Question 2(a)

I will take full history concerning the diagnosis, bearing in mind factors affecting drug
choices in gout management, including;

 Past medical history - Comorbidities especially of kidney, liver, cardiovascular,

gastrointestinal disease and diabetes; concomitant medication use; allergies.
 Gout history – Total flare number, recent flare frequency rate, prior flare experience
with specific treatment (anti-inflammatory agent tolerability and effectiveness).
 Characteristics of gout flare – Duration of symptom onset to therapeutic assessment,
number of affected joints, and the clinical setting in which the flare is occurring (e.g.,
during initiation of urate-lowering therapy).
 Differential diagnosis of flare symptoms – If current flare is atypical than prior gout
flares, or if flare occurs in high-risk setting, pay attention towards possibility of
alternative or accompanying cause of acute inflammatory arthritis (eg, infection).
I will perform thorough physical examination of the joints, looking for tophi or signs of
inflammation. Look for eye involvement in chronic gout, such as tophi in the eyelids,
conjunctival nodules, or marginal keratitis. Referral to ophthalmologist if ocular involvement
suspected.
For diagnosis of gouty arthritis; first metatarsophalangeal joint involvement, local erythema,
maximal inflammation within 24 hours with hyperuricaemia are suggestive, however a
response to colchicine and the presence of tophi have a higher diagnostic usefulness1.
Definitive diagnosis is by urate crystals demonstrated in synovial fluid or tophus by
diagnostic aspiration.
Plain radiograph is not useful in diagnosing initial acute gouty arthritis. Radiologic features
in chronic gout include tophi, an overhanging edge of cortex, and erosion of bone with
sclerotic borders. Mineralization and joint spaces are preserved2.
Imaging modalities as ultrasound and CT scan may be helpful if the diagnosis is uncertain or
to detect complications.
Management for gouty arthritis includes non-pharmalogical and pharmalogical approaches.
Research suggested that patients with gout who lack confidence in their treatments have
reduced adherence to their medications. Hence, patient’s education is vital. I will assist
interactive communication with the patient to achieve thorough understanding of gouty
arthritis, emphasizing patient’s active participation on lifestyle modification and medication
adherence.
Any predisposing medical conditions or habits must be addressed. Lifestyle advice includes
maintenance of ideal body weight and avoidance of excess alcohol, sugar-sweetened drinks
and other known triggers. There is little evidence that supports low purine diet reduces the
risk of flare in established gout, though restriction is advised. Adequate fluid intake of 2-3L
daily to keep urine diluted.
Any medication regimens that may have contributed to the gout attack must be altered.
Several medications can alter serum urate concentrations. Losartan, atorvastatin,
fenofibrate and calcium channel blockers have weak urate-lowering properties. Low-dose
aspirin and thiazide diuretics increase serum urate3.
Acute flare treatment
Treatment of acute flares should begin as soon as possible. NSAIDs or colchicine are first-
line; or oral corticosteroids for those who cannot tolerate or have contraindications to first-
line agents.
Hence one of the following is chosen considering patient’s circumstances;
 NSAIDS, Tab Indomethacin 50mg TID for 3-5 days. Appropriate in younger patients
who lack renal, cardiovascular, or active gastrointestinal disease, without NSAID
allergy, not on anticoagulants.
 Colchicine 1.2mg immediately, then 0.6mg once or twice daily for 3-5 days, for those
with normal renal function. Lower doses required in renal or hepatic impairment or
receiving CYP3A4 or P-glycoprotein inhibitors.
 Oral corticosteroids, Prednisone 0.5 mg/kg/day and tapered off over 5-10 days.
If the patient is already on Allopurinol, it should not be stopped during acute flares of gout.
However, it should not be started during a flare4.
Patient Monitoring
I would discharge the patient with a follow-up appointment in 2 weeks. However, if any red-
flags symptom such as worsening or non-resolving pain, he should seek medical attention
immediately.

During follow-up, review patient’s wellbeing, perform baseline laboratory tests, and
consider starting urate-lowering therapy (if not been started).

Baseline investigations include full blood count (to exclude infection, lympho- or
myeloproliferative disease), renal profile and urinalysis (to exclude renal disease), and
serum uric acid.

Urate-lowering therapy
Allopurinol is the first-line agent.
As indicated, I should consider urate-lowering therapy in at least one of the following:
 tophi
 two or more attacks a year
 chronic kidney disease (stage 2 or worse)
 urolithiasis
The American College of Rheumatology recommends commencing Allopurinol 100 mg daily,
except those with stage 4 or worse chronic kidney disease, where the recommended
starting dose is 50 mg per day. It is titrated up until target serum uric acid is achieved.

Recommended target of uric acid is <0.36 mmol/L(without tophi) and <0.30 mmol/L(with
tophi)5. A normal or low serum urate does not exclude the diagnosis of acute gout, as it may
not be elevated during acute attack.
Prophylaxis of acute gout flares
Recommended in those commencing urate-lowering therapy. NSAIDs and low-dose
colchicine are first line, and low-dose prednisolone as second line.
The American College of Rheumatology recommends:

 at least six months’ duration, or

 three months’ duration after achieving target serum urate in patients without tophi, or
 six months’ duration after achieving target serum urate in patients with tophi on
examination.

Consideration of medication contraindications and use of gastric protection may be

appropriate6.

Long-term Monitoring
If Allopurinol is started, I would then arrange another follow-up in 2 weeks to ensure that no
untoward toxicity has developed, and then every 1-2 months while medication dosages are
adjusted to achieve the target uric acid level. Once target level is achieved and maintained,
patients can be monitored every 6 months.

1
Finch A, Kubler P. The management of gout. Australian Prescriber. 2016 Aug 1;39(4).
2
Pittman JR, Bross MH. Diagnosis and management of gout. American family physician. 1999 Apr;59(7):1799-
806.
3
Jordan KM, Cameron JS, Snaith M, Zhang W, Doherty M, Seckl J, Hingorani A, Jaques R, Nuki G. British Society
for Rheumatology and British Health Professionals in Rheumatology guideline for the management of gout.
Rheumatology. 2007 Aug 1;46(8):1372-4.
4
Becker MA, Gaffo AL. Treatment of gout flares. UpToDate. 2019.
5
Robinson PC, Stamp LK. The management of gout: much has changed. Australian family physician. 2016
May;45(5):299.
6
Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, Pillinger MH, Merill J, Lee S, Prakash S, Kaldas
M. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic
nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis care & research.
2012 Oct;64(10):1431-46.