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Special
considerations in
the management
of gout
Pathophysiology
of pseudogout
Clinical
presentation of
pseudogout
Diagnosis and
treatment of
pseudogout
Authors’ case
studies
GOUT and other
crystal arthropathies
— Part 2
The authors
DR CHANDI PERERA,
consultant rheumatologist,
Inflammatory Diseases
Research Unit, school of
medicine, University of NSW,
and Sydney Adventist Hospital,
Wahroonga, NSW.
Last week, Part 1 of this series looked at the pathogenesis, clinical features, diagnosis and treatment of gout. This week, Part 2
concludes with a discussion of special considerations in the management of gout, and an overview of the pathophysiology,
clinical presentation, diagnosis and treatment of calcium pyrophosphate dihydrate deposition disease (pseudogout).
Special considerations in the management of gout
Specialist referral for gout
AN often-asked question is when to
refer a patient with gout. Our opinion
is that it is best to consider specialist
referral in complex gout, poorly controlled disease, younger patients requiring further investigation, when there
is doubt about the diagnosis, to reinforce lifestyle advice and, where
required, to review ongoing management of uncomplicated gout.
Special considerations
Nephropathy
Acute uric acid nephropathy is the
single acute presentation of urate
crystal deposition that needs urgent
intervention. All other initial manifestations of renal crystal deposition
disease are readily treatable. In
patients with hyperuricaemia and
renal disease who have bland urine
sediment it is important to consider
the possibility of lead toxicity as an
alternative aetiology especially if
hyperuricaemia is out of proportion
to the degree of renal disease.
Urolithiasis
Increasing rates of urinary uric acid
excretion are associated with a higher
risk of uric acid and calcium oxalate
stone formation. Uric acid calculi form
about 20% of renal stones with
approximately 80% of the stones
occurring in males and a peak incidence in the sixth decade in both sexes.
Most patients with urate stones do
not have gout or hyperuricosuria. Fifty
per cent of stone formers have diabetes
or impaired glucose tolerance.
Diagnosis is made by non-contrast
helical computerised tomography. Pure
uric acid calculi are radiolucent and
often missed on conventional X-rays
although stone analysis shows that
some uric acid stones are partially
composed of calcium oxalate.
Treatment involves increasing alkalinisation of urinary pH usually using
sodium bicarbonate and increasing urinary volume together with allopurinol
to reduce excretion as recommended in
the CARI (Caring for Australasians
12
with Renal Impairment) guidelines.
Therapeutic failure in gout
Non-compliance is an important but
remediable cause of failure. It is a relatively common clinical problem due to
a combination of factors including a
natural history of self-limiting recurrences, therapeutic intolerance, its
potential curability and lack of patient
understanding of disease pathophysiology or appreciation of the need for
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long-term treatment. Usually the
patient will have discontinued treatment due to lack of symptoms and
over the years will have presented to
several primary care physicians for
treatment of acute episodes; and subsequently will have failed to follow up.
Patient education at disease onset is
arguably the single most important
factor determining therapeutic success.
Alcohol ingestion is an important part
of the problem and needs to be clearly
identified and broached at the time of
instituting therapy.
DR ANDREW BROOK,
consultant rheumatologist and
visiting medical officer,
department of rheumatology,
Canberra Hospital; and Canberra
Rheumatology, Canberra, ACT.
Emerging therapies for gout
Febuxostat
Febuxostat, a newer selective xanthine
oxidase inhibitor (inhibiting both oxidised and reduced forms) represents
an alternative to allopurinol for
cont’d next page
DR KATHIE TYMMS,
consultant rheumatologist and
visiting medical officer,
department of rheumatology,
Canberra Hospital; and Canberra
Rheumatology, Canberra, ACT.
28 August 2009 | Australian Doctor |
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HOW TO TREAT Gout and other crystal arthropathies – Part 2
from previous page
patients with gout. It is metabolised
via hepatic conjugation and oxidation with less than 5% excreted
unchanged by the kidney. No dose
adjustment is required in patients
with mild to moderate renal impairment. No clinically significant drug
interactions were observed with
colchicine, hydrochlorothiazide,
indomethacin or warfarin.
The Febuxostat versus Allopurinol Controlled Trial (FACT)
demonstrated it was more efficacious at both 80mg and 120mg
doses than the commonly used
dose of allopurinol 300mg in
meeting the primary endpoint
(serum uric acid level of
13
<0.36mmol/L). While rates of
flares on treatment after 52 weeks
in all groups were similar, it
remains unclear as to what the
optimal dose of febuxostat is and
if higher doses of allopurinol
would be more effective than the
doses of febuxostat used. Further
safety and efficacy data, especially
with respect to cardiovascular
events and its usefulness in meta-
bolic syndrome and hepatic and
renal impairment, are needed.
However, at first glance it offers a
promising alternative to allopurinol-hypersensitivity patients on azathioprine or 6-mercaptopurine and
a possible solution to the perennial
problem of co-existing renal impairment. The long-term cost of treatment is likely to be a factor in
uptake.
Rasburicase
Rasburicase is a recombinant
preparation of urate-oxidase (uric-
ase) synthesised from Aspergillus
flavus that acts by converting uric
acid to allantoin, an inactive and
soluble uric acid metabolite with
no effect on formation of uric acid.
Currently rasburicase is used to prevent acute urate nephropathy precipitated by chemotherapy-induced
tumour lysis in patients with
leukaemia and lymphoma. It is of
limited value in treating chronic
gout largely due to a short half-life
(approximately 18 hours), mode of
administration (infusion) and
potential immunogenicity.
Pegloticase
A pegylated mammalian recombinant uricase currently in phase III
clinical trials, pegloticase has
demonstrated rapid reduction of
urate levels and in several cases
tophus size during phase II development. It is likely to have a
niche role in tophaceous gout,
particularly when patients are
intolerant or resistant to allopurinol.
