Dr. Abhijeet Bhosikar
Crystal & Metabolic

Gout — Treatment in Pune

Also known as: Gouty Arthritis · Crystal Arthritis · High Uric Acid

The most curable form of arthritis — and the most commonly mistreated.

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What is Gout?

Gout is caused by monosodium urate crystals depositing in and around joints when blood uric acid stays persistently above roughly 6.8 mg/dL — the level at which urate saturates body fluid.

An attack is one of the most painful things in medicine: the joint becomes red, hot and so tender that a bedsheet is intolerable. It classically hits the base of the big toe (podagra), but the ankle, knee, wrist and fingers are also common.

Gout is genuinely curable in the sense that with sustained urate-lowering therapy the crystals dissolve, attacks stop permanently and tophi shrink away. Almost all treatment failure comes from treating only the attacks and never lowering the urate.

Close-up of tablets in a blister packIllustrative
Conventional DMARDs control the majority of patients and cost a fraction of biologics.

In the Indian context

Reported gout prevalence in Indian COPCORD data is around 0.05%, but clinic experience suggests substantial under-diagnosis. Rising rates of obesity, metabolic syndrome, alcohol use and diuretic prescription are increasing the burden across urban Pune.

Symptoms of Gout

Early signs

  • Sudden severe joint pain, often waking the patient in the early hours
  • Redness, warmth and shiny skin over the joint, peaking within 12–24 hours
  • Extreme tenderness — even light touch or bedding is unbearable
  • The attack settles over 7–14 days even untreated, leaving the joint apparently normal
  • Peeling or itching of skin over the joint as the attack resolves

If left untreated

  • Tophi — chalky white nodules over the ear cartilage, elbows, fingers or Achilles tendon
  • More frequent attacks involving more joints, with less complete recovery between them
  • Chronic joint damage and deformity mimicking rheumatoid arthritis
  • Kidney stones and reduced kidney function from urate nephropathy
  • Draining tophi that ulcerate through the skin

Causes & risk factors

  • Reduced renal excretion of urate — the mechanism in about 90% of patients, often genetic (URAT1 and SLC2A9 variants)
  • Diuretics, especially thiazides, plus low-dose aspirin, ciclosporin and some anti-TB drugs
  • Chronic kidney disease and metabolic syndrome
  • Beer and spirits, and fructose-sweetened soft drinks
  • High-purine intake: organ meat, red meat and shellfish

How Gout is diagnosed

No single test diagnoses a rheumatic disease. The diagnosis comes from combining the pattern of symptoms, the examination findings, and only the investigations that answer a specific question.

  1. Joint fluid aspiration with polarised microscopy

    The gold standard — needle-shaped, negatively birefringent urate crystals confirm the diagnosis definitively and simultaneously exclude infection.

  2. Serum uric acid, timed correctly

    Crucially, uric acid can be normal or low during an acute attack. Testing must be repeated at least two weeks after the attack settles, or gout gets wrongly excluded.

  3. Ultrasound double-contour sign

    A bright band of urate coating the cartilage surface — a non-invasive, highly specific sign of urate deposition, and useful for tracking crystal dissolution over time.

  4. Dual-energy CT (DECT)

    Colour-codes urate deposits without a needle. Valuable for atypical presentations and for demonstrating hidden tophus burden.

  5. Metabolic and renal workup

    Kidney function, lipids, HbA1c, blood pressure and a drug review — gout is a marker of cardiometabolic risk and often a signal to change a diuretic.

Treatment options

Treat the attack fast

Low-dose colchicine, an NSAID, or a short steroid course started within the first 24 hours. Speed of initiation matters far more than choice of drug.

Urate-lowering therapy to a target

Allopurinol started low and titrated up, or febuxostat, aiming for serum urate below 6 mg/dL — or below 5 mg/dL where tophi are present. The dose is titrated to the number, not fixed at the starting dose.

Flare prophylaxis during initiation

Low-dose colchicine for the first three to six months of urate-lowering therapy. Skipping this causes early flares, which is why patients wrongly conclude allopurinol 'does not suit them' and stop.

HLA-B*58:01 awareness

This allele markedly raises the risk of severe allopurinol hypersensitivity and is more common in some Asian populations — a reason for cautious low-dose initiation and clear rash warnings.

Lifestyle and drug rationalisation

Weight reduction, cutting beer, spirits and sugary drinks, good hydration, and switching a thiazide to losartan or a calcium channel blocker where blood pressure allows.

Long-term crystal clearance

Therapy is lifelong. Urate stays below target for years while existing deposits dissolve — attacks then stop entirely and tophi visibly regress.

Living with Gout

  • Drink two to three litres of water daily unless your doctor has restricted fluids
  • Cherries, low-fat dairy and vitamin C have modest urate-lowering effects
  • Alcohol — particularly beer — is the most reliable single trigger to remove
  • Do not stop urate-lowering therapy during an attack; that prolongs the problem
  • Keep a rescue dose of the flare medication at home and at work for immediate use

Seek urgent medical attention if you have

  • A single hot swollen joint with fever — septic arthritis can look identical and is an emergency
  • Any rash appearing after starting allopurinol — stop the drug and seek review immediately
  • Loin pain or blood in urine suggesting urate stones
  • Ulcerating or discharging tophi
  • Rapidly rising creatinine

Do not wait for a scheduled appointment for any of the above. Call the clinic on +91 70571 19999 or attend the nearest emergency department.

Frequently asked questions about Gout

My uric acid is high but I have no pain. Do I need treatment?
Asymptomatic hyperuricaemia usually does not require urate-lowering drugs. It does require attention to kidney function, blood pressure, weight, alcohol and any medications causing it. Drug treatment is generally started once there has been a proven attack, a tophus, urate stones or significant kidney disease.
Should I stop dal, tomatoes and spinach?
This is the most common piece of misinformation in Indian gout care. Vegetable purines have little effect on gout risk, and tomatoes are not a meaningful trigger for most people. Beer, spirits, sugary drinks, organ meat, red meat and shellfish are what actually matter, along with overall weight.
Why did my gout get worse after starting allopurinol?
Lowering urate mobilises existing crystals, which can provoke flares in the first few months. This is expected and temporary. It is exactly why low-dose colchicine cover is prescribed alongside, and why the answer is to continue rather than stop.
Can gout be cured permanently?
Effectively, yes. If serum urate is held below 6 mg/dL continuously, crystal deposits dissolve, attacks cease, and tophi disappear over months to years. The condition returns if medication stops, because the underlying handling of urate is unchanged.

Get an expert opinion on Gout in Pune

Consultations at the Ravet clinic in Pimpri-Chinchwad. Bring your previous reports — a properly reviewed history usually saves repeating tests.

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Part of a wider group

Gout & Crystal ArthritisThe most curable arthritis there is — and the most commonly mistreated.

Related conditions

  • Pseudogout (CPPD)

    Gout's mimic — same fury, different crystal, different treatment.

  • Osteoarthritis

    India's most common joint disease — and far more treatable than 'nothing can be done'.

  • Rheumatoid Arthritis

    Symmetric small-joint swelling that responds best when treated within the first 12 weeks.

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