Gout
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Direct answer
An exquisitely painful monoarthritis of the first metatarsophalangeal joint (podagra) waking a middle-aged man overnight is the classic presentation of gout — crystal-deposition arthritis from monosodium urate supersaturation of joints and tissues. Definitive diagnosis is needle aspiration showing needle-shaped, strongly negatively birefringent crystals under compensated polarised light. Acute attacks are treated with non-steroidal anti-inflammatory drugs, low-dose colchicine or corticosteroids; urate-lowering therapy (allopurinol first line) is started after the attack settles, titrated to a serum urate below 6 mg per dL.
What you must remember
- Crystal signature: needle-shaped monosodium urate crystals that are strongly negatively birefringent and found within neutrophils during acute attacks — contrast with the rhomboid, weakly positive birefringent calcium pyrophosphate crystals of pseudogout.
- Risk factors: male sex, obesity, alcohol (especially beer), purine-rich diets, diuretics, low-dose aspirin, chronic kidney disease and cyclosporine; in women it typically appears after menopause.
- Acute treatment: full-dose NSAIDs (with gastroprotection), low-dose colchicine (0.5 mg two to three times daily — as effective and far better tolerated than high-dose regimens), or oral/intra-articular corticosteroids when both are contraindicated.
- Urate-lowering therapy: allopurinol first line, started at 100 mg daily (50 mg in chronic kidney disease) and titrated monthly; febuxostat is an alternative; probenecid suits under-excreters with preserved renal function; target serum urate below 6 mg per dL (below 5 with tophi).
- Never initiate urate-lowering therapy during an acute flare; continue it without interruption if already established, and cover initiation with prophylactic colchicine or an NSAID for some months.
- Chronic tophaceous gout: hard, non-inflamed urate deposits over olecranon, helix of ear and finger pulps; longstanding disease causes punched-out juxta-articular erosions with overhanging edges on radiographs.
- Secondary causes: myeloproliferative and lymphoproliferative disease, tumour lysis after chemotherapy, renal impairment and Lesch-Nyhan syndrome (hypoxanthine-guanine phosphoribosyltransferase deficiency).
- Losartan and fenofibrate are uricosuric — useful comorbidity choices — whereas thiazides and loop diuretics raise urate.
One attack, then years of urate management
A 46-year-old man on a thiazide wakes at 3 am with a red, hot, exquisitely tender great toe. The first decision is honest: a hot joint is septic arthritis until aspiration proves otherwise, and the tap serves double duty — Gram stain and culture, and crystal analysis showing needle-shaped, strongly negatively birefringent monosodium urate (against the rhomboid, weakly positive pyrophosphate of pseudogout, which favours the knee with chondrocalcinosis). A normal serum urate at the peak of the attack would not exclude gout, since levels paradoxically fall during flares. Treat the flare: full-dose NSAIDs with gastroprotection, or low-dose colchicine 0.5 mg two to three times daily — as effective and far better tolerated than the high-dose regimens of older textbooks — or corticosteroids when both are contraindicated. Then think in years. His risk profile (male, obese, beer, thiazide; women typically only after menopause) is audited — losartan and fenofibrate are uricosuric choices, thiazides and loop diuretics are not. After the attack settles, start allopurinol 100 mg daily (50 mg in chronic kidney disease), titrating monthly toward urate below 6 mg per dL — below 5 with tophi — with colchicine or an NSAID covering the first months, because urate-lowering begun mid-flare worsens the attack, while established therapy continues through flares. Look for the chronic signs: Ask why he is hyperuricaemic — myeloproliferative disease, tumour lysis, renal impairment, or Lesch-Nyhan syndrome.
Where students slip
Three mix-ups recur. Gout versus septic arthritis: both can coexist, steroids mask infection, and the aspirate answers both. Gout versus pseudogout: settled by crystal shape and birefringence plus chondrocalcinosis — "needle, negative" against "rhomboid, positive" carries the mark. The allopurinol timing rule is the third — never start during a flare, never stop established therapy during one — with the target numbers (below 6, below 5 with tophi) attached. The pharmacology list completes the set: losartan alone among antihypertensives lowers it.
Frequently asked questions
What crystal is seen in gout synovial fluid?
Needle-shaped monosodium urate crystals showing strong negative birefringence under compensated polarised light, often inside neutrophils.
What is the first-line treatment of an acute attack?
NSAIDs at full anti-inflammatory dose; low-dose colchicine or corticosteroids are equally acceptable alternatives depending on comorbidity.
When should allopurinol be started?
Not during an acute flare — begin after it settles, at low dose titrated upward, with anti-inflammatory prophylaxis for several months.
What is the target serum urate?
Below 6 mg per dL (below 5 mg per dL in tophaceous disease) to dissolve crystal deposits and prevent attacks.
Which drugs raise serum urate?
Thiazide and loop diuretics, low-dose aspirin, cyclosporine, niacin and pyrazinamide; losartan is uniquely uricosuric among antihypertensives.
How does gout differ from pseudogout?
Pseudogout shows rhomboid, weakly positively birefringent calcium pyrophosphate crystals, chondrocalcinosis and a predilection for the knee, often in older adults.