Medically reviewed by Dr. Tom Biernacki, DPM — Board-Certified Podiatric Surgeon — Balance Foot & Ankle, Howell & Bloomfield Hills, MI. Last updated April 2026.

Gout vs. Pseudogout: How to Tell the Difference

Both gout and pseudogout cause sudden, severe joint inflammation — often waking patients from sleep. Both are crystal arthropathies (caused by crystal deposits in joints), but the crystals are different, the joints most commonly affected differ, and the long-term management diverges significantly. Here’s how to distinguish them.

Gout: The Basics

Gout is caused by monosodium urate (MSU) crystals — the crystallized form of uric acid. When serum urate levels rise above 6.8 mg/dL (the saturation point), urate precipitates into joints and soft tissues. The crystals trigger an intense inflammatory response mediated by neutrophils and the NLRP3 inflammasome.

Classic Features of Gout

• Joint distribution: 50–70% of first attacks involve the first MTP joint (big toe joint) — a pattern called podagra. Also: ankle, midfoot (Lisfranc), knee, wrist, and elbow.
• Demographics: Predominantly men (men are 3–4× more commonly affected); women’s risk increases after menopause when estrogen loss reduces uric acid excretion
• Onset: Rapid — full intensity pain typically within 12–24 hours of onset; often waking at night
• Appearance: Intense redness, warmth, swelling; the skin may peel during resolution
• Triggers: High-purine foods (red meat, shellfish), alcohol (especially beer), dehydration, diuretics, certain medications, illness or surgery
• Tophi: Chronic gout causes tophaceous deposits (chalky white urate nodules) in soft tissues — around joints, ear helices, Achilles tendon

Pseudogout: The Basics

Pseudogout (calcium pyrophosphate dihydrate deposition disease — CPPD) is caused by calcium pyrophosphate (CPP) crystals depositing in joint cartilage and synovium. Unlike gout, it’s not caused by dietary factors.

Classic Features of Pseudogout

• Joint distribution: The knee is most commonly affected (>50% of cases). Also: wrist, ankle, shoulder, hip. The big toe is rarely the primary site (distinguishing it from gout).
• Demographics: Both sexes equally; strongly age-related — prevalence increases dramatically after age 70. Very uncommon before age 60.
• Onset: Similar to gout — sudden, severe flares
• Associations: Hyperparathyroidism, hypomagnesemia, hemochromatosis, hypothyroidism, hypophosphatasia — metabolic workup is indicated at first diagnosis
• Chondrocalcinosis: CPP crystals in cartilage are visible on X-ray as calcification (chondrocalcinosis) — a key diagnostic finding

How to Differentiate Gout from Pseudogout

Definitive Diagnosis: Joint Aspiration

The gold standard for distinguishing gout from pseudogout (and both from septic arthritis, which is a medical emergency) is joint aspiration with synovial fluid crystal analysis under polarized light microscopy. This is an office procedure.

Treatment: Similarities and Differences

Acute Attack (Both Conditions)

• NSAIDs (indomethacin, naproxen): First-line; start within hours of attack onset
• Colchicine: Highly effective if started within 24 hours of attack
• Corticosteroids: Oral or intra-articular; use when NSAIDs/colchicine are contraindicated

Long-Term Management: Key Differences

Gout: Urate-lowering therapy (allopurinol, febuxostat) targets serum urate below 6.0 mg/dL to prevent crystal formation. Diet modification (reduce red meat, shellfish, alcohol, fructose). Long-term commitment to urate management.

Pseudogout: No urate-lowering therapy. Treat underlying metabolic causes (check calcium, PTH, magnesium, iron studies, thyroid). Low-dose colchicine or NSAIDs for prevention of recurrent attacks. No dietary modification proven effective.

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Gout vs Pseudogout: Get the Right Diagnosis

Gout and pseudogout have different causes and treatments despite similar symptoms. Our podiatrists use joint fluid analysis and imaging to ensure accurate diagnosis.

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Clinical References

1. Neogi T. Gout. Ann Intern Med. 2016;165(1):ITC1-ITC16.
2. Rosenthal AK, et al. Calcium pyrophosphate deposition disease. N Engl J Med. 2016;374(26):2575-2584.
3. Schlesinger N. Diagnosis of gout: clinical, laboratory, and radiological findings. Am J Manag Care. 2005;11(15 Suppl):S443-S450.

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Dr. Tom Biernacki, DPM is a double board-certified podiatrist and foot & ankle surgeon at Balance Foot & Ankle Specialists in Southeast Michigan. With over a decade of clinical experience, he specializes in heel pain, bunions, diabetic foot care, sports injuries, and minimally invasive surgery. Dr. Biernacki is a member of the APMA and ACFAS, and his patient education content on MichiganFootDoctors.com and YouTube has reached over one million views.