
diovascular risk associated with febuxostat, which has
been confirmed recently in comparison with allopurinol.65
This is of great relevance to older patients with cardiovas-
cular comorbidities and risk factors, leading some com-
mentators to opine that this drug should not be
considered as a first-line drug.66
PUBLIC HEALTH OPPORTUNITIES
Gout is the ‘Cinderella’ of musculoskeletal conditions;
prevalent, impactful and eminently treatable with a
close to 100% success rate, but the condition is sadly
overlooked. The barriers to effective treatment on a
national scale are clear.67 Improved rates of treatment
persistence, based upon education of patients and health
Journal of Pharmacy Practice and Research (2019) 49, 90–97
R. O. Day et al.
professionals, including pharmacists, are needed. Inno-
vative and cost-effective public health interventions are
also needed. As a current example in Australia, the use
of a mobile app to educate and receive individualised
feedback regarding serum urate concentrations is under-
going testing in a double-blind cluster-randomised con-
trolled trial in primary care.68
Indigenous Australians are at risk for gout and its
consequences, and more recent recognition of this
propensity is a step towards culturally-appropriate pro-
grams to improve the lives of those afflicted.12
WHAT’S NEW IN GOUT?
The move towards ‘treat to target’ serum urate concen-
trations has emerged in the past decade and has shown
that most people can achieve target concentrations by
allopurinol dose adjustments. The concerns about this
practice in people with renal impairment have largely
been allayed, although more evidence for safety is
needed. The challenge is to implement this change
across primary care. In this sector, changing dosing
practice is difficult because restriction of maximum
doses had previously been strongly promoted.
The best methods for establishing effective ULT, with
the express purpose of building confidence that the con-
dition can be controlled without increased risk of serious
toxicity, remains a work in progress. Most authorities rec-
ommend starting with low doses of ULT according to
renal function, then increasing the dose in small incre-
ments until the target urate concentration is achieved,
with coverage for acute attacks. The optimal duration of
this cotherapy is not yet established, but most guidelines
suggest 6 months. This could vary depending on the
duration of gout, the baseline urate and the presence of
gouty tophi, the latter being associated with a longer per-
iod of risk.29 Recent work supports early initiation of
ULT, even during an acute attack, and, importantly, not
ceasing ULT if an attack occurs.69,70
POTENTIAL FOR PHARMACY CONTRIBUTION
Persistence with ULT is the greatest challenge in the suc-
cessful management of gout. Because pharmacists inter-
act regularly with people with gout who are taking ULT
and prophylactic treatment for acute attacks of gout,
there is an opportunity to monitor and improve persis-
tence. Community pharmacists, as trusted advisers to
their clients, can also identify patients who are having
acute gout attacks. These patients may not have started
ULT and this effective option can be canvassed. During
© 2019 The Society of Hospital Pharmacists of Australia
Management of gout in older people
the initiation of ULT, patients experiencing acute attacks
can be reassured that these will cease when serum urate
concentrations remain below 0.36 mmol/L for 6 months.
In addition, these patients can be advised regarding the
benefits of continuing to take ULT even if an acute attack
occurs in this 6-month ‘establishment phase’. An increase
in the dose of a patient’s prophylactic colchicine may be
appropriate if not exceeding 0.5 mg twice a day, and
referral back to the patient’s general practitioner (GP)
could be recommended accordingly. Finally, when peo-
ple present with features of a gout attack, for example
very painful acute pain, most commonly at the base of
their great toe, this diagnostic suggestion can be made
and referral to their GP recommended. Innovative collab-
orative public health programmes involving community
pharmacists, district nurses, GPs and specialists are
being explored. Point-of-care testing for urate and allop-
urinol dose adjustments undertaken by community phar-
macists has demonstrated promising results in the effort
to reduce the burden of gout among the M~aori peoples
of New Zealand.71
CONCLUSION
The effectiveness of gout management in the community
is poor, resulting in impaired quality of life for sufferers.
There is widespread lack of understanding about the
condition and how to manage it effectively. There is
stigma associated with the label, with some even sug-
gesting a name change to ‘crystal arthritis’. There are
challenges in commencing ULT that are hard to convey
to people who have gout, and these challenges are not
well understood by prescribers. Comorbidities,
polypharmacy, organ function decline, drug interactions
and drug–disease interactions all add to the complexity
and challenges of dealing with gout in the older person.
Given the centrality of pharmacotherapy to this condi-
tion, the opportunity for pharmacists to make a major
contribution to improving outcomes is obvious.
ACKNOWLEDGEMENTS
Dr Rohan Elliott, BPharm, MClinPharm, PhD, BCGP,
FSHP, FASCP Lead Pharmacist, Aged and Continuing
Care, Austin Health, Heidelberg, VIC 3084 for his
invaluable review of the manuscript and advice.
Conflicts of interest statement
Richard Day declares that the National Health and Med-
ical Research Council (NHMRC) Partnership Grant
© 2019 The Society of Hospital Pharmacists of Australia
95
#1094708, ‘Patient-centred eHealth approach to improv-
ing outcomes for gout sufferers’, lists Menarini Aus-
tralia, AstraZeneca Australia, Lexy Davies Trust, NPS
MedicinesWise, Arthritis Australia, Pharmaceutical Soci-
ety of Australia and the Australian Rheumatology Asso-
ciation as Funding Partners with the NHMRC.
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Received: 06 September 2018
Revised version received: 13 October 2018
Accepted: 20 October 2018
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Journal of Pharmacy Practice and Research (2019) 49, 90–97