Gout & Pseudogout

Gout and calcium pyrophosphate deposition (CPPD) are inflammatory arthritides caused by crystals: monosodium urate (MSU) in gout and calcium pyrophosphate (CPP) in CPPD.

Gout affects about 2.5% of the UK population and is rising with obesity, ageing and diuretic use. Acute CPP crystal arthritis, historically 'pseudogout', mainly affects older adults.

In every acute hot swollen joint, exclude septic arthritis first. Gout and infection can coexist, so finding crystals does not exclude sepsis.

Hyperuricaemia is the prerequisite for gout: above a serum urate of about 360 micromol/L, MSU crystals can form. Most comes from reduced renal excretion (chronic kidney disease (CKD), diuretics, low-dose aspirin, ciclosporin, alcohol); less from overproduction (purine-rich diet, myeloproliferative disease, tumour lysis).

Crystals favour cooler peripheral joints such as the 1st metatarsophalangeal (MTP) joint and activate the NLRP3 inflammasome, releasing interleukin-1 beta and driving neutrophil inflammation. Untreated, gout runs from flares, through intercritical gout with crystals persisting, to chronic tophaceous gout.

In CPPD, CPP crystals form in fibrocartilage (menisci, triangular fibrocartilage of the wrist, symphysis pubis), seen on X-ray as chondrocalcinosis. Most cases are age-related. Hyperparathyroidism, haemochromatosis and hypomagnesaemia are recognised metabolic associations.