Condition Guide

Gout

Gout is the most common inflammatory arthritis in adults, caused by uric acid crystals depositing in joints. Attacks are excruciatingly painful but highly treatable.

Written by Suman Konda, PharmD, Clinical Pharmacist · Based on peer-reviewed sources · Editorial policy · Not medical advice

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What is gout?

Gout is a form of inflammatory arthritis caused by hyperuricaemia: abnormally high uric acid levels in the blood. When uric acid exceeds its solubility limit (around 6.8 mg/dL), it crystallises into monosodium urate crystals that deposit in joints, tendons and surrounding tissues. An acute gout attack occurs when the immune system reacts to these crystals, causing intense inflammation. The classic presentation is sudden, severe pain in the big toe joint (first metatarsophalangeal joint), often waking the patient at night, with redness, swelling and warmth.

Uric acid blood test

GroupUric Acid LevelInterpretation
Men<7.2 mg/dLNormal
Women<6.0 mg/dLNormal
Gout risk threshold≥6.8 mg/dLSaturation point: crystals can form
HyperuricaemiaMen >7.2; Women >6.0Elevated: gout risk

Important: uric acid levels may be NORMAL or even LOW during an acute gout attack, because the inflammatory response causes uric acid to redistribute. A normal uric acid during an attack does not rule out gout. Recheck 2–4 weeks after the attack resolves.

A Normal Uric Acid Does Not Rule Out Gout

This is the single most useful thing to know about the uric acid test, and it is the opposite of what most people assume. A blood test taken during an acute attack can come back normal in someone who genuinely has gout, and a normal result is regularly used to dismiss the diagnosis.

The size of the effect is well documented. Across two trials of acute gout treatment covering 339 patients, 14% had a genuinely normal urate at presentation, and 32% had a level at or below 8 mg/dL during the attack. Attacks occurred even below the concentration at which urate crystallises.2

There are two reasons for this. Crystals that formed months or years ago are already sitting in the joint, and an attack is the immune system reacting to them — it does not require the blood level to be high at that moment. And during an attack, urate often shifts out of the blood, so the timing of the test works against you.

What this means practicallyUrate is a test for planning treatment, not for confirming an attack. The level that matters is the one measured once things have settled, a few weeks after the flare, because that is what reflects your usual state and guides whether urate-lowering treatment is needed and whether it is working. If a normal result during a flare was used to tell you it was not gout, that reasoning does not hold.

The same study showed why context matters: people already taking allopurinol had markedly lower urate during their attacks than those not taking it.2 Being on treatment does not prevent every flare, particularly early on, and a flare while taking allopurinol is not evidence the drug has failed.

Where the diagnosis is genuinely uncertain, the definitive test is not a blood test at all — it is examining fluid drawn from the joint for urate crystals under a microscope, which also distinguishes gout from a joint infection, an entirely different emergency that can look similar.

Joints commonly affected by gout

JointFrequencyNotes
Big toe (podagra)~70% of first attacksClassic presentation
AnkleCommonOften second attack site
KneeCommonLarge joint attacks can mimic septic arthritis
Wrist / fingersLess commonMore common in chronic gout
ElbowLess commonTophi (crystal deposits) visible here

What causes high uric acid?

Overproduction of uric acid

Purine-rich diet (red meat, organ meats, seafood, beer), alcohol excess (alcohol both increases uric acid production and reduces renal excretion), rapid cell turnover (haematological malignancies, tumour lysis syndrome after chemotherapy), and rare enzyme deficiencies.

Underexcretion of uric acid

Accounts for 90% of gout cases. Causes: kidney disease (reduced excretion), dehydration, diuretics (especially thiazides and loop diuretics), low-dose aspirin, cyclosporine, hypertension, metabolic syndrome and hypothyroidism.

Diet changes to lower uric acid

  • Limit red meat, organ meats (liver, kidney) and shellfish (highest purine content)
  • Avoid beer and spirits; moderate wine consumption
  • Drink at least 2 litres of water daily (dilutes uric acid)
  • Increase low-fat dairy (milk, yoghurt): shown to lower uric acid
  • Eat cherries or tart cherry juice: evidence supports modest uric acid reduction
  • Avoid high-fructose corn syrup (soft drinks, fruit juices)
  • Maintain a healthy weight: obesity doubles gout risk

Medications for gout

MedicationUseNotes
NSAIDs (ibuprofen, indomethacin)Acute attack treatmentFirst-line for acute attacks
ColchicineAcute attack + preventionVery effective when started early
CorticosteroidsAcute attack if NSAIDs/colchicine contraindicatedUsed when kidney disease prevents NSAIDs
AllopurinolLong-term uric acid loweringStarted 2–4 weeks after acute attack resolves; target uric acid <6.0 mg/dL
FebuxostatUric acid lowering (alternative to allopurinol)Used if allopurinol not tolerated

Questions to ask your doctor

  • Should I start uric acid-lowering therapy (allopurinol)?
  • What uric acid target should I aim for?
  • Which foods are highest in purines that I should avoid?
  • Is my diuretic worsening my gout?
  • Do I need a joint aspiration to confirm gout and rule out infection?

Related reading

Medical Disclaimer: This page is for general educational purposes only and does not constitute medical advice. Always consult a qualified doctor for diagnosis and treatment.

References

The clinical information on this page is based on peer-reviewed sources indexed in PubMed, the biomedical literature database of the US National Library of Medicine.

  1. FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology guideline for the management of gout. Arthritis Care Res (Hoboken). 2020;72(6):744-760. doi:10.1002/acr.24180 · PMID 32391934
  2. Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis. 2017;76(1):29-42. doi:10.1136/annrheumdis-2016-209707 · PMID 27457514
  3. Schlesinger N, Norquist JM, Watson DJ. Serum urate during acute gout. J Rheumatol. 2009;36(6):1287–9. PMID 19369457 · doi:10.3899/jrheum.080938