What's the difference between a gout flare and the underlying disease?

A flare is the inflammatory reaction to urate crystals already deposited in a joint — sudden, exquisite pain in a single joint (classically the big toe), peaking around 24 hours and settling over 7–14 days. The underlying disease is sustained hyperuricaemia — uric acid above the saturation point of about 0.41 mmol/L — that lets crystals form and silently accumulate between flares. Treating the flare with anti-inflammatories ends the attack but does nothing to clear crystals. Without urate-lowering therapy, flares recur, tophi grow, and joint erosions develop. Treating both layers is the point.

Do I have to take allopurinol forever, or can diet alone fix gout?

Diet alone rarely reaches the urate target. Strict purine restriction and weight loss can lower urate by roughly 0.05–0.10 mmol/L, but most patients with established gout need a sustained level below 0.36 mmol/L (below 0.30 with tophi) for crystals to dissolve. That usually requires allopurinol, titrated monthly to target. Most patients stay on it lifelong. Diet still matters — alcohol (especially beer and spirits), sugar-sweetened drinks, and excess red or organ meat are real triggers — but framing diet as an alternative to medication leads to undertreatment, recurrent flares, and progressive joint damage.

Why does my GP check HLA-B*5801 before starting allopurinol?

HLA-B*5801 is a genetic marker strongly linked to severe allopurinol hypersensitivity — a rare but potentially fatal reaction involving rash, fever, hepatitis, and acute kidney injury, usually in the first two months. The variant is much more common in people of Han Chinese, Korean, Thai and Filipino ancestry. Australian guidelines recommend testing before starting allopurinol in these higher-risk populations; if positive, febuxostat is used instead. The test is Medicare-rebatable. In lower-risk ancestry, routine screening is not recommended, but any new rash, fever or unwell feeling in the first two months still needs urgent review.

Is gout just a joint problem, or does it affect the rest of my health?

Gout is now considered a cardiovascular risk equivalent. It travels with hypertension, type 2 diabetes, dyslipidaemia, chronic kidney disease, obstructive sleep apnoea, and fatty liver disease, and is independently associated with heart attack and stroke. The 2023 Australian CVD risk guideline lists gout as an upclassifier in cardiovascular risk assessment. That changes the management mindset — a gout consultation is also a cardiovascular and kidney check. Blood pressure, lipids, glucose, kidney function, weight, alcohol and sleep all sit on the same page.

What should I do if a hot, swollen joint comes on suddenly?

If a single joint becomes hot, swollen and exquisitely painful — particularly the big toe — and you have known gout, start the anti-inflammatory plan agreed with your GP (NSAID, colchicine or short course of oral steroid) as early as possible; treatment within 24 hours works best. Seek urgent assessment the same day if it is your first attack, if you have fever or feel systemically unwell, if the joint is intensely red and you cannot move it, or if you are immunosuppressed — these can signal septic arthritis, which requires joint aspiration before antibiotics. Do not stop your daily urate-lowering tablet during a flare.

Gout

Gout: treat-to-target urate, not just the flare — the AU GP approach

By Dr HB Lo, FACRRM Reviewed 19 May 2026 11 min read

Gout is a crystal arthritis caused by monosodium urate crystals depositing in joints when blood uric acid stays above the saturation point (~0.41 mmol/L). It affects around 6.5% of Australian adults, with very high prevalence in Aboriginal and Torres Strait Islander, Pacific Islander and Maori populations.

Acute flares respond within days to NSAIDs, colchicine, or oral prednisolone. The bigger picture is lifelong urate-lowering therapy — usually allopurinol — titrated to a serum urate target below 0.36 mmol/L (below 0.30 with tophi). Diet helps but rarely controls gout alone.

What gout actually is

Gout is an inflammatory arthritis driven by monosodium urate (MSU) crystals depositing in joints and soft tissue when blood uric acid sits above its saturation point of roughly 0.41 mmol/L. Crystals are silent for years, then a sudden release triggers an intense inflammatory response — the classic hot, swollen, exquisitely tender joint, very often the base of the big toe (“podagra”). Around 6.5% of Australian adults — roughly 1.7 million people — have gout, four times more often in men than pre-menopausal women, and with very high prevalence in Aboriginal and Torres Strait Islander, Pacific Islander, and Maori populations (Robinson AFP 2016; eTG — Rheumatology: Gout).

