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The pharmacological history of gout is unusually long. Hippocrates wrote of the "unwalkable disease" in the fifth century BCE; the [[wikipedia:Aulus Cornelius Celsus|Celsus]] description of inflammatory arthritis in the first century is recognisable; the English physician [[wikipedia:Thomas Sydenham|Thomas Sydenham]] published his ''Tractatus de Podagra et Hydrope'' in 1683, one of the most precise clinical descriptions of gout ever written, drawn from his own suffering of the disease. The chemical recognition of [[wikipedia:Uric acid|uric acid]] in renal calculi by [[wikipedia:William Hyde Wollaston|William Hyde Wollaston]] in 1797 and its identification by Wollaston in 1813 as the substance of gouty tophi established the biochemical foundation of the disease;<ref name="wollaston1797">Wollaston WH. On gouty and urinary concretions. ''Philosophical Transactions of the Royal Society of London''. 1797;87:386-400.</ref> the demonstration by [[wikipedia:Alfred Baring Garrod|Alfred Garrod]] in 1848 that gout patients had elevated serum uric acid (by his "thread test" using a thread suspended in serum to crystallize uric acid) closed the diagnostic argument and gave the framework that has persisted to the present. | The pharmacological history of gout is unusually long. Hippocrates wrote of the "unwalkable disease" in the fifth century BCE; the [[wikipedia:Aulus Cornelius Celsus|Celsus]] description of inflammatory arthritis in the first century is recognisable; the English physician [[wikipedia:Thomas Sydenham|Thomas Sydenham]] published his ''Tractatus de Podagra et Hydrope'' in 1683, one of the most precise clinical descriptions of gout ever written, drawn from his own suffering of the disease. The chemical recognition of [[wikipedia:Uric acid|uric acid]] in renal calculi by [[wikipedia:William Hyde Wollaston|William Hyde Wollaston]] in 1797 and its identification by Wollaston in 1813 as the substance of gouty tophi established the biochemical foundation of the disease;<ref name="wollaston1797">Wollaston WH. On gouty and urinary concretions. ''Philosophical Transactions of the Royal Society of London''. 1797;87:386-400.</ref> the demonstration by [[wikipedia:Alfred Baring Garrod|Alfred Garrod]] in 1848 that gout patients had elevated serum uric acid (by his "thread test" using a thread suspended in serum to crystallize uric acid) closed the diagnostic argument and gave the framework that has persisted to the present. | ||
The acute-gout medicines have all been used for centuries in some form. Colchicine, extracted from the autumn crocus ''[[wikipedia:Colchicum autumnale|Colchicum autumnale]]'' by [[wikipedia:Pierre Joseph Pelletier|Pelletier]] and [[wikipedia:Joseph Bienaimé Caventou|Caventou]] in 1820, has been used for acute gout in some form since the Byzantine era (Alexander of Tralles in the sixth century described the use of ''Colchicum''). Colchicine's antigout mechanism (microtubule disruption that inhibits neutrophil chemotaxis and crystal-driven inflammasome activation) was elucidated in the twentieth century, but the medicine had been used effectively for fifteen hