1. Let clinical presentation be your primary guide. Forget the gold standard of diagnosis — demonstrating negatively birefringent crystals within synovial aspirate. Aspirating small joints in a family practice setting is asking for trouble. Even measuring plasma urate can be deceptive, as most people with high levels don’t have gout, and besides, urate levels actually fall during acute gouty attacks. It’s not uncommon for urate to score high a month after an attack.
2. The theoretical limit of solubility of urate is 420 µmol/l (7.0 mg/dl). Above that, it must be forming crystals somewhere. Gout risk is elevated above roughly 300 µmol/l (5.0 mg/dl).
3. The main differential diagnosis is septic arthritis. Telling the difference isn’t always easy. Both can cause redness, local warmth, and desquamation. Gout tends to strike the first metatarsophalangeal joint, but can also appear elsewhere in the foot, or the ankle, knee or wrist. Bilateral involvement suggests a rheumatoid cause.
4. Warning signs of septic arthritis are: major swelling, pyrexia, large joint, recent trauma, and no previous attack. Clues that point towards gout include: recent diuretic use, recent drinking (i.e. Christmas presentation), and family history.
5. Useful investigations: blood tests will show raised ESR, CRP, maybe high white cells and thrombocytosis — not very helpful in narrowing the possibilities. Check liver and especially renal function, as renal capacity will influence optimal therapy. It’s also worth checking B12 and thyroid hormones, as deficiencies can cause hyperuricemia.
6. Acute treatment and chronic treatment are very different and often incompatible. Never initiate allopurinol for control of chronic gout until an acute attack is over. Even then, allopurinol can trigger breakthrough attacks, so add prophylactic oral colchicine or NSAID for 3-12 months.
7. Start allopurinol at 50 or 100 mg daily and titrate upwards. Some patients develop rashes on this drug. Uricosuric drugs are an alternative, but avoid them in poeple with kidney stones. Don’t expect the newest xanthine oxidase inhibitor febuxostat (Uloric) to radically outperform allopurinol.
8. The debate continues over which drug — colchicines or NSAID — is better for acute care and preventing breakthrough attacks. Colchicine causes diarrhea, but some experts argue that’s preferable to a GI bleed. The risk of more serious colchicine complications — myopathy and neuropathy — rises fast as renal function declines. A good conservative acute dose is 0.5 mg colchicine tid, a good prophylactic dose is 0.5 mg bid. Among NSAIDs, none stands out above the others.
9. Diuretic-induced gout can sometimes be prevented by adding an ACE inhibitor or ARB. Low-dose aspirin can also increase urate levels.
10. Conventional wisdom says to cut out purine-rich foods to help symptoms. But the only large study to test that proposition failed to back it up. Nevertheless, it’s wise to reduce red meat, sardines, salmon, shellfish, liver and kidneys. Weight loss helps. Alcohol, especially beer, definitely leads to gout. One anecdotal claim that has stood up to research is that consuming dairy helps prevent gout.