The clinical model is two-layered: the flare is the inflammatory reaction to crystals; the disease is the sustained hyperuricaemia that lets crystals form. Modern Australian general practice treats both — anti-inflammatory cover for the flare, urate-lowering therapy for the disease.

A. Core clinical — the AU general practice framework

What gout looks like

The Australian Rheumatology Association and eTG describe four overlapping phases:

Asymptomatic hyperuricaemia — raised urate without crystal disease. Usually not treated on its own.
Acute flare — sudden, severe single-joint pain peaking around 24 hours, resolving over 7–14 days. The first MTP joint is the classic site in about half of first attacks; ankle, mid-foot, knee, wrist and fingers are common.
Intercritical gout — symptom-free between flares, but crystals continue to deposit silently.
Chronic tophaceous gout — palpable lumps (tophi) on the ear helix, olecranon bursa, finger pads, Achilles or patellar tendons; bone erosions; chronic joint pain.

A urate stone or urate-related kidney problem can also be the first presentation.

Diagnosis

The reference standard is joint aspiration with polarising microscopy, looking for negatively birefringent needle-shaped MSU crystals (eTG; Australian Prescriber — The management of gout). In Australian general practice, aspiration is strongly preferred at the first presentation of a hot single joint — partly to confirm gout, partly to exclude septic arthritis, which can co-exist and is a surgical emergency.

When aspiration is not feasible, the ACR/EULAR 2015 classification framework supports a clinical diagnosis based on the joint pattern, peak-pain timing, hyperuricaemia, tophi, and imaging features such as the double-contour sign on musculoskeletal ultrasound or punched-out erosions on X-ray (ACR 2020 Guideline).

Useful tests:

Serum urate — supports the diagnosis but can be falsely low during a flare; recheck 2–4 weeks later. A baseline urate below 0.36 mmol/L makes gout unlikely in most cases (eTG).
Inflammatory markers (ESR, CRP) — typically raised; a raised CRP does not rule out septic arthritis.
Kidney function, liver enzymes, full blood count, lipids, HbA1c — for comorbidity workup.
HLA-B*5801 genotyping before starting allopurinol in higher-risk ancestry (Han Chinese, Korean, Thai, Filipino) (Hung PNAS 2005); Medicare-rebatable.
MSK ultrasound — non-invasive, sensitive for early urate deposition; widely available across Australia.

Differentials

The big-three differentials are septic arthritis, pseudogout (CPPD — positively birefringent rhomboid crystals, often the knee or wrist, with chondrocalcinosis on X-ray), and cellulitis overlying a joint. Reactive arthritis, psoriatic arthritis, rheumatoid arthritis flare, osteoarthritis flare, bursitis and trauma round out the list. Any single hot joint with fever or systemic upset is septic arthritis until proven otherwise (RACGP — The management of gout).

A few common general practice pitfalls worth naming (eTG; Australian Prescriber):

Diagnosing every acute monoarthritis as gout without aspiration — gout and septic arthritis can co-exist, and missing the latter is catastrophic
Stopping the daily allopurinol during a flare — this prolongs the flare and resets crystal equilibrium
Starting urate-lowering therapy without flare prophylaxis — the early mobilisation of crystals can precipitate further flares for the first 3–6 months
Failing to titrate allopurinol to the urate target — most patients are undertreated, drifting at sub-target levels that never dissolve crystals
Missing HLA-B*5801 testing in higher-risk ancestry before allopurinol
Treating the joint and ignoring the cardiovascular and kidney comorbidity that almost always travels with gout

B. Acute management

The Australian primary tier — eTG, the Australian Medicines Handbook, Australian Prescriber — converges on three first-line options for an acute flare. The best one depends on comorbidities, not effect size; all three resolve a typical flare in days when started early (ideally within 24 hours of onset).

Option	Typical AU adult regimen	Best when	Avoid / caution
NSAID	Naproxen 500 mg BD, ibuprofen 400 mg TDS, indomethacin 50 mg TDS, or diclofenac 50 mg TDS for 5–7 days, with PPI cover	Younger, no GI/CKD/HF/anticoagulation issues	Severe CKD, heart failure, peptic ulcer, anticoagulation
Colchicine	1 mg PO stat, then 0.5 mg one hour later, then 0.5 mg BD for 5 days	NSAID contraindicated; fits AU script	eGFR <30 (avoid or markedly reduce); fatal toxicity with clarithromycin, ciclosporin, ketoconazole
Oral prednisolone	30–50 mg daily for 3–5 days	CKD, heart failure, GI risk, anticoagulation	Brittle diabetes, severe infection, recent psychosis
Intra-articular corticosteroid	Methylprednisolone 40 mg or triamcinolone 20–40 mg	Single-joint flare, sepsis excluded	Septic joint not excluded

Severe or polyarticular flares can combine modalities — for example, oral prednisolone plus colchicine, or NSAID plus colchicine (eTG).

Two practice points the RACGP and Australian Prescriber consistently flag (RACGP; Australian Prescriber):

Do not stop urate-lowering therapy during a flare. Stopping allopurinol mid-flare worsens and prolongs it.
It is reasonable to start urate-lowering therapy during a flare, provided flare prophylaxis (low-dose colchicine or NSAID) is added — modern trial data show this does not worsen the flare and improves long-term adherence (Taylor Am J Med 2012).

All three first-line agents are on the PBS general schedule in Australia, with colchicine carrying quantity restrictions because of its narrow toxic margin (AMH).

C. Urate-lowering therapy (ULT) and prevention

The structural treatment for gout is daily urate-lowering therapy, titrated to a serum urate target rather than a symptom target. This is the single most important shift in modern gout management (eTG; Australian Prescriber).

Indications for ULT

eTG and Australian Rheumatology Association advice align on starting ULT for any of:

Two or more flares per year
Tophi (clinical or imaging)
Urate kidney disease or urate stones
Chronic kidney disease stage 2 or worse
Erosive joint changes on imaging
A severe single flare in a younger patient

Targets

Standard target: serum urate <0.36 mmol/L (<6 mg/dL)
With tophi or recurrent flares: <0.30 mmol/L — needed to actually dissolve crystal deposits

Allopurinol — first-line

Allopurinol is the AU first-line urate-lowering drug (eTG; AMH).

HLA-B*5801 genotyping before starting in Han Chinese, Korean, Thai or Filipino ancestry (Hung PNAS 2005). If positive, switch to febuxostat.
ATSI considerations. Gout is markedly more common in Aboriginal and Torres Strait Islander people; access to ULT is often delayed. Annual ATSI Health Assessment (MBS 715) is the AU mechanism to surface and treat hyperuricaemia, comorbidities, and ULT adherence.
Start low, go slow: 50–100 mg daily (50 mg if CKD stage 3 or worse), titrating up by 50–100 mg monthly to the urate target. The historical “cap at 300 mg in CKD” is no longer supported — careful uptitration with monitoring beats undertreatment (Stamp Arthritis Care Res 2017).
Flare prophylaxis during titration — colchicine 0.5 mg daily (or a low-dose NSAID) for at least 3–6 months, continuing 6 months after the target is reached or until tophi resolve.
Lifelong in most patients with established gout.

Febuxostat — second-line

Febuxostat (Adenuric, Uloric) is the second-line urate-lowering drug, used when allopurinol is not tolerated, in HLA-B*5801-positive patients, or when allopurinol cannot reach the target at the maximum tolerated dose. The CARES trial (NEJM 2018) raised concern about cardiovascular mortality versus allopurinol in patients with established cardiovascular disease; the larger FAST trial (Lancet 2020) was reassuring. Current AU practice uses febuxostat with caution in established cardiovascular disease and discusses the trade-off with the patient. It is PBS Authority Required (Streamlined) for allopurinol intolerance, hypersensitivity, contraindication, or failure to reach target on maximum tolerated allopurinol (AMH).

Probenecid and pegloticase

Probenecid is a uricosuric used selectively in under-excretors with normal renal function — third-line, PBS general schedule. Pegloticase is a recombinant uricase reserved for severe refractory tophaceous gout under specialist care; it is not PBS-subsidised in most contexts and is accessed via the TGA Special Access Scheme.