However further clinical studies need to confirm its efficacy
across different populations.
Pseudogout or CPPD-deposition disease
PSEUDOGOUT is a crystal
arthropathy associated with
ageing. The term pseudogout
describes an acute arthritis
with characteristic calcifications in cartilage (chondrocalcinosis) and calcium
pyrophosphate dihydrate
(CPPD) crystals in the synovial fluid.
The acute attacks of
pseudogout, which are similar to those of gout, are followed by spontaneous resolution. Over time, recurrent
episodes can result in
chronic arthritis with degeneration of cartilage and
bone.
Joints commonly involved
22
The acute attacks
of pseudogout,
which are similar
to those of gout,
are followed by
spontaneous
resolution.
| Australian Doctor | 28 August 2009
include the knees, wrists,
shoulders, hips and ankles.
Hyperparathyroidism, hereditary haemochromatosis,
hypothyroidism and hypomagnesaemia are recognised
metabolic associations.
The diagnosis of pseudogout is established clinically
and by demonstrating
weakly positive bi-refringent crystals on polarised
light microscopy with supporting radiographic features, which include chondrocalcinosis and the usual
characteristic degenerative
changes seen in osteoarthritis (including cartilage loss,
subchondral cyst formation
and osteophyte formation).
Radiological features of
pyrophosphate arthropathy
overlap those of osteoarthritis; however, the pattern of
joint involvement may help
to discriminate it from primary osteoarthritis. Both
conditions are common in
the elderly and the role of
each process in the pathogenesis of the other is uncertain, and it is important to
consider both processes
together rather than in isolation.
The differential diagnosis
for pseudogout includes
gout, septic arthritis, inflammatory
osteoarthritis,
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rheumatoid arthritis and,
occasionally,
spondyloarthropathy.
Terminology
Before further discussion
there are a number of terms
used that require clarification:
• Pseudogout describes the
clinical syndrome of acute
arthritis associated with
CPPD deposition in articular cartilage.
• Chondrocalcinosis simply
describes calcification of
articular cartilage.
• The term pyrophosphate
arthropathy indicates
structural abnormality of
cartilage and bone associated with CPPD deposition.
• CPPD-deposition disease is
a term that seems to
encompass both pseudogout and pyrophosphate
arthropathy, although it is
often loosely used as a synonym implying either or
both of these conditions.
Often confusion surrounding these terms stems from
a combination of factors,
including the coexistence of
CPPD crystals in asymptomatic osteoarthritis, incidental chondrocalcinosis in
osteoarthritis and loose use
of terminology.
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Epidemiology and aetiology of pseudogout
Prevalence
CPPD crystals formed
induce an intra-articular
acute inflammatory response,
with neutrophil degranulation and release of reactive
oxygen species, resulting in
acute pseudogout. Recent
findings suggest a crucial role
for interleukin-1 in pseudogout, and may explain the
success of treatment with
anakinra, the interleukin-1
inhibitor, in resistant cases.
WHILE the prevalence of
CPPD-deposition disease is
unclear and depends on the
definition used, about 35%
of patients presenting for
total knee replacement for
osteoarthritis have evidence
of CPPD deposition.
Framingham sub-cohort
analysis showed an overall
prevalence of 8% for
chondrocalcinosis in the 6393 year age group, with the
greatest prevalence in those
14
over 85 years. Increasing
age seems to be the main risk
factor for sporadic chondrocalcinosis.
Genetics
Scanning electron
micrograph of
calcium phosphate
crystals on the
surface of cartilage
in a knee joint.
Pathophysiology
CPPD-deposition disease is a
disorder of articular cartilage,
associated with overproduction of inorganic pyrophosphates by chondrocytes.
CPPD crystals and basic calcium phosphate ([BCP] carbonated-substituted hydroxyapatite, tricalcium phosphate
and octacalcium phosphate)
crystals are associated with
CPPD-deposition disease.
Both CPPD and BCP crystals
increase in vitro chondrocyte
mitogenesis, metalloproteinase elaboration and
prostaglandin E2 production.
Worsening osteoarthritis
has been demonstrated after
introduction of CPPD crystals in animal models, suggesting these crystals probably play a role in causing or
accelerating degeneration of
cartilage.
BCP crystals have been
demonstrated in patients with
primary osteoarthritis. While
BCP crystals seen in
osteoarthritic joints lack clear
radiological associations and
are difficult to find in synovial fluid, these crystals are
thought to be markers of
severe osteoarthritis and have
been proposed as potential
therapeutic targets. However,
symptomatic arthritis associated with BCP crystals, such
as Milwaukee shoulder syndrome, is uncommon in
patients under 60.
While deposition of calcium-containing crystals can
occur in most tissues, deposition is frequently intra-articu-
lar and peri-articular. The
exact mechanism of cartilage
calcification is uncertain; it is
thought to depend on concentrations of extracellular inorganic phosphate, pyrophosphate and calcium and
soluble factors such as transforming growth factor-ß
which modulate extracellular
pyrophosphate. Excess extracellular pyrophosphate results
in CPPD crystal deposition, a
phenomenon that probably
increases with ageing.
While chondrocalcinosis
may be sporadic, and
uncommonly associated with
some metabolic disorders, a
rare familial predisposition
has also been reported. No
studies to date have quantified the different aetiologies
and cases attributed to familial predisposition.
Historically, scientific attention to a genetic link to calcium-crystal-related arthritis
was first raised in a series of
cases in the late 1950s; patients
in this cohort presented by
Sit’aj and Zitnan belonged to
15
five families.
Familial inheritance is largely
autosomal dominant and
seems to have a relatively early
initial clinical presentation.
