Gout vs. Pseudogout: Key Differences and How to Tell Them Apart

Gout and pseudogout are both crystal-induced arthropathies, meaning they cause joint inflammation triggered by crystal deposits, but they involve entirely different crystals, tend to affect different joints, and require different long-term management strategies. The only definitive way to distinguish between them is through joint fluid analysis performed by a healthcare provider. For a broader overview of gout specifically, see our complete guide to understanding gout.

Medical Disclaimer: This article is for educational purposes only and is not a substitute for professional medical diagnosis. Both gout and pseudogout can present with symptoms similar to joint infections and other serious conditions. If you are experiencing sudden, severe joint pain, especially with fever, seek prompt medical evaluation. Do not attempt to self-diagnose based on symptom descriptions alone.

What Are the Two Different Crystal Types?

The fundamental difference between gout and pseudogout lies in the type of crystal causing the inflammation.

Gout is caused by monosodium urate (MSU) crystals. These form when uric acid, a byproduct of purine metabolism, exceeds its solubility limit in the blood (approximately 6.8 mg/dL at body temperature) and crystallizes in joint tissues. Under polarized light microscopy, MSU crystals appear as needle-shaped structures with strong negative birefringence, meaning they appear yellow when aligned parallel to the compensator axis.

Pseudogout, formally known as calcium pyrophosphate deposition disease (CPPD), is caused by calcium pyrophosphate dihydrate (CPP) crystals. These form when calcium pyrophosphate accumulates in cartilage and joint tissues. CPP crystals are typically rhomboid or rectangular in shape and show weak positive birefringence under polarized light, appearing blue when aligned parallel to the compensator axis.

These crystal differences are not just academic. They reflect entirely different metabolic processes and lead to different approaches to long-term management.

Which Joints Does Each Condition Prefer?

One of the most useful clinical clues for distinguishing gout from pseudogout is which joint is affected.

Gout most commonly strikes the first metatarsophalangeal joint (big toe), a presentation called podagra. Other frequently affected joints include the ankle, midfoot, knee, wrist, and finger joints. Gout has a strong predilection for peripheral joints, particularly in the lower extremities.

Pseudogout most commonly affects the knee, which is the single most frequently involved joint. The wrists are the second most common site. Pseudogout can also affect the ankles, shoulders, elbows, and hands. Notably, pseudogout rarely involves the big toe, and when a patient presents with acute big toe inflammation, gout is the far more likely diagnosis.

Feature	Gout	Pseudogout (CPPD)
Most common joint	Big toe	Knee
Other common joints	Ankle, midfoot, knee	Wrist, ankle, shoulder
Big toe involvement	Very common	Rare

How Do the Symptoms Compare?

Both conditions produce acute episodes of joint pain, swelling, redness, and warmth, and the clinical presentations can be remarkably similar.

Gout flares typically have a dramatic and rapid onset, often reaching peak intensity within 12 to 24 hours. The pain is frequently described as the most severe the patient has ever experienced. Flares often start at night and may be preceded by a recognizable prodrome of tingling or mild discomfort in the joint. For a detailed breakdown of these warning signs, see our guide on gout symptoms.

Pseudogout attacks can also be sudden and severe, but they sometimes develop more gradually over the course of a day or two. The pain, while significant, is often described as somewhat less intense than a severe gout flare, though this is highly variable between individuals and episodes. Pseudogout attacks may last longer, sometimes persisting for weeks.

Both conditions can produce low-grade fever during acute attacks, which adds to the diagnostic challenge since joint infection can also cause fever and joint inflammation.

Who Gets Each Condition?

The demographics and risk factors differ meaningfully between the two conditions.

Gout predominantly affects men, with a male-to-female ratio of approximately 3 to 1. It is relatively uncommon in premenopausal women because estrogen has a uricosuric effect, promoting uric acid excretion. Risk factors include elevated uric acid, family history of gout, obesity, metabolic syndrome, chronic kidney disease, certain medications (particularly diuretics), and dietary factors including alcohol and fructose. For a deeper dive into these drivers, see our article on what causes gout. Gout can occur at any age but most commonly presents in men between the ages of 40 and 60.

Pseudogout affects men and women roughly equally and is strongly associated with advancing age. It is rare before age 50 and becomes increasingly common with each decade. Risk factors include age, osteoarthritis, prior joint trauma or surgery, hyperparathyroidism, hemochromatosis, hypothyroidism, and hypomagnesemia. Unlike gout, pseudogout does not have strong dietary or lifestyle associations.

How Is Each Condition Diagnosed?

The gold standard for diagnosing both conditions is arthrocentesis, also known as joint aspiration. A doctor inserts a needle into the affected joint, withdraws a sample of synovial fluid, and sends it for analysis.

Under polarized light microscopy, the two crystal types are readily distinguishable:

• MSU crystals (gout): Needle-shaped, strongly negatively birefringent
• CPP crystals (pseudogout): Rhomboid or rod-shaped, weakly positively birefringent

Joint fluid analysis also allows the laboratory to check for bacteria, which rules out or confirms joint infection. This is critically important because septic arthritis is a medical emergency that requires immediate antibiotic treatment.

Imaging can also help. X-rays may show chondrocalcinosis, which is calcification of joint cartilage visible on plain radiographs. Chondrocalcinosis is highly suggestive of CPPD, though not all patients with pseudogout show it. Dual-energy CT can detect monosodium urate crystal deposits in gout. Ultrasound can identify the “double contour sign” characteristic of urate deposition on cartilage surfaces.

Blood uric acid levels can support a gout diagnosis but are not definitive. Uric acid can be normal during an acute gout flare, and many people with elevated uric acid never develop gout.

How Does Treatment Differ?

Acute attacks of both conditions are treated with similar anti-inflammatory strategies:

• NSAIDs such as indomethacin or naproxen
• Colchicine, which is effective for both gout and pseudogout flares
• Corticosteroids, either oral, injected into the joint, or intramuscular

The critical difference lies in long-term management. Gout has effective urate-lowering therapies, including allopurinol, febuxostat, and probenecid, that reduce uric acid production or increase its excretion. When uric acid is maintained below approximately 6.0 mg/dL over time, existing urate crystals gradually dissolve and flares diminish.

Pseudogout currently has no equivalent long-term crystal-dissolving therapy. There is no medication that reliably reduces calcium pyrophosphate crystal formation or promotes their dissolution. Management focuses on treating acute attacks, preventing recurrences with low-dose colchicine or anti-inflammatories, addressing any underlying metabolic conditions (like hyperparathyroidism), and managing joint symptoms with physical therapy and supportive care.

Why Does Accurate Diagnosis Matter?

Getting the right diagnosis matters because it determines your long-term management strategy. A patient misdiagnosed with pseudogout who actually has gout will miss out on urate-lowering therapy that could prevent progressive joint damage. Conversely, a gout diagnosis in someone with CPPD may lead to unnecessary allopurinol use without benefit.

If you have been diagnosed with gout and are tracking your condition using tools like Urica, the data you collect about your flare patterns, dietary triggers, and response to treatment can be valuable information for your rheumatologist. Understanding your specific crystal type and how your body responds to different factors is essential for effective personalized management.

This article is for informational and educational purposes only. It is not intended as medical advice and should not be used for self-diagnosis. Both gout and pseudogout require professional medical evaluation for accurate diagnosis, as their symptoms can mimic serious conditions including joint infections. Always consult a qualified healthcare provider for proper diagnosis and treatment.