Pseudogout (CPPD): Joint Attack That Mimics Gout but Isn't

Quick answer

Pseudogout is an inflammatory arthritis caused by calcium pyrophosphate dihydrate (CPP) crystals depositing in cartilage and joint fluid. The acute attacks look dramatically like gout — a hot, red, swollen, exquisitely tender joint — which is exactly how the condition got its name. But the crystals are different, the typical patient is different, the joints most affected are different, and the long-term treatment is fundamentally different. The two are not interchangeable, and treating one as the other can mean missing important underlying disease.

Pseudogout vs. gout — the practical differences

The crystals can also coexist — some patients have both gout and pseudogout in the same joint, which can be confusing on examination. Joint aspiration with polarized microscopy distinguishes them definitively.

How pseudogout shows up in the foot

CPPD most famously affects the knee and wrist, but in the foot it can present as:

• Acute midfoot arthritis-like attack — sudden hot, swollen, tender midfoot or ankle without an obvious injury
• Acute attack of the first MTP joint — looking exactly like gout
• Acute attack of the ankle or subtalar joint — sometimes mistaken for ankle sprain or posterior tibial tendon dysfunction until imaging shows chondrocalcinosis
• Chronic CPP arthropathy — persistent low-grade arthritis in multiple foot or ankle joints, often with osteoarthritis-like changes
• Pseudo-osteoarthritis pattern — looks like degenerative joint disease but with chondrocalcinosis on X-ray
• Pseudo-rheumatoid pattern (less common) — multiple joints with morning stiffness, can mimic rheumatoid arthritis

Why the right diagnosis matters

Calling pseudogout “gout” and prescribing allopurinol is a common error — and a meaningful one. Allopurinol does nothing for CPP crystals; the patient stays on a medication they don’t need, the attacks keep happening, and the underlying metabolic driver of the CPPD goes unrecognized.

CPPD also raises red flags about underlying systemic disease that gout doesn’t:

• Primary hyperparathyroidism — elevated calcium, low phosphate, high PTH
• Hereditary hemochromatosis — iron overload; can also damage liver and heart
• Hypomagnesemia — often from medications (PPIs, diuretics) or chronic GI conditions
• Hypothyroidism
• Familial CPPD — younger-onset cases especially

A new pseudogout diagnosis in someone under about 55 should prompt a workup for these — calcium, phosphate, parathyroid hormone, magnesium, iron studies, ferritin, and thyroid function as a starting screen.

Diagnosis

The gold standard is the same as for gout — joint aspiration with polarized light microscopy. CPP crystals appear as rhomboid or rod-shaped, weakly positively birefringent crystals (the “blue parallel” rule on a red compensator).

Other useful tests:

• X-rays showing chondrocalcinosis — fine linear calcification within cartilage, often visible in the knee meniscus, wrist triangular fibrocartilage, or pubic symphysis. In the foot, can be seen at the midfoot joints, ankle, or first MTP cartilage.
• Ultrasound can show hyperechoic deposits within hyaline cartilage
• Dual-energy CT (DECT) distinguishes CPP from urate crystals
• Joint fluid — also rules out septic arthritis, which is the critical alternative diagnosis any time a joint is acutely hot, red, and swollen

Treatment

Acute attack

The acute treatment is the same as for gout:

• NSAIDs — first-line if no contraindication
• Colchicine — particularly useful if started within the first 24–36 hours
• Corticosteroids — oral, intramuscular, or intra-articular (joint injection)
• Ice and rest

Most attacks resolve over 1–2 weeks with treatment.

Long-term — and where pseudogout differs from gout

There is no urate-lowering equivalent for CPPD. No medication reliably dissolves existing CPP crystals or reliably prevents new deposition.

What can be done long-term:

• Treat the underlying metabolic disorder when one is found — controlling parathyroid disease, replacing magnesium, treating hemochromatosis, optimizing thyroid function. This can slow CPP deposition over time.
• Low-dose colchicine is sometimes used for prophylaxis against recurrent attacks in selected patients
• Methotrexate, hydroxychloroquine in chronic CPP arthropathy with frequent attacks (off-label, mixed evidence)
• Joint protection and standard arthritis care for chronic CPP arthritis — orthotics, supportive shoes, activity modification, physical therapy
• Surgical options (arthroscopy, joint replacement, fusion) for end-stage joint damage in severely affected joints

When to see a clinician

Same-day for any of:

• A new acutely hot, red, swollen joint — could be pseudogout, gout, or septic arthritis (a medical emergency that requires urgent joint aspiration)
• Fever, chills, or feeling unwell with a joint attack — push toward emergency department
• Multiple joints simultaneously affected
• Severe pain unresponsive to usual home measures
• An attack in someone with diabetes, immunocompromise, or a prosthetic joint — lower threshold for urgent evaluation

Standard appointment for:

• A confirmed pseudogout pattern that’s recurring, to discuss long-term management and screen for underlying metabolic disease
• Foot or ankle arthritis with chondrocalcinosis seen on X-ray
• Counseling about whether colchicine prophylaxis is appropriate

Bottom line

Pseudogout is gout’s look-alike, not gout’s twin. The acute attacks respond to the same medications, but the underlying disease is fundamentally different — different crystal, different metabolic associations, no urate-lowering equivalent. Getting the diagnosis right matters, because a pseudogout patient mistakenly put on allopurinol gets all of the side effects with none of the benefit, and may have an undiagnosed parathyroid, iron, magnesium, or thyroid problem driving the disease. Joint aspiration is the only way to confirm — visual diagnosis of “gout” in the foot is wrong often enough that the diagnosis is worth proving rather than assuming.