Using linkage analysis
studies in families with
CPPD arthropathy, loci have
been identified on chromosome eight (CCAL1) and
five, with that on 5p
(CCAL2) considered to be
particularly important, as it
has been linked to disease
phenotype in apparently
unrelated families.
However not all familial
inheritance can be explained
by these two genes, suggesting genetic loci heterogeneity even in so-called familial
CPPD-deposition disease. A
mutation of the ANKH gene
(a transmembrane protein
involved in inorganic phosphate transport) responsible
for familial CPPD-deposition
disease has been described
16
by Williams, et al.
Patients with familial
CPPD-deposition disease are
likely to develop early and
more aggressive disease.
CPPD-deposition disease
linked with metabolic associations tends to present at an
earlier age. A familial form
of chondrocalcinosis associated with diffuse idiopathic
skeletal hyperostosis (DISH)
has also been reported.
cont’d next page
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HOW TO TREAT Gout and other crystal arthropathies – Part 2
Clinical presentation of pseudogout
CPPD-DEPOSITION disease
has a wide spectrum of intraarticular and extra-articular
clinical manifestations,
including monoarticular and
polyarticular pseudogout,
axial spinal inflammation
and tenosynovitis. The knee
joints are commonly affected,
with the elbows, wrists,
shoulders, hips and ankles
also affected. Metacarpophalangeal (MCP) joints may
also be involved.
Direct joint trauma,
stress response related to
intercurrent illness, surgery
and parenteral fluid administration leading to altered
fluid-balance states will
often precipitate the usually
self-limiting acute episodes.
A typical acute attack of
pseudogout will reach its
peak within 24 hours and
usually resolve over 1-3
weeks. Clinical features are
due to inflammation of the
joint and may mimic the
intensity of gout, with erythema, swelling, pain, loss
of function and exquisite
tenderness — hence the
name pseudogout.
Pseudogout may uncommonly present with systemic
features, including fever,
leukocytosis and elevated
inflammatory markers more
commonly seen in gout and
infection, and in such cases it
is important to exclude pos-
sible sepsis. Elderly patients
may present with delirium.
Atypical presentations
include neck pain and
headache associated with
fevers, and low-grade, diffuse, symmetrical polyarticular inflammation that may
be mistaken for meningitis
and rheumatoid arthritis,
respectively. Occasionally a
low-positive rheumatoid
factor titre may further add
to the confusion.
A subgroup of patients
presents with proximal
inflammatory symptoms
not unlike polymyalgia
rheumatica. Features suggestive of CPPD arthritis in
this group of patients
include calcific tendinopathy, tibiofemoral osteoarthritis and ankle involvement.
Reported cases of CPPDdeposition disease and
hypomagnesaemia
in
patients with short bowel
syndrome mean that primary-care
physicians
should be alert to this possibility.
Chondrocalcinosis associated with metabolic disorders and familial chondrocalcinosis is uncommon
but must be considered in
patients presenting before
age 55 or if there is widespread polyarticular chondrocalcinosis.
Diagnosis of pseudogout
WHEN there is clinical doubt
about the diagnosis, demonstration
of crystals by synovial fluid analysis
is essential, as is the exclusion of
infection. The presence of typical
radiographic calcifications supports
the diagnosis. Crystals show either
no or weakly positive bi-refringence
on polarised light microscopy and
are often difficult to detect.
Where the symptomatic joint distribution overlaps that of typical
osteoarthritis, and in the absence
of associated chondrocalcinosis
and/or demonstrated crystals in
synovial fluid, a diagnosis is made
more difficult.
The possibility of CPPD crystal
deposition disease needs to be considered particularly when radiological features of osteoarthritis are
evident in joints not commonly
affected in primary osteoarthritis.
While there is an established radiographic association between chondrocalcinosis and osteoarthritis, the
absence of chondrocalcinosis does
not exclude a clinical diagnosis of
pseudogout.
CPPD crystals seen in both
pseudogout and asymptomatic
osteoarthritic joints can also coexist
with uric acid crystals and BCP
crystals. The association between
calcium crystals and osteoarthritis is
complex, and direct correlation
between chondrocalcinosis and car17
tilage loss is at best tenuous. Also,
the presence of intracellular crystals in synovial fluid from the knee
joint is not clearly associated with
18
inflammatory symptoms.
The differential diagnosis of acute
monoarticular pseudogout includes
gout and septic arthritis. As mentioned above, chronic CPPD-deposition disease may be polyarticular
or oligoarticular and is often mis-
Table 5: Diseases associated
with pseudogout
• Haemochromatosis
• Hypomagnesaemia
• Hyperparathyroidism
• Hypothyroidism
• Wilson’s disease
Table 6: Standard
investigations
Clinical features of pseudogout may include erythema, swelling, pain, loss of
function and tenderness of the joint. Exclusion of infection is essential.
taken for rheumatoid arthritis or
primary generalised osteoarthritis;
investigations are tailored to differentiate between pseudogout and
these conditions.
After a diagnosis of CPPD-deposition disease has been established,
screening for associated conditions
(table 5) should be undertaken.
Investigations include:
• Iron studies.
• Calcium level.
• Magnesium level.
• Phosphate level.
• Uric acid level.
• Thyroid function tests.
• Liver function tests.
• Parathyroid hormone level.
• Caeruloplasmin level (tables 6
and 7).
Wilson’s disease and hypophosphatasia are unlikely to be associated with radiological chondrocalcinosis in people over 60.
Likewise, manifestations of
haemochromatotic iron overload
are unlikely in a premenopausal
woman. A high degree of clinical
suspicion is required to diagnose
haemochromatosis.
