What Is Gout?
Gout is the most common inflammatory arthritis in India, affecting an estimated 1–2% of the adult population. It is caused by elevated uric acid (hyperuricaemia) in the blood, which leads to urate crystal deposition in joints, causing excruciatingly painful acute attacks and, if untreated, chronic joint damage.
Gout is eminently curable and preventable with the right treatment. Yet in India, it is massively undertreated — patients manage flares with painkillers but never treat the underlying high uric acid.
What Causes High Uric Acid?
Uric acid is the end product of purine metabolism. Purines are found in certain foods (red meat, organ meats, seafood, alcohol) and are also produced naturally by the body during cell turnover. High uric acid results from:
- Overproduction — genetic tendency, rapid cell turnover (psoriasis, blood cancers), high purine diet
- Underexcretion — kidney disease (the commonest cause in India), dehydration, alcohol, certain medications (diuretics, cyclosporine, low-dose aspirin)
Note: Most Indians with high uric acid have reduced kidney excretion as the primary mechanism — not dietary excess alone.
Symptoms of Gout
Acute Gout Attack
The classic presentation is sudden, severe pain in the big toe joint (podagra) — often waking the patient at night. The joint becomes intensely red, hot, swollen, and so tender that even the touch of a bedsheet causes agony. Attacks peak within 12–24 hours and self-resolve in 3–10 days without treatment, though treatment shortens the attack.
While the big toe is most classic, acute gout can affect the ankle, knee, wrist, and elbow. It almost never affects the small joints of the fingers (which helps distinguish it from RA).
Intercritical Gout
The period between attacks. The patient is asymptomatic but urate crystals continue accumulating in joints and soft tissues. Without urate-lowering therapy, attacks become more frequent and severe.
Tophaceous Gout
With long-standing high uric acid, chalky white deposits of urate crystals (tophi) accumulate in soft tissues — ear cartilage, Achilles tendon, fingers, and around joints. Tophi indicate chronic undertreated gout and are associated with joint destruction.
Pseudogout — Another Crystal Arthritis
Pseudogout is caused by calcium pyrophosphate crystals (CPPD), not urate. It typically affects larger joints (knee most common) in older patients. The acute attack mimics gout. Managed similarly with anti-inflammatories but urate-lowering drugs have no role.
Diagnosing Gout
- Serum uric acid — elevated (>6.8 mg/dL), though it may paradoxically fall during acute attacks
- Joint fluid aspiration — gold standard: identification of negatively birefringent monosodium urate crystals under polarised microscopy
- Ultrasound — double contour sign over cartilage, tophi identification
- DECT (Dual Energy CT) — highly accurate for urate deposition, available at major centres
- X-rays — in chronic gout show punched-out erosions with overhanging edges
Treatment of Acute Gout Attack
- NSAIDs (indomethacin, naproxen, etoricoxib) — first-line if no kidney disease
- Colchicine — very effective, especially if started within first 12 hours. Low dose (0.5mg twice daily) is as effective as high dose with fewer GI side effects
- Steroids — oral prednisolone or joint injection for those with kidney disease where NSAIDs are contraindicated
- Rest, ice, elevation of the affected joint
Do NOT start allopurinol during an acute attack — it can prolong the attack. Wait 2–4 weeks after the attack resolves.
Long-Term Urate-Lowering Therapy (ULT)
This is the crucial step most Indian gout patients miss. Allopurinol is the gold-standard ULT and one of the best value-for-money drugs in all of rheumatology:
- Allopurinol — start at 100mg/day and titrate monthly to achieve target uric acid <6 mg/dL (or <5 mg/dL in tophaceous gout). Cost: ₹50–150/month. Requires HLA-B*5801 screening in Indian patients (increased risk of severe skin reaction — Stevens-Johnson syndrome) before starting.
- Febuxostat — alternative to allopurinol, more potent. Start at 40mg, increase to 80mg if needed. Cost: ₹300–600/month.
- Benzbromarone — for patients who under-excrete uric acid with normal kidney function
When to start ULT: After the second gout attack, or after the first attack if: serum uric acid >9 mg/dL, kidney stones, tophi present, or kidney disease.
Co-prescribe colchicine 0.5mg twice daily for the first 3–6 months of ULT initiation to prevent the “mobilisation flares” that commonly occur as crystals dissolve.
Gout Diet — What Actually Matters
Diet alone cannot cure gout — medications are essential. But dietary changes can reduce uric acid by 1–2 mg/dL:
- Avoid: Alcohol (especially beer), organ meats (kidney, liver, brain), anchovies, sardines, shellfish, high-fructose corn syrup (in soft drinks and packaged foods)
- Limit: Red meat, mutton, venison
- Safe/Protective: Dairy products (milk, curd — actually protective), cherries, vegetable proteins (lentils, tofu), coffee, water (drink 2–3L/day)
- Myth: Dal and pulses do NOT significantly raise uric acid in gout patients — they are safe to eat
Gout and Associated Conditions
Gout is a systemic metabolic disease associated with: hypertension, type 2 diabetes, chronic kidney disease, cardiovascular disease, and metabolic syndrome. Every gout patient should have their cardiovascular risk factors addressed holistically, not just their uric acid.
FAQs About Gout in India
Should I take allopurinol lifelong?
In most patients, yes. Stopping allopurinol allows uric acid to rise again and attacks to recur. Think of it like blood pressure medication — it controls the problem but doesn’t cure the underlying tendency.
Can I take allopurinol with kidney disease?
Yes, with dose adjustment. Allopurinol is actually beneficial in chronic kidney disease as uric acid independently damages kidneys. Febuxostat is better tolerated in CKD.
Written by Dr. Keerthivardhan, Rheumatologist, NIMS Hospital Hyderabad.