Lifestyle inputs

Australian primary-tier advice (RACGP; eTG; NPS MedicineWise) is consistent:

Alcohol — beer and spirits are the strongest dietary triggers; wine is less harmful but still a trigger (Choi Lancet 2004).
Sugar-sweetened drinks and high-fructose syrups are strong triggers; eliminate (Choi BMJ 2008).
Red meat, organ meat and seafood in moderation — extreme purine restriction is rarely necessary and rarely sustained.
Low-fat dairy, coffee, vitamin C 500–1000 mg/day, hydration — modest protective effects.
Weight optimisation of even 5–10% lowers urate modestly and reduces flare frequency.
Drug review — switch a thiazide to losartan (mildly uricosuric) where the indication allows; do not stop low-dose aspirin for gout alone, as cardiovascular benefit usually outweighs the modest urate rise.

Lifestyle change is part of the package, not an alternative to ULT for most people with established gout.

Monitoring rhythm

eTG and the Australian Rheumatology Association outline a practical follow-up cadence:

Acute flare — review at 1–2 weeks to confirm resolution and plan urate-lowering therapy if not already in place
ULT initiation and titration — monthly review with serum urate, kidney function, liver enzymes and full blood count; titrate by 50–100 mg until target reached
Stable on target urate — 6-monthly clinical review with serum urate; annual UEC, LFTs, lipids, HbA1c, blood pressure and CVD risk re-stratification
Tophi — expect gradual clinical resolution over 6–24 months on sustained urate <0.30 mmol/L; document size at each review
Safety-netting in the first two months of allopurinol — any new fever, rash, jaundice, blood in urine or feeling acutely unwell warrants urgent assessment to exclude severe drug hypersensitivity (Hung PNAS 2005)

D. Australian operations

The PBS and MBS frame the prescribing and billing pathway:

Allopurinol — PBS general schedule, multiple strengths.
Febuxostat (Adenuric, Uloric) — PBS Authority Required (Streamlined) for allopurinol intolerance, hypersensitivity, contraindication, or failure to reach target on maximum tolerated allopurinol.
Colchicine — PBS general schedule with quantity restrictions reflecting its narrow toxic window.
Probenecid, NSAIDs, prednisolone, intra-articular corticosteroids — PBS general schedule.
Pegloticase — not PBS-subsidised in most contexts; SAS pathway.

MBS items that commonly apply to a gout work-up in general practice (MBS Online) include standard consultations 23 / 36 / 44, serum urate 66578, HLA-B*5801 73337, musculoskeletal ultrasound 55844 / 55848, synovial fluid microscopy and culture 69300, GP Chronic Condition Management Plan 965 / 967, and ATSI Health Assessment 715. Chronic gout qualifies for a Chronic Condition Management Plan with allied health referrals (dietitian, exercise physiologist).

Rheumatology referral is the standard pathway for refractory disease, suspected coexisting inflammatory arthritis, candidacy for febuxostat or pegloticase, and complex CKD limiting management. The Australian Rheumatology Association’s find-a-rheumatologist directory is the public starting point.

(MBS/PBS items verified 2026-05-19 via WebSearch — workspace egress to mbsonline.gov.au and pbs.gov.au still blocked; spot-check confirms current.)

E. Special populations

Chronic kidney disease. Gout and CKD are intertwined — CKD raises urate, and crystals damage kidneys. Allopurinol can still be used; the starting dose is reduced (50 mg daily in CKD stage 3 or worse), and titration is slower with closer monitoring of kidney function, liver enzymes and blood counts. The old practice of capping allopurinol at 300 mg in CKD is no longer supported, as it locks patients into an undertreated urate (Stamp Arthritis Care Res 2017). Severe allopurinol hypersensitivity (acute kidney injury, rash, fever, hepatitis in the first two months) is more common in CKD and demands urgent assessment (eTG).

Transplant patients. Ciclosporin and tacrolimus markedly raise urate and increase flare risk. Management is shared with the transplant team — allopurinol carries an azathioprine interaction that requires dose review; febuxostat is often preferred in this group.

Menopause. Oestrogen is mildly uricosuric, so urate typically rises after menopause and gout incidence in women climbs, often presenting as a polyarticular pattern on a background of osteoarthritis and diuretic use. The same treat-to-target principles apply; thiazide diuretics for blood pressure can often be switched to losartan (RACGP).

Cardiovascular comorbidities. The 2023 Australian CVD Risk Guideline treats gout as a cardiovascular risk upclassifier. A gout consultation is the moment to check blood pressure, lipids, glucose, kidney function, weight and smoking — and to address them in parallel with urate-lowering.

Aboriginal and Torres Strait Islander health. Higher prevalence, earlier age of onset, and structural barriers to long-term ULT mean an ATSI Health Assessment and a Chronic Condition Management Plan should be considered routinely in this population.