Radiological assessment of
pseudogout
Most joints with radiological evidence of CPPD crystal deposition are
asymptomatic, leading to the assertion that, unlike in gout, the exact
role of imaging in CPPD-deposition
disease is unclear. However plain
radiography and ultrasonography
remain important tools and assist in
diagnosing these disorders.
The typical appearance of CPPD
crystal arthropathy on plain radiography is chondrocalcinosis, and is
commonly seen in fibrocartilage of
the knee, triangular ligament of the
wrist and pubic symphysis.
Degenerative changes of MCP
joints and patellofemoral joints
should raise suspicion of an associated CPPD crystal deposition
arthropathy and its related metabolic
associations. Squaring of bone ends
and presence of hook-like osteophytes
in MCP joints, particularly if involving the second and third, raises the
possibility of haemochromatosis and
associated CPPD arthropathy, while
severe isolated patellofemoral jointspace degeneration may be seen in
• Synovial fluid for crystals, Gram
stain, microscopy for cells and
culture and sensitivity
• FBC
• Urea, electrolytes, creatinine;
LFTs; calcium, magnesium, phosphate
• Uric acid
• CRP, ESR
• X-ray
Table 7: Additional
investigations
• Iron studies
• Parathyroid hormone
• Thyroid function tests
• Caeruloplasmin
• Haemochromatosis gene studies
• Blood cultures
hyperparathyroidism with or without CPPD crystal deposition.
Plain radiographic features of BCP
crystal disease are non-specific,
although plain X-rays are a useful tool
for diagnosing acute calcific tendonitis. A radiological association
between osteophyte burden and chondrocalcinosis has been noted. Calcification is often an incidental radiolog-
ical feature noted in asymptomatic
individuals, with no clear relationship
to disease severity.
Further evidence of a possible contributory role for CPPD crystals in the
causation of degenerative changes of
‘pseudo-osteoarthritis’ accompanying
CPPD crystal deposition is suggested
by these changes accompanying chondrocalcinosis in joints such as MCP
and wrist, and accompanying joints
that are unusual sites for classic
osteoarthritis.
Recent advances in ultrasonography have improved diagnostic utility
in CPPD arthropathy. Crystal deposits
in articular cartilage, fibrocartilage
and tendons produce intracartilage
focal hyper-echoic signals on ultrasonography.
Advances in resolution have
resulted in appreciating differences
between the patterns of articular cartilage crystal deposition in gout and
CPPD arthropathy. At present, more
work is underway to understand the
predilection of different crystals for
particular sites in articular cartilage.
Ultrasound also has a useful role in
therapy, to assist local injection in
selected cases of calcific shoulder tendonitis. It is also fast emerging as a
diagnostic tool to detect CPPD
deposits that are too small to be visible on plain radiographs, such as
those seen in peri-articular structures
(enthesitis).
CT imaging has a limited but useful
role in assessing atypical presentations
related to CPPD deposition, such as
cervical canal stenosis and myelopathy
caused by a retro-odontoid calcified
mass lesion (the so-called ‘crowned
dens syndrome’) presenting with acute
neck pain. MRI is useful for assessing
the uncommon cervical spinal canal
compression due to CPPD deposition
in the axial skeleton.
Treatment of pseudogout
NO available treatment is
known to halt progression
of CPPD-deposition disease.
Treatment of acute pseudogout is similar to that of
acute gout, with NSAIDs,
glucocorticoids and colchicine.
The principles governing
use of NSAIDs and intraarticular and oral steroids
are similar to those of gout
management. In the event
that NSAIDs are contraindicated, treatment with ACTH
is an option used with variable success. Simple joint
24
aspiration has been shown
to improve symptoms and,
when feasible, should be
undertaken for both diagnostic and therapeutic reasons.
Treatment of any underlying metabolic condition is
important and may reduce
frequency of pseudogout
attacks, but does not usually
result in resolution of cartilage calcification. There is no
equivalent to uricosuric therapy used in gout, and the
difficulty is treating recurrent or chronic pseudogout.
| Australian Doctor | 28 August 2009
For recurrent pseudogout,
studies show that colchicine
at a dose of 0.5mg twice
daily has varying success as
prophylactic treatment.
Although the long-term
safety of this approach is
untested, the usual precautions relating to the use of
colchicine apply. When gastrointestinal side effects prevail, particularly in elderly
patients, a dose of 0.5mg
orally once daily is proposed,
although the value of lowdose therapy is uncertain.
NSAIDs, are the usual pre-
ferred option but should not
be prescribed lightly, given
known risks and usual comorbidities found in elderly
patients with pseudogout.
Resistant pseudogout is an
uncommon entity and, as a
general principle, in such
cases it is important to
revisit and review the diagnosis. In established resistant cases, systemic steroids
are used for lack of a better
option.
Probenecid inhibits transforming growth factor-ßinduced
extracellular
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pyrophosphate upregulation;
this effect is independent of
cell membrane injury or
phosphodiesterase inhibition, suggesting a potential
therapeutic role in CPPD
disease. However, welldesigned randomised controlled trials are needed
before probenecid becomes
a mainstream therapeutic
tool for managing particularly resistant pseudogout.
A small study recommends
19
using methotrexate. Although a two-month lag
between initiation of therapy
and response was evident,
this may be preferable to
long-term steroid use. A case
study has demonstrated a
good response in a patient
with resistant pseudogout
and steroid-related side
effects using anakinra, the
20
interleukin-1 inhibitor.
The judicious principles
used to determine individually tailored suitability for
surgical intervention including joint replacement in
osteoarthritis remain the
same in pseudogout-related
joint degeneration.
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Haemochromatosis and CPPD-deposition arthropathy
HAEMOCHROMATOSIS
is a condition associated
with CPPD-depositionrelated arthritis. While
almost any joint can be
involved and the entire spectrum of radiographic findings of CPPD-deposition disease may be seen in
haemochromatosis, osteoarthritic changes of the
second and third MCP joints
are characteristic, and their
presence should raise the
possibility of haemochromatosis and associated
CPPD-deposition disease.
