What Is Pseudogout? Symptoms, Causes, and Treatment

Pseudogout is a form of arthritis caused by calcium crystals building up in your joints, triggering sudden episodes of pain, swelling, and stiffness. It most commonly strikes the knees and tends to affect older adults, with radiological signs appearing in 30% to 40% of people over age 80. Despite sharing a name with gout, pseudogout involves a completely different type of crystal and behaves differently in important ways.

What Causes Pseudogout

The culprit behind pseudogout is a buildup of calcium pyrophosphate crystals inside joint cartilage. Your body normally produces pyrophosphate as a byproduct of cell metabolism, and small amounts circulate through cartilage without causing problems. In pseudogout, an imbalance of pyrophosphate in the cartilage causes it to bind with calcium, forming tiny sharp crystals that embed in the joint tissue.

These crystals can sit quietly in your cartilage for years without symptoms. But when they shed into the joint space, your immune system treats them as foreign invaders. White blood cells swarm the area, releasing inflammatory chemicals that cause the intense pain, redness, and swelling of a pseudogout attack. This inflammatory cascade also damages the joint lining over time, which is why repeated flares can lead to progressive joint deterioration.

How It Differs From Gout

Gout and pseudogout look similar on the surface, both causing hot, swollen, painful joints, but they have different causes and different triggers. Gout results from uric acid crystals, which form when blood levels of uric acid get too high. Diet plays a major role in gout: eating red meat, seafood, and drinking alcohol can trigger flares by raising uric acid levels.

Pseudogout doesn’t work this way. There’s no strong link between what you eat and pseudogout attacks. The calcium pyrophosphate crystals form due to changes in cartilage chemistry, not from dietary excess. This means the dietary restrictions that help manage gout (cutting back on purines and alcohol) generally won’t prevent pseudogout flares. Gout also favors the big toe as its signature joint, while pseudogout gravitates toward the knees, wrists, and ankles.

Who Gets Pseudogout

Age is the single biggest risk factor. Crystal deposits show up on imaging in 6% to 15% of people over 60, and that number jumps to 30% to 40% after age 80. The condition is rare in younger adults unless an underlying metabolic condition is driving it.

Several health conditions raise the risk significantly. Overactive parathyroid glands (hyperparathyroidism) carry nearly five times the odds of developing pseudogout compared to the general population. Osteoarthritis roughly triples the risk. Advanced kidney disease, particularly in people on dialysis or with stage 5 kidney disease, more than doubles the likelihood. Certain medications, including loop diuretics commonly prescribed for high blood pressure or heart failure, are also associated with increased risk. Joint trauma or surgery can sometimes trigger crystal shedding and set off a first attack.

What a Flare Feels Like

A pseudogout attack typically comes on fast, sometimes within hours. The affected joint becomes swollen, warm to the touch, and intensely painful. Moving the joint or putting weight on it feels difficult or impossible. The knee is the most common target, though the wrists, ankles, hips, and occasionally smaller joints like fingers and toes can be affected too.

Flares last days to weeks, which is generally longer than the typical gout attack. Some people experience isolated episodes separated by months or years of no symptoms. Others develop a more chronic pattern, with low-grade pain and stiffness that persists between flares, resembling rheumatoid arthritis closely enough to cause diagnostic confusion.

How Pseudogout Is Diagnosed

The gold standard for diagnosis is examining fluid drawn from the affected joint under a special polarized light microscope. Calcium pyrophosphate crystals have a distinctive appearance that differentiates them from the uric acid crystals of gout. This joint fluid analysis is the most definitive test available.

Imaging also plays an important role. X-rays and ultrasound can both detect calcium deposits in cartilage, a finding called chondrocalcinosis. Studies comparing the two methods at the wrist found similar accuracy: ultrasound picked up crystal deposits about 78% of the time, while X-rays caught them about 76% of the time. Both methods have high specificity, meaning that when they do detect calcifications, it’s very likely real. In 2023, the ACR and EULAR (two major rheumatology organizations) published updated classification criteria that combine demographic factors, clinical features, imaging findings, and crystal analysis to standardize how the condition is identified.

Treatment for Acute Flares

There is no treatment that dissolves the crystals once they’ve formed. Management focuses on controlling inflammation during flares and reducing their frequency over time.

Anti-inflammatory medications are the first-line approach for acute attacks, though they come with caveats. Because pseudogout predominantly affects older adults, the stomach bleeding and kidney risks associated with these drugs make them a less-than-ideal long-term solution in this population. When only one joint is involved, particularly the knee, draining fluid from the joint and injecting a corticosteroid directly into it can provide fast, targeted relief. For flares affecting multiple joints, a short course of oral corticosteroids with a quick taper is a common alternative.

Colchicine, a medication also used for gout, is sometimes prescribed at low doses to reduce the frequency of recurrent attacks. It works better as a preventive measure than as a treatment for flares already underway. Ice, rest, and keeping weight off the affected joint during a flare all help manage symptoms alongside medication.

Long-Term Joint Effects

Repeated pseudogout flares aren’t just painful in the moment. Each episode of inflammation damages the joint lining (the synovium) and can gradually erode cartilage. Over years, this can lead to a form of degenerative arthritis that looks and feels a lot like osteoarthritis, with chronic stiffness, reduced range of motion, and persistent low-level discomfort even between flares.

Because the underlying crystal deposits can’t currently be removed or dissolved, the long-term strategy centers on minimizing inflammation. If you’re having frequent flares, your doctor may recommend a low-dose preventive medication to reduce how often attacks occur and slow cumulative joint damage. Staying active, maintaining joint mobility, and addressing any underlying metabolic conditions (like hyperparathyroidism or low magnesium) that might be fueling crystal formation are all practical steps that can change the trajectory of the disease.