Diagnosis: Chronic Tophaceous Gout (with diuretic-exacerbated hyperuricaemia)

Clinical Reasoning

• Anti-CCP (ACPA) negative — sensitivity ~70%, specificity ~95% for RA; its absence significantly lowers RA probability
• RF is non-specific and can be positive in gout, especially in the elderly
• Asymmetric erosion pattern on X-ray
• No juxta-articular osteopenia
• Dramatically elevated urate

Management

1. Acute/Ongoing Inflammation

• Colchicine 500 mcg BD–TDS — preferred over NSAIDs given renal impairment (GFR 55) and existing NSAID use (diclofenac should be reduced/stopped)
• Low-dose prednisolone is already in use; can be continued for flare control but not as urate-lowering therapy
• Intra-articular corticosteroid injection to the knee effusion can provide rapid relief
• Avoid NSAIDs long-term — renal impairment + existing diclofenac increases risk of further AKI

2. Urate-Lowering Therapy (ULT) — the cornerstone

• Allopurinol — first-line xanthine oxidase inhibitor
  • Start at low dose (50–100 mg/day) given reduced GFR (55) — titrate slowly to avoid triggering acute flare
  • Target serum urate < 360 µmol/L (ideally < 300 µmol/L in tophaceous disease)
  • Cover with colchicine for 3–6 months when initiating ULT to prevent mobilisation flares
• Febuxostat — alternative xanthine oxidase inhibitor if allopurinol intolerant; caution given cardiovascular comorbidities (AF, hypertension)

3. Address Aggravating Factors

4. Carpal Tunnel Syndrome

• If due to urate crystal deposition in the carpal tunnel, ULT will improve this over time
• Consider nerve conduction studies to quantify severity
• Corticosteroid injection or surgical decompression if severe

5. Olecranon Bursa

• Aspiration if tense/painful (send fluid for crystal analysis to confirm MSU crystals — needle-shaped, negatively birefringent under polarised light)
• Intralesional corticosteroid injection

6. Monitoring

• Recheck serum urate at 4–6 weeks after starting allopurinol
• Monitor renal function, FBC, LFTs on allopurinol
• DEXA if long-term steroid use (already on prednisolone + self-medicating with oral steroids)

Summary

Complete Diagnosis & Management

DIAGNOSIS: Chronic Tophaceous Gout

Pathophysiology

Why Chronic Tophaceous Gout (not RA)

MANAGEMENT

1. Acute Flare Control

• Mechanism: depolymerises tubulin → impairs neutrophil migration into inflamed joint → blocks NLRP3 inflammasome → reduces IL-1β
• Dose: 0.5–1 mg stat, then 0.5 mg 6–12 hourly (low-dose regimen preferred)
• Must be given within 36 hours of onset of attack to be effective
• Caution: GFR 55 — dose-adjust; avoid in severe renal impairment (GFR <30). Monitor for GI toxicity (nausea, vomiting, diarrhoea). Hepatic metabolism via CYP3A4.

• Renal impairment (GFR 55) → risk of further AKI
• Already on diclofenac — should be weaned off and replaced

• Patient already on prednisolone 5 mg daily (for asthma) — can utilise short-course dose increase during flares
• Intra-articular corticosteroid injection into the knee effusion — appropriate for monoarticular/oligoarticular flare; aspirate first to exclude septic arthritis

2. Urate-Lowering Therapy (ULT) — Cornerstone of Chronic Management

• 2 attacks per year

• Chronic kidney disease (GFR 55)
• Tophi present (olecranon bursa, MCP joints)
• Serum urate markedly elevated

First-line: Allopurinol (xanthine oxidase inhibitor)

• Inhibits the last two steps of uric acid biosynthesis (hypoxanthine → xanthine → uric acid)
• Preferred over febuxostat and probenecid as first-line ULT
• Starting dose: 50–100 mg/day — start LOW because GFR 55 (dose adjustment mandatory when GFR <30; titrate slowly at any level of renal impairment to avoid precipitating flares)
• Titrate upward every 2–4 weeks
• Target: serum urate <360 µmol/L (ideally <300 µmol/L in tophaceous disease)
• Adverse effects: rash (most common), hypersensitivity reactions (risk increased with renal impairment), hepatotoxicity — monitor LFTs and FBC
• Drug interaction: allopurinol inhibits xanthine oxidase → do not combine with azathioprine (patient is not on this, but relevant given chronic steroid use in future)
• Interaction with theophylline (not relevant here) and warfarin (monitor INR if anticoagulation started for AF)

Alternative: Febuxostat (if allopurinol intolerant)

• Non-purine xanthine oxidase inhibitor; inhibits both reduced and oxidised forms of XO
• Less renal elimination than allopurinol — less dose adjustment needed in renal impairment
• Caution in this patient: increased risk of cardiovascular events (MI, stroke) vs. allopurinol; patient has AF and hypertension — febuxostat should be reserved for allopurinol intolerance only
• Goldman-Cecil Medicine states: "Allopurinol can prevent gouty attacks more safely than febuxostat"

Uricosuric agents (e.g., probenecid) — avoid

• Probenecid is contraindicated if creatinine clearance <50 mL/min — this patient's GFR is 55, borderline; also risks urate stone formation

3. Addressing Aggravating Factors

4. Specific Complications

• Aspirate: send fluid for Gram stain, culture, and crystal microscopy (to confirm MSU and exclude septic bursitis)
• Intralesional corticosteroid once infection excluded
• ULT will dissolve tophi over months–years

• Likely due to MSU crystal deposition in the carpal tunnel
• Nerve conduction studies to quantify severity
• ULT alone may resolve it over time
• Corticosteroid injection if symptomatic; surgical decompression if severe/unresponsive

• Aspirate for diagnosis + therapeutic relief
• Intra-articular corticosteroid injection

5. Monitoring Plan

Summary Algorithm

Acute flare  →  Colchicine ± intra-articular steroid
                ↓
Stop/replace diclofenac  →  Colchicine for analgesia
                ↓
Start allopurinol 50–100 mg (low dose, titrate)
+ Colchicine prophylaxis × 6 months
                ↓
Switch enalapril → losartan
Reduce/stop alcohol
                ↓
Target serum urate < 360 µmol/L (<300 in tophaceous disease)
                ↓
Manage AF (rate control + anticoagulation)
Bone protection (long-term steroids)
Carpal tunnel / knee / bursa as needed