Stiffness, pain and bony
swelling are more prominent
than ‘boggy synovitis’.
Osteophyte formation at
MCP joints and chondrocalcinosis are notable radiological features. Late clinical
features of iron overload
include diabetes and other
endocrine manifestations,
liver disease, cardiomyopathy and increased skin pigmentation.
Investigations include iron
studies and relevant gene
testing after counselling.
Carefully monitored NSAID
therapy for symptomatic
arthritis remains the mainstay of treatment. The use of
Investigations
include iron
studies and
relevant gene
testing after
counselling.
intra-articular and systemic
steroids has a role, particularly if NSAIDs are unsuitable and in monoarticular
presentations. Monitoring
for and treating osteoporosis in haemochromatosis and
iron overload is important
and should not be overlooked.
The two common genetic
mutations
found
in
haemochromatosis
are
C282Y and H63D. C282Y
is more common in the Caucasian population, with
about 11% carrying the
gene, although H63D is seen
in about 23% of the population worldwide.
Summary
The relationship between
haemochromatosis variants
and arthritic manifestations
is inconsistent. Some studies
have found no relationship
between C282Y and selfreported rheumatological
symptoms or chondrocalcinosis, while others report an
association between C282Y
and late-onset osteoarthritis
and chondrocalcinosis.
Heterozygosity for the
C282Y gene mutation may
be associated with an
increased risk of late-onset
osteoarthritis in patients over
65 years, but this finding
needs substantiation by
better-designed studies, as
there are implications for
directed therapy in such subgroups
at
risk
for
osteoarthritis.
Younger
individuals
(under 65) homozygous for
H63D present with polyarthralgia, chondrocalcinosis of the hips and knees
and osteophytic joints of the
hands with joint-space narrowing, while older compound heterozygotes (over
65) have more arthralgia,
chondrocalcinosis of the hip
and increased osteophyte
burden in knee joints.
CPPD-DEPOSITION
disease and associated
clinical manifestations
encompassing pseudogout
and pyrophosphate
arthropathy should be
considered in patients
presenting with clinical
features mimicking gout,
inflammatory osteoarthritis,
septic arthritis and
rheumatoid arthritis,
especially in the elderly.
Chondrocalcinosis
associated with a metabolic
disorder tends to present at
an earlier age.
cont’d next page
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treated and healing following nasal surgery should have occurred before use. Class effect: rare instances of glaucoma, increased intra-ocular pressure and nasopharyngeal candidiasis. Special care should be taken with patients who may be susceptible to candida infections (e.g. diabetics).
Excessive dosing may cause suppression of the HPA axis, reduction in bone density and growth retardation in adolescents and children. Children receiving prolonged treatment should have their height regularly monitored. Other precautions: pregnancy (category B3), lactation. For more
details, refer to full PI. Interactions: There is no theoretical basis for anticipating interactions between Avamys and the cytochrome P450 mediated metabolism of other compounds at clinically relevant intranasal doses of Avamys. Based on data with another glucocorticoid metabolised by
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is achieved, dose reduction to one spray in each nostril once daily (total daily dose, 55 mcg) may be effective for maintenance. Children (2 to 11 years of age):The recommended starting dosage is one spray (27.5 mcg per spray) in each nostril once daily (total daily dose, 55 mcg). Patients
not adequately responding to one spray in each nostril once daily may use two sprays in each nostril once daily (total daily dose, 110 mcg). Once adequate control of symptoms is achieved, dose reduction to one spray in each nostril once daily (total daily dose, 55 mcg) is recommended.
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References: 1. Avamys Product Information; 2. Vasar M et al. Allergy Asthma Proc 2008; 29:313-321; PC0905044 GSKA 6/09
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28 August 2009 | Australian Doctor |
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HOW TO TREAT Gout and other crystal arthropathies – Part 2
Authors’ case studies
References and further
reading
Young man with podagra
MR X, a 40-year-old man
with a seven-year history of
recurrent podagra, presented
with three months of persistent pain in his wrists, elbows,
knees and ankles with intermittent swelling and associated early morning stiffness
lasting for about an hour. He
had no recorded fevers,
rigors or night sweats, no
known nephrolithiasis or
renal impairment and no
recent diarrhoeal illness.
There was a possible past
history of connective tissue
disorder with Raynaud’s phenomenon and an intermittent
pruritic truncal rash. There
were no known medication
allergies.
Family history
His uncle may have had gout
and his father had a myocardial infarction at age 60.
Comorbidities
• Gastro-oesophageal reflux
disease treated with
esomeprazole 40mg daily.
• Hypertension treated with
perindopril 5mg/indapamide 1.25mg daily.
Examination
Mr X looked well and was
afebrile. His BP was
140/95mmHg, pulse rate 96
beats/minute and SaO2 94%
(room air). He had a BMI of
29, with central adiposity.
There was synovitis in both
wrists, knees and ankles.
There were effusions in the
left knee and both ankles,
with gouty tophi of the right
elbow. Examination of the
cardiovascular and respiratory systems was unremarkable.
Investigations
• White cell count (WCC) —
9
15.3 × 10 /L.
• ESR — 136mm in 1 hour .
• CRP — 221mg/L.
• Rheumatoid factor —
<10IU/L.
• Serum creatinine —
168μmol/L (normal range
60-130μmol/L) (known to
be 106μmol/L six months
ago).
• Serum urate — 628μmol/L
(NR 260-440μmol/L).
