Derangement in purine metabolism resulting in hyperuricaemia; monosodium urate crystal deposits in tissue (tophi), synovium (microtophi) and kidneys (urate nephropathy)
Demographics
Common, 1% population
Males, adults
Maori
Aetiology
Primary Gout 90%: Genetic (unknown) due to decreased uric acid excretion. Rarely due to enzyme defects (HGPRT def.)
Secondary Gout 10%: increased production due to excess cell breakdown (cancers), renal disease, high protein diet, alcohol abuse, Obesity, thiazide diuretics, Lead toxicity.
Pathophysiology
↑ uric acid (insufficient excretion/increased purine production), acidosis, low temperatures → urate crystal formation caused by supersaturation in ECF → uric acid crystal (coated with IgG) deposition in synovial fluid and tissue → polymorphonuclear cell phagocytosis → inflammatory mediator release → localised joint inflammation
Collections of MSU crystals, called tophi, develop in the soft tissues and appear as firm lumps under the skin. Tophi generally develop around 10 years after the first attack of gout
crystals → inflammation → neutrophils engulf and become lysed by crystals → release of lysosomal enzymes → cartilage and joint damage.