Gout and pseudogout are both caused by crystals building up inside your joints, but the crystals are different, the joints they target are different, and the long-term outlook is different. Gout comes from uric acid crystals, while pseudogout comes from calcium pyrophosphate crystals. That single distinction drives nearly every difference between the two conditions, from which joints flare up to whether you can prevent future attacks with diet and medication.
Different Crystals, Different Diseases
Gout is caused by monosodium urate crystals that form when uric acid levels in your blood stay elevated over time. These needle-shaped crystals settle directly onto the surface of cartilage inside a joint, triggering intense inflammation. Your body treats the crystals like a foreign invader, flooding the area with immune cells and producing the rapid-onset swelling and pain that gout is known for.
Pseudogout is caused by calcium pyrophosphate dihydrate (CPPD) crystals. Instead of landing on the cartilage surface, these crystals tend to deposit within the cartilage itself and in surrounding ligaments and joint capsules. They’re also harder to spot under a microscope because they’re smaller and often don’t light up under polarized light the way urate crystals do. This is one reason pseudogout is sometimes missed or misdiagnosed as gout.
Where Each Condition Strikes
Gout has a strong preference for the big toe, especially during a first attack. It can also hit the ankle, midfoot, and knee, but the base of the big toe is the classic location. If you wake up at 2 a.m. with a red, swollen big toe that feels like it’s on fire, gout is the leading suspect.
Pseudogout favors the knee more than any other joint. The wrist is the second most common site. It can also affect the ankle, shoulder, and elbow, and occasionally the small joints of the hand. When someone over 60 develops sudden inflammatory arthritis in the knee or wrist without an obvious cause, pseudogout is high on the list of possibilities.
Who Gets Each Condition
Gout is far more common in men, particularly between the ages of 30 and 50. Women’s risk rises after menopause, when the protective effect of estrogen on uric acid excretion fades. Overall, gout is one of the most common forms of inflammatory arthritis, affecting roughly 4% of American adults.
Pseudogout tends to appear later in life. Symptom onset after age 60 is a hallmark feature, and the condition becomes increasingly common with each decade after that. It affects men and women more equally than gout does. Having certain metabolic conditions significantly raises your risk, including hyperparathyroidism (overactive parathyroid glands), hemochromatosis (iron overload), thyroid disease, chronic kidney disease, and hypomagnesemia (low magnesium levels). If you’re diagnosed with pseudogout before age 60, your doctor will likely screen for these underlying conditions.
How Attacks Feel
Both conditions can cause sudden, intense joint pain, swelling, redness, and warmth. During a flare, the affected joint can become so tender that even the weight of a bedsheet is unbearable. In both cases, attacks often come on fast, sometimes reaching peak intensity within 12 to 24 hours.
That said, pseudogout attacks are sometimes less dramatic than gout. They can build more gradually and last longer, sometimes simmering for weeks. Pseudogout can also present as a chronic, low-grade inflammatory arthritis that mimics rheumatoid arthritis, with persistent stiffness and swelling in multiple joints. This chronic form doesn’t always have the obvious “attack” pattern that gout typically follows, which adds to the diagnostic challenge.
How Doctors Tell Them Apart
The gold standard for both conditions is joint aspiration: drawing a small sample of fluid from the inflamed joint with a needle and examining it under a microscope. Urate crystals from gout are needle-shaped and light up brightly under polarized light. Calcium pyrophosphate crystals from pseudogout are shorter, rhomboid-shaped, and often appear faint or invisible under the same polarized light. This single test gives a definitive answer in most cases.
Imaging helps too. X-rays in pseudogout often show a characteristic finding called chondrocalcinosis, which is visible calcification within the cartilage, particularly in the knees, wrists, and the pubic symphysis. Gout doesn’t produce this pattern. On ultrasound, urate deposits in gout create a “double contour sign” where crystals coat the cartilage surface and move together with the underlying bone during joint motion. Calcium pyrophosphate deposits sit in the capsule or ligaments above the cartilage, so they move in the opposite direction on ultrasound, a distinction researchers have called the “pseudo double contour sign.”
Blood tests can support a gout diagnosis if uric acid levels are elevated, but they’re not conclusive on their own. Some people with gout have normal uric acid during a flare, and high uric acid alone doesn’t prove gout. There is no equivalent blood marker for pseudogout.
Diet and Lifestyle Factors
This is one of the starkest differences between the two conditions. Gout has well-established dietary triggers. Foods high in purines, such as red meat, organ meats, shellfish, and certain fish, break down into uric acid and can raise your blood levels enough to trigger a flare. Alcohol, especially beer, and sugary drinks sweetened with fructose are also significant risk factors. Losing weight, staying hydrated, and limiting these foods can meaningfully reduce gout flare frequency for many people.
Pseudogout has no known dietary triggers. The calcium pyrophosphate crystals that cause it aren’t influenced by what you eat or drink. There’s no “pseudogout diet.” The underlying drivers are age, genetics, and the metabolic conditions mentioned earlier. This means lifestyle changes that help with gout simply don’t apply to pseudogout.
Treatment for Acute Flares
When either condition flares, the immediate goal is the same: reduce inflammation and pain. The first-line options are identical for both. Anti-inflammatory medications (NSAIDs like ibuprofen or naproxen), colchicine, and corticosteroids all work for acute attacks of gout and pseudogout. Corticosteroids can be taken by mouth or injected directly into the inflamed joint. The choice depends on your other health conditions and what you tolerate best.
Most acute flares resolve within a few days to two weeks with treatment. Applying ice to the joint and resting it also helps during an attack.
Long-Term Management
Here the two conditions diverge sharply. Gout has effective long-term prevention. If you have frequent attacks (more than two per year), visible uric acid deposits called tophi, kidney stones, or kidney disease, you’re a candidate for urate-lowering therapy. These medications reduce the amount of uric acid your body produces or help your kidneys excrete more of it. The goal is to bring your uric acid level below 6 mg/dL, or below 5 mg/dL if you have tophi. With consistent treatment, many people with gout can eliminate flares entirely and even dissolve existing crystal deposits over time.
Pseudogout has no equivalent. No medication can dissolve calcium pyrophosphate crystals or stop new ones from forming. If an underlying metabolic condition is identified, treating it can slow further crystal deposition, but it won’t clear crystals already in the joint. Long-term management focuses on controlling symptoms when they arise and, in some cases, taking low-dose anti-inflammatories or colchicine to reduce flare frequency. For people with chronic pseudogout that resembles rheumatoid arthritis, treatment strategies borrow from the rheumatoid arthritis playbook to manage ongoing inflammation.
This difference in treatability is perhaps the most important practical distinction. Gout, despite being painful and disruptive, is one of the few forms of arthritis that can be effectively “cured” at the crystal level with proper management. Pseudogout is managed but not reversed, making symptom control and monitoring for underlying conditions the primary focus.