• Microscopy, culture and
sensitivity (MCS) of joint
aspirates (left knee × 2 and
gouty tophus of right
elbow aspirated) — WCC
6
>50,000 × 10 /L mainly
neutrophils; Gram stain —
no organisms seen; culture
— no growth seen after
one week; crystals — negatively bi-refringent needleshaped crystals seen.
Management
The diagnosis of gout was
confirmed as above and the
patient was educated about
gout, its precipitants and curability. The possibility of the
metabolic syndrome and its
implications were raised in
the context of his young age.
26
Treatment options were discussed taking into consideration his renal impairment
and comorbidities. Further
investigations revealed a
raised LDL cholesterol, low
HDL cholesterol and an elevated BSL. No secondary
cause of hyperuricaemia was
found.
Prednisone was commenced
at 10mg daily for three days,
7.5mg daily for five days, 5mg
daily for 10 days, 2.5mg daily
for one week and then ceased.
Allopurinol 50mg daily was
commenced while he was on
prednisone 5mg daily (a week
after symptoms had completely resolved). Serum creatinine was repeated fortnightly
and Mr X was reviewed in the
outpatient clinic after six
weeks and at three-monthly
intervals thereafter. Allopurinol was increased to 100mg
daily at seven weeks and to
150mg daily at 12 weeks;
serum creatinine was monitored at monthly intervals. He
was referred to the diabetic
clinic for a persistently elevated BSL and to a cardiologist for a cardiac risk assessment and management.
Elderly patient with
swollen joints
• Hypercholesterolaemia
(stable on treatment).
Patient’s history of gout
Crystal diagnosis was established 15 years ago; initially
this was mono-articular (podagra), but in the last three years
he had had polyarticular
episodes. Since worsening of
his CCF about two years ago,
a concomitant increase and relative persistence of flares had
been noted, that is, 3-4
episodes each year with
episodes lasting progressively
longer.
Previously he had been
taking allopurinol 300mg daily,
but he was now taking 100mg
daily due to worsening renal
failure. Acute episodes had
been treated with colchicine
and an NSAID. He was aware
of precipitants and abstained
from alcohol.
Medications
• Ramipril 7.5mg mane.
• Frusemide 40mg daily.
• Aspirin 100mg daily.
• Glyceryl trinitrate spray I-II
sublingual prn.
• Meloxicam 7.5mg daily.
• Allopurinol 100mg daily.
• Calcium 600mg daily.
• Ostelin 1000 IU daily.
• Simvastatin 20mg nocte.
Mr Y, 80, presented to the
emergency department in congestive cardiac failure (CCF),
with widespread ischaemic
changes on ECG, acute on
chronic renal impairment, and
a swollen left elbow with
tophi and associated cellulitis, sepsis and confusion.
There was a history of penicillin allergy (rash), but he
had tolerated cephalexin in
the past. Premorbidly he was
independent and self-caring
and lived with his wife of 52
years. His temperature was
38.7°C, BP 90/55mmHg and
pulse was 108 beats/minute
and regular (low volume).
• FBC — Hb 100g/L, WCC —
9
20 × 10 /L with raised neutrophils
• ESR — 80mm in 1 hour
• CRP — 200mg/L
• EUC — Na 134mmol/L, K
3.5mmol/L,
HCO 317mmol/L, Cr 270μmol/L
and U 24mmol/L
• Raised CK and troponin
• Cholestatic LFTs, raised
serum uric acid
• Positive blood cultures —
Methicillin-sensitive Staphylococcus aureus
• Chest X-ray – cardiomegaly
and cardiac failure
Past medical history
Diagnosis
• Ischaemic heart disease,
mitral regurgitation and heart
failure.
• Renal failure and prostate
cancer (stable on no treatment).
• Gout (stable until two years
ago).
• Hypertension.
Mr Y was diagnosed with
polyarticular gout worsening
due to renal impairment and
increased diuretic therapy.
| Australian Doctor | 28 August 2009
Investigations
Treatment
Mr Y was admitted to the
coronary care unit for monitoring and treatment of CCF
and acute coronary syndrome; the ACE inhibitor
and meloxicam were ceased
and frusemide was increased
to 80mg mane and 40mg
midi; he was rehydrated
gently (monitoring fluid balance) and commenced on
cephazolin, and infectious
disease and renal colleagues
were consulted.
Progress (day 7)
Mr Y was afebrile on cephazolin and his cardiac failure stable. Coronary
angiogram revealed triple
vessel disease. While the cellulitis had largely resolved,
he still had a painful,
swollen left elbow and had
developed painful, swollen
hands and ankles in the last
two days. Blood cultures
were negative and transthoracic echocardiogram was
negative for subacute bacterial endocarditis. He also
complained of painful and
burning soles and was
unable to mobilise. A
rheumatology consult was
requested.
Treatment of gout
He was commenced on
10mg prednisone daily for
three days, reducing to
7.5mg daily for one week
and 5mg daily for one week
with clear improvement of
symptoms noted within 48
hours; prednisone was continued at a dose of 2.5 mg
daily for a further three
weeks without complications. His left elbow joint
was aspirated for symptomatic relief (uric acid crystals seen on microscopy).
Three months later Mr Y
had completed six weeks
(total) of antibiotics and
while on 2.5mg prednisone
daily his allopurinol was
increased to 150mg daily following discussion with his
renal physician. His prednisone was stopped a month
later with no immediate
flare.
Older man with painful
hands
MR H, a 65-year-old retiree,
presented for further management of his osteoarthritis, which was interfering
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with his golf, tennis and jogging.
He had had painful hands
for the past five years, with
bilateral involvement of the
first carpometacarpal (CMC)
joints at onset and gradual
swelling of the second, third
and fourth MCP joints,
second and fourth distal
interphalangeal (DIP) joints
and both wrists, which occasionally became very painful
with swelling lasting for
three days.