When to escalate

Seek urgent assessment, usually via ED or rheumatology, when:

A single hot, swollen joint comes on with fever, rigors or feeling systemically unwell — septic arthritis until proven otherwise
The sternoclavicular joint or spine is involved — atypical and potentially serious
Rash, fever, eosinophilia, hepatitis or acute kidney injury develop within two months of starting allopurinol or febuxostat — severe drug hypersensitivity
A first attack of gout in an older adult on diuretics with a polyarticular pattern — overlapping inflammatory arthritis needs sorting out
Gout that remains uncontrolled despite optimised allopurinol — for febuxostat or pegloticase candidacy
Recurrent urate stones or worsening kidney function — for nephrology input

What this article is and is not

This is general health information drawn from current Australian primary-tier sources — Therapeutic Guidelines, the RACGP, the Australian Medicines Handbook, NPS MedicineWise, the Australian Rheumatology Association, and the Heart Foundation — together with major gout trials. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about specific treatment, including allopurinol dosing, febuxostat candidacy, and HLA-B*5801 testing, are made with your own GP and treating specialists.

For Australian consumer-friendly sources: HealthDirect — Gout, Better Health Channel — Gout, Arthritis Australia, Australian Rheumatology Association.

Sources cited

Frequently asked questions

What's the difference between a gout flare and the underlying disease?

A flare is the inflammatory reaction to urate crystals already deposited in a joint — sudden, exquisite pain in a single joint (classically the big toe), peaking around 24 hours and settling over 7–14 days. The underlying disease is sustained hyperuricaemia — uric acid above the saturation point of about 0.41 mmol/L — that lets crystals form and silently accumulate between flares. Treating the flare with anti-inflammatories ends the attack but does nothing to clear crystals. Without urate-lowering therapy, flares recur, tophi grow, and joint erosions develop. Treating both layers is the point.
Do I have to take allopurinol forever, or can diet alone fix gout?

Diet alone rarely reaches the urate target. Strict purine restriction and weight loss can lower urate by roughly 0.05–0.10 mmol/L, but most patients with established gout need a sustained level below 0.36 mmol/L (below 0.30 with tophi) for crystals to dissolve. That usually requires allopurinol, titrated monthly to target. Most patients stay on it lifelong. Diet still matters — alcohol (especially beer and spirits), sugar-sweetened drinks, and excess red or organ meat are real triggers — but framing diet as an alternative to medication leads to undertreatment, recurrent flares, and progressive joint damage.
Why does my GP check HLA-B*5801 before starting allopurinol?

HLA-B*5801 is a genetic marker strongly linked to severe allopurinol hypersensitivity — a rare but potentially fatal reaction involving rash, fever, hepatitis, and acute kidney injury, usually in the first two months. The variant is much more common in people of Han Chinese, Korean, Thai and Filipino ancestry. Australian guidelines recommend testing before starting allopurinol in these higher-risk populations; if positive, febuxostat is used instead. The test is Medicare-rebatable. In lower-risk ancestry, routine screening is not recommended, but any new rash, fever or unwell feeling in the first two months still needs urgent review.
Is gout just a joint problem, or does it affect the rest of my health?

Gout is now considered a cardiovascular risk equivalent. It travels with hypertension, type 2 diabetes, dyslipidaemia, chronic kidney disease, obstructive sleep apnoea, and fatty liver disease, and is independently associated with heart attack and stroke. The 2023 Australian CVD risk guideline lists gout as an upclassifier in cardiovascular risk assessment. That changes the management mindset — a gout consultation is also a cardiovascular and kidney check. Blood pressure, lipids, glucose, kidney function, weight, alcohol and sleep all sit on the same page.
What should I do if a hot, swollen joint comes on suddenly?

If a single joint becomes hot, swollen and exquisitely painful — particularly the big toe — and you have known gout, start the anti-inflammatory plan agreed with your GP (NSAID, colchicine or short course of oral steroid) as early as possible; treatment within 24 hours works best. Seek urgent assessment the same day if it is your first attack, if you have fever or feel systemically unwell, if the joint is intensely red and you cannot move it, or if you are immunosuppressed — these can signal septic arthritis, which requires joint aspiration before antibiotics. Do not stop your daily urate-lowering tablet during a flare.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.