Gout vs Pseudogout: Telling Them Apart
Gout and pseudogout produce almost the same picture at the bedside — a joint that swells, reddens and hurts within hours — but they are caused by two different crystals, and only one of them responds to urate-lowering treatment. Gout is monosodium urate; pseudogout is calcium pyrophosphate. Telling gout vs pseudogout apart matters less in the first 48 hours, when the anti-inflammatory treatment overlaps almost completely, and enormously after that, when the long-term plans diverge entirely.
Two different crystals
In gout, urate builds up in the blood until it exceeds its solubility limit — around 6.8 mg/dL (about 400 µmol/L) at body temperature — and needle-shaped monosodium urate crystals form in and around joints. The immune system treats those needles as foreign, and the resulting inflammation is the attack. That whole chain is explained in more detail in our plain-language guide to gout.
Pseudogout, properly called acute calcium pyrophosphate crystal arthritis, involves a completely unrelated crystal: calcium pyrophosphate dihydrate, which deposits in cartilage rather than forming out of a blood level you can measure. There is no “serum calcium pyrophosphate” test. Nothing you eat or drink changes the deposit, and no drug currently dissolves it. This is the single most important practical difference: gout is a condition you can reverse the chemistry of, and pseudogout is not.
The joints each one picks
Gout’s signature site is the base of the big toe — roughly half of first attacks land there, for reasons of temperature and mechanical load covered in why gout hits the big toe first. After that it favours the midfoot, ankle and knee.
Pseudogout goes the other way. The knee is far and away its commonest joint, followed by the wrist. A hot, swollen wrist in a person over 70 is much more likely to be calcium pyrophosphate than urate. Pseudogout also has a habit of involving the second and third knuckles of the hand, which gout rarely does early on.
Who gets which
- Gout skews male and starts earlier — often between 30 and 60 in men. It travels with obesity, alcohol, chronic kidney disease, and with drugs that raise urate, especially thiazide and loop diuretics.
- Pseudogout is a disease of age. It is uncommon before 60, climbs steeply after 70, and affects men and women roughly equally. Its risk factors are joint trauma, previous meniscal surgery, and a handful of metabolic conditions — haemochromatosis, hyperparathyroidism, hypomagnesaemia and hypophosphatasia.
- Pseudogout is often set off by an unrelated illness, an operation or a hospital admission, which is why it turns up so often in inpatients a day or two after surgery.
Age is a useful nudge rather than a rule. Plenty of 75-year-olds have gout — in women it tends to arrive late, in the hands, alongside diuretics — and pseudogout does occasionally show up in people in their fifties with one of the metabolic triggers above.
What the X-ray shows
A plain radiograph is where the two diseases start to separate. Calcium pyrophosphate deposits are radio-opaque, so they show up as a thin line of calcification within cartilage — chondrocalcinosis — classically in the knee menisci, the wrist’s triangular fibrocartilage and the pubic symphysis. Urate crystals are not radio-opaque and show nothing at all in early gout.
Two caveats stop chondrocalcinosis from being a diagnosis on its own. It is common and often silent: a large share of people over 80 have it on X-ray with no symptoms whatsoever. And its presence does not exclude gout — the two can sit in the same joint in the same person.
Why aspiration settles it
Drawing fluid from the joint and looking at it under a polarising microscope is the only test that gives a definite answer, and it answers three questions at once. Monosodium urate crystals are needle-shaped and strongly negatively birefringent — yellow when aligned parallel to the compensator. Calcium pyrophosphate crystals are rhomboid or rod-shaped and weakly positively birefringent — blue in the same orientation.
The third question is the one that actually matters for safety. A joint infection looks like both of these, and it destroys cartilage within days. Aspiration sends fluid for Gram stain and culture at the same time as crystal analysis, which is why guidance keeps pushing it. A hot, swollen joint with fever, rigors or feeling systemically unwell needs urgent medical assessment the same day — not a wait-and-see and not self-treatment. Blood tests will not rescue you here: a serum urate can be normal or even low during an acute attack, and CRP rises in all three conditions. How gout is diagnosed goes through the full sequence.
Gout vs pseudogout at a glance
| Gout | Pseudogout | |
|---|---|---|
| Crystal | Monosodium urate, needle-shaped | Calcium pyrophosphate, rhomboid |
| Microscopy | Strongly negative birefringence | Weakly positive birefringence |
| Favourite joints | Big toe, midfoot, ankle, knee | Knee, wrist, knuckles, shoulder |
| Typical age | 30–60 at onset in men; later in women | Mostly over 60, rising sharply over 70 |
| Sex balance | Strongly male until menopause | Roughly equal |
| Blood test | Serum urate, target below 6 mg/dL (360 µmol/L) | No equivalent blood marker |
| X-ray | Normal early; erosions late | Chondrocalcinosis in cartilage |
| Diet’s role | Modest but real | None |
| Long-term drug | Urate-lowering therapy, indefinitely | No deposit-dissolving drug exists |
Treatment overlaps, then diverges completely
For the attack itself, the playbook is nearly identical, because you are suppressing the same inflammatory response to a crystal regardless of which crystal it is: an NSAID, a corticosteroid by mouth or injected into the joint, or colchicine. Colchicine is used in both, though the evidence base in pseudogout is thinner — dosing and timing are covered in our colchicine guide.
After the attack the paths part. In gout, the work is bringing serum urate below the target and keeping it there, which dissolves the existing deposits and, given time, stops attacks happening at all — see the uric acid target that actually matters and the practical guide to allopurinol. Gout is controlled rather than cured, but controlled can mean zero attacks for years.
In pseudogout, none of that applies. Allopurinol does nothing for calcium pyrophosphate; prescribing it would be treating the wrong disease. Management is treating attacks as they come, checking for the metabolic causes listed above in anyone diagnosed young, and low-dose colchicine prophylaxis for people with frequent recurrences.
Worth remembering: if a joint has been called “gout” for years but nobody has ever aspirated it and the urate has always come back normal, the label deserves a second look — particularly if the joint in question is a knee or a wrist in someone over 70.
Frequently Asked Questions
Can you have gout and pseudogout at the same time?
Yes, and it is not rare in older adults. Both crystal types have been found in a single joint sample. It is one more reason the microscopist looks at the whole slide rather than stopping at the first crystal.
Does a high uric acid level mean an attack is gout rather than pseudogout?
It shifts the odds but proves nothing. High urate is common and mostly silent, and urate frequently dips into the normal range during an acute attack. Someone with asymptomatic hyperuricaemia can still be having a pseudogout flare.
Is pseudogout less painful than gout?
On average the attacks build a little more slowly and are somewhat less savage than a classic first-toe gout attack, but the overlap is wide. A pseudogout knee can leave someone unable to bear weight for a week.
Will a gout diet help pseudogout?
No. Calcium pyrophosphate is not made from anything you eat, and no dietary change has been shown to alter deposition. Eating well is worth doing for other reasons, but it is not treatment here.
What to read next
- How gout is diagnosed — what each test can and cannot tell you
- Gout symptoms: what a first attack feels like
- Normal uric acid but still gout?
- Gout attack: what to do first