He also had had mechanical knee pain and mild loss
in range of movement of the
knee joint, with more recent
self-limiting episodes of pain
and swelling.
Mr H was an active and
fit man who lived with his
partner. He was a nonsmoker and consumed 10g
of alcohol every second day.
He had no known medication allergies.
Mr H’s past history was of
rheumatic fever at age seven
years, hypertension and a
duodenal ulcer. There was a
strong family history of
ischaemic heart disease and
diabetes mellitus.
Examination revealed
osteoarthritic changes of the
joints of the hands, with
prominent second and third
MCP joints, due to bony
swelling, but no active synovitis.
X-rays of the knees in
1989, 1994 and 2003
showed tri-compartmental
osteoarthritis with chondrocalcinosis. X-rays of the
hands and wrists in 2000
showed a calcified triangular ligament and bilateral
degenerative changes of the
first, second and third MCP
joints with hook-osteophyte
formation.
FBC and inflammatory
markers were normal, as
were urea, electrolytes, creatinine, LFTs, blood glucose
level, calcium, magnesium,
phosphate, uric acid, TSH
and parathyroid hormone
levels. However, iron studies
showed a transferrin saturation of 70% and an elevated
ferritin level of 600μg/L.
Mr H’s diagnosis was
haemochromatosis with
chondrocalcinosis
and
pseudogout. Subsequent gene
studies demonstrated that he
was homozygous for C282Y.
Management consisted of
venesection and monitoring
iron studies. Arthritic flares
were treated with NSAID,
proton-pump inhibitor therapy and intra-articular and
systemic steroids. Mr H also
received physiotherapy for
patellofemoral symptoms.
He was screened for osteoporosis because treatment
for this — particularly in
advanced haemochromatosis
— is important, but no intervention was required.
His family were counselled
and genetic screening of children was advised.
Available on request from
julian.mcallan@reedbusiness
.com.au
Online resources
Australian Rheumatology
Association:
www.rheumatology.org.au
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HOW TO TREAT Gout and other crystal arthropathies – Part 2
GP’s contribution
DR MARG TAIT
Picnic Point, NSW
Case study
A 67-YEAR-old man presented with painful swelling of
his left hand consistent with
synovitis. He had a background of gastro-oesophageal
reflux disease, ischaemic heart
disease, hypertension, L5
decompression surgery and
bilateral knee replacements.
He was commenced on
meloxicam 7.5mg daily.
Two days later the hand
was worse and he reported
that he had sustained a penetrating injury to his hand
shortly after the initial consultation. Cephalexin 1g qid was
commenced but after 48
hours there was little change
and he was referred to ambu-
latory care for IV antibiotics.
A few days later he was
admitted for management of
possible septic arthritis of his
right hand following an infection associated with the cannulation. The infection settled
but bilateral synovitis persisted
in the wrists and MCP joints.
He was tried on a COX-2
inhibitor with no effect. Seven
weeks after his presentation
and when the ESR and CRP
had returned to normal, prednisone 5mg bd was commenced with good effect, as
well as colchicine 0.5mg bd.
X-ray of the left wrist
demonstrated marked changes
of osteoarthritis in CMC and
MCP joints as well as chondrocalcinosis of the triradiate
cartilage. There was no erosive arthropathy.
Other X-rays showed widespread
and
advanced
osteoarthritis complicating
underlying chondrocalcinosis.
Serum calcium and parathyroid hormone levels were
normal. Serum uric acid was
0.45mmol/L and rheumatoid
ration unless there is unstable
coagulopathy, overlying skin
infection (cellulitic) or a prosthetic joint. It is reasonable to
perform joint aspiration to
confirm the diagnosis and
inject steroid for symptomatic
relief.
factor was mildly positive. Iron
studies were normal as was a
TSH level.
Steroids were withdrawn
and colchicine ceased with
time. There has been no recurrence for three years.
Questions for the authors
This patient is now warfarinised. If he developed
painful acute swelling of his
knee, would you aspirate his
knee joint to exclude infection,
confirm diagnosis and inject
steroids?
Anticoagulation is not a
contraindication to joint aspi-
How to Treat Quiz
How often is the synovitis
bilateral?
In pseudogout bilateral synovitis is not uncommon, especially of the wrists although a
relapsing pattern, that is, one
wrist followed by the other is
also commonly seen, as is
monoarthritis. Symmetrical
synovitis of the MCP joints of
the hands is unusual and
seronegative rheumatoid
arthritis needs to be considered.
General questions for the
authors
How is the diagnosis of
pseudogout affecting the
Achilles tendon made and
how does the treatment differ
from that of a joint affected
by pseudogout?
Calcaneal tendon calcifications are frequently seen in
asymptomatic chondrocalcinosis. Ultrasound scanning
and power Doppler studies
correlate well with conventional radiography in depicting calcifications. Ultrasound
scanning is useful at detecting
early calcification which may
have a normal appearance on
conventional X-ray. Inflammatory changes of calcaneal
soft tissues are frequently
demonstrated by ultrasound
and power Doppler studies in
patients with CPPD-deposition-related tendonitis and in
this setting ultrasound and
power Doppler studies may
1
be more useful.
The diagnosis of enthesopathy associated with CPPDdeposition disease in a
younger age group should
also include consideration of
an associated metabolic disorder and requires appropriate
investigation if clinically indicated.
The treatment of CPPDrelated enthesopathy is diffi-
cult. NSAIDs, corticosteroid
injections and rarely colchicine
have been used to treat acute
presentations.
Should all patients with X-ray
changes be investigated further for the disorders associated with chondrocalcinosis,
or only those under 55 years
or with polyarticular chondrocalcinosis?
