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Gout is a crystal arthropathy caused by deposition of monosodium urate crystals in joints and tissues, typically affecting the first metatarsophalangeal joint. Pseudogout is caused by calcium pyrophosphate dihydrate crystal deposition, most commonly affecting fibrocartilaginous structures like the knee menisci and triangular fibrocartilage complex of the wrist.
Gout results from hyperuricemia leading to supersaturation and precipitation of uric acid crystals, which trigger intense neutrophilic inflammation through activation of the NLRP3 inflammasome. Pseudogout occurs due to chondrocalcinosis, where calcium pyrophosphate dihydrate crystals deposit in cartilage and are shed into joint spaces, causing acute inflammatory attacks similar to gout but through different crystal-mediated pathways.
Gout typically presents as sudden-onset, severe monoarticular arthritis with predilection for the great toe, while pseudogout more commonly affects larger joints like knees with less dramatic onset. Joint aspiration revealing negatively birefringent needle-shaped crystals confirms gout, whereas positively birefringent rhomboid crystals indicate pseudogout. Treatment differs significantly, with gout responding to urate-lowering therapy and colchicine, while pseudogout management focuses on anti-inflammatory agents and joint aspiration.