Gout is one of the most common types of inflammatory arthritis, caused by the accumulation of urate crystals in the joints. It occurs when there is either an overproduction or underexcretion of uric acid, leading to its buildup in the blood and crystal urate deposits in the joints. This can trigger inflammation and sudden, severe pain, most commonly in the first metatarsophalangeal joint.

Genetic factors are the most important cause of gout. Impaired renal function and obesity also significantly contribute to hyperuricaemia.

Gout is diagnosed on the basis of clinical history, physical examination, and lab tests. Aspiration of an affected joint or bursa to confirm the presence of monosodium urate crystals is the gold standard for confirming a diagnosis of gout.

When ordering a joint synovial analysis ask for:

• crystal analysis
• MCS
• cell count

Note:

• Crystal analysis and MCS - Can be done with tubes provided by the radiologist.
• Cell count - Provide patients with a K2 EDTA tube (small purple top) as this is often not stocked at most radiology companies and the sample will clot without it.

Serum urate testing during an acute flare may not be beneficial for diagnosing gout, as levels may be normal to low. This happens because the urate crystals precipitate out of the bloodstream and into the joint space, and reduce the measurable serum uric acid concentration.

Dual-energy CT (DECT) is a non-invasive imaging technique that can be useful in complex or atypical cases:

• where the diagnosis is not clear cut and it is difficult to obtain a joint aspirate
• where there is multiple joint involvement
• to quantify or monitor disease burden

DECT is not recommended as a routine diagnostic tool. Its sensitivity is lower in patients with early-stage gout or those without visible tophi, making it less reliable compared to joint aspiration in such cases.

Other limitations include the higher cost, limited availability, and the risk of radiation exposure, making it less suitable for widespread use.

Triggers may include:

• excessive consumption of certain purine-rich foods (like red meat, shellfish, and alcohol)
• dehydration
• sudden weight changes
• kidney dysfunction,
• certain medications e.g. thiazide, loop diuretics and ciclosporin.

Gout flares are more common at night and early morning when cortisol levels are low and can last approximately 7-10 days if left untreated.

It is common for patients to need more than 300 mg daily of allopurinol. However, it is essential to start at a low dose, and gradually up-titrate every 4 weeks, until the target serum urate is met. Gradual up-titration reduces the risk of hypersensitivity reactions and acute changes in uric acid concentration that could trigger a gout flare. The maximum dose of allopurinol recommended in guidelines is 900 mg daily. See the QUM Alliance gout treatment algorithm for guidance and alternatives to allopurinol if contraindicated.

It is most important to check and confirm adherence before increasing the dose of allopurinol as allopurinol is rarely ineffective.

For patients with renal impairment, the dosing of allopurinol should be adjusted based on the estimated glomerular filtration rate (eGFR) as follows: See the QUM Alliance gout treatment algorithm for guidance.

Starting Dose

• eGFR 15–30 mL/min/1.73 m2: Start with 50 mg of allopurinol on alternate days.
• eGFR <15 mL/min/1.73 m2: Start with 50 mg twice a week.

Dose Titration

• Increase the dose every 4 weeks as follows:
  • eGFR <60 mL/min/1.73 m2: Increase by 50 mg increments.
  • eGFR ≥60 mL/min/1.73 m2: Increase by 100 mg increments.

Maximum dose

• 900 mg per day, regardless of renal function.

The maximum dose of allopurinol that can be used in renal impairment is the same as above, 900mg. However, up-titration will occur at a lower dosage and/or a slower dosing interval. See the QUM Alliance gout treatment algorithm for guidance.

A rapid reduction in serum uric acid levels after starting urate-lowering therapy (ULT) is thought to destabilise urate crystals within the joints. The displaced crystals interact with cells in the synovium, triggering a gout flare, which is most common in the first few months of ULT.

The risk of an allopurinol hypersensitivity reaction is low, occurring in less than 1% of patients.

However, individuals who carry the HLA-B5801 allele have a higher risk of severe hypersensitivity to allopurinol. If your patient is from an at-risk group, such as certain Asian populations (eg Han Chinese, Korean, Thai) or African-American, you may want to consider genetic testing for the HLA-B5801 allele before starting allopurinol.

The test costs about $75 and isn’t covered by Medicare. If the test is positive, allopurinol should not be prescribed due to significantly increased risk of a serious reaction. See the QUM Alliance gout treatment algorithm for alternative ULT options.

After starting urate-lowering therapy, serum urate levels should be monitored every 4 weeks until target levels are reached. In those with non-tophaceous gout aim for <0.36 mmol/L. For those with tophaceous gout, gouty arthritis or recurrent flares aim for < 0.30 mmol/L. Once stable, monitor in 6 months then annually.

Yes, lifestyle changes can help in managing gout, although they’re not a complete solution. While managing diet is unlikely to prevent gout in the first place, it can reduce the risk of having a gout flare.

Here’s how:

1. Diet and alcohol: while diet and alcohol don't play as big a role as once thought, managing intake can still help. Limiting high-purine foods from animal sources (like red meat and shellfish) and alcohol, especially beer, may reduce the risk of triggering flares.
2. Maintain a healthy weight and balanced diet: while no specific diet is endorsed, maintaining a healthy weight and balanced diet can significantly benefit gout management.
3. Supplements and alternative therapies: although popular, supplements like vitamin C and tart cherry juice have limited and inconsistent evidence for gout management. Vitamin C has minimal impact on urate levels, and tart cherry juice lacks strong evidence for preventing flares.

While medication, such as allopurinol, is the most effective way to manage urate levels, these lifestyle adjustments can support overall gout management and help reduce flare triggers. When counselling patients regarding diet and lifestyle also be considerate of:

• comorbidities: consider existing dietary advice for other conditions to avoid conflicting guidance
• culturally-specific beliefs: for better adherence to dietary recommendations, consider culturally-specific beliefs about health and lifestyle.

In susceptible people, excess consumption of certain high-purine foods or alcohol can lead to an acute change in serum urate concentration that triggers a gout flare. Yet while there is strong evidence that lifestyle factors can increase the risk of gout, evidence that correcting these factors improves outcomes is lacking.

For patients who are well managed on ULT, no specific diet is endorsed, although maintaining a healthy weight and balanced diet are encouraged. This includes staying hydrated, advising patients who drink alcohol to do so in moderation and recommending reduced consumption of beverages high in fructose (added or natural) such as non-diet soft drinks and fruit juices.

Other points to consider when counselling patients regarding diet and lifestyle:

• be mindful of comorbidities: consider existing dietary advice for other conditions to avoid conflicting guidance
• address culturally-specific beliefs: for better adherence to dietary recommendations, consider culturally-specific beliefs about health and lifestyle.