I think it is reasonable to
investigate confirmed or suspected cases of pseudogout for
metabolic associations especially in a younger age group
and polyarticular presentations; however extensive investigation of age-appropriate
sporadic monoarticular presentations with no other clinical findings is less likely to
yield similar associations.
In acute presentations of
either scenario one should aim
to establish a crystal-based
diagnosis of pseudogout.
Reference
1. Journal of Rheumatology
2004; 31:2242-50.
INSTRUCTIONS
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by post or fax.
The mark required to obtain points is 80%. Please note that some questions have more than one correct answer.
Gout and other crystal arthropathies —
Part 2 — 28 August 2009
1. Which THREE statements about the
terminology surrounding calcium
pyrophosphate dihydrate (CPPD) deposition
disease are correct?
a) Chondrocalcinosis describes deposition of
CPPD crystals in articular cartilage
b) Pseudogout describes the clinical syndrome
of acute arthritis associated with CPPD
deposition in articular cartilage
c) Pyrophosphate arthropathy indicates
structural abnormality of cartilage and bone
associated with CPPD deposition
d) CPPD-deposition disease is often used as a
synonym for pseudogout
2. Which TWO statements about the
epidemiology and aetiology of CPPDdeposition disease are correct?
a) A rare familial predisposition to CPPDdeposition disease has been reported,
however most cases are sporadic
b) Familial inheritance of CPPD-deposition
disease is largely autosomal recessive
c) Patients with familial CPPD-deposition
disease are likely to have milder disease
d) CPPD-deposition disease linked with
metabolic associations tends to present at
an earlier age
3. Which THREE statements about the
pathophysiology of CPPD-deposition
disease are correct?
a) CPPD-deposition disease is associated with
overproduction of inorganic pyrophosphates
by chondrocytes
b) Excess extracellular pyrophosphate
resulting in CPPD crystal deposition
probably increases with ageing
c) There is no association between basic
calcium phosphate (BCP) crystals and
CPPD-deposition disease
d) CPPD crystals induce an intra-articular
acute inflammatory response, resulting in
acute pseudogout
4. Which TWO statements about clinical
features of CPPD-deposition disease are
correct?
a) CPPD-deposition disease has a wide
spectrum of intra-articular and extraarticular clinical manifestations
b) An acute attack of pseudogout will typically
resolve over 1-3 weeks
c) Episodes of pseudogout can be
distinguished from acute gout by the
absence of erythema
d) Polyarticular inflammation excludes a
diagnosis of pseudogout
5. Which TWO statements about
presentation of CPPD-deposition disease
are correct?
a) CPPD-deposition disease commonly affects
the knee joints
b) Wrists, elbows, shoulders, hips and ankles
are rarely affected in CPPD-deposition
disease
c) Elderly patients with pseudogout may
present with delirium
d) Pseudogout does not produce an increase
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in the white blood cell count or
inflammatory markers
6. Which TWO of the following conditions
may be associated with CPPD-deposition
disease?
a) Haemochromatosis
b) Hyperparathyroidism
c) Hyperthyroidism
d) Hypermagnesaemia
7. Which TWO statements about diagnosis
of CPPD-deposition disease are correct?
a) The diagnosis of pseudogout is established
clinically and by demonstrating CPPD
crystals on synovial fluid analysis with
supporting radiographic features
b) In CPPD-deposition disease, crystals are
negatively bi-refringent on polarised light
microscopy
c) In pseudogout, crystals are very easy to
detect on synovial fluid analysis
d) In pseudogout, CPPD crystals can coexist
with uric acid crystals
8. Which THREE statements about the
radiological assessment of CPPDdeposition disease are correct?
a) The typical appearance of CPPD crystal
arthropathy on plain radiography is
chondrocalcinosis
b) Chondrocalcinosis is commonly seen in
fibrocartilage of the knee, triangular
ligament of the wrist and the pubic
symphysis
c) Radiological features of pyrophosphate
arthropathy overlap those of osteoarthritis
d) There is no role for ultrasound in CPPDdeposition disease
9. Which TWO statements about treatment
of CPPD-deposition disease are correct?
a) Treatment of acute pseudogout is similar to
that of acute gout
b) For recurrent pseudogout, prophylaxis with
low-dose colchicine may be tried, however
the long-term safety of this approach is
uncertain
c) Pseudogout that is resistant to therapy is
common
d) Treatment of any underlying metabolic
condition does not have any effect on the
frequency of pseudogout attacks
10. Which THREE statements about
haemochromatosis and CPPD-deposition
arthropathy are correct?
a) Osteoarthritic changes of the second and
third MCP joints should prompt
consideration of haemochromatosis and
associated CPPD arthropathy
b) In CPPD arthropathy associated with
haemochromatosis, stiffness, pain and bony
swelling are more prominent than ‘boggy
synovitis’
c) Patients with confirmed haemochromatosis
should be monitored for osteoporosis
d) Studies have shown consistent relationships
between haemochromatosis variants and
arthritic manifestations
CPD QUIZ UPDATE
The RACGP now requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2008-10 triennium. You
can complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept the quiz by post
or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online.
HOW TO TREAT Editor: Dr Wendy Morgan
Co-ordinator: Julian McAllan
Quiz: Dr Wendy Morgan
NEXT WEEK Thyroid nodules are a very common finding in Australian adults. While most thyroid nodules are benign, about 5% of nodules coming to operation will be thyroid cancer. The next How to Treat gives
an up-to-date account of the aetiology, assessment, diagnosis and treatment of thyroid nodules. The author is Professor Leigh Delbridge, professor of surgery, University of Sydney; visiting surgeon, Royal North
Shore, Hornsby, Mater and North Shore Private Hospitals; honorary thyroid surgeon, The Children’s Hospital at Westmead, NSW; and president-elect of the International Association of Endocrine Surgeons.
28
| Australian Doctor | 28 August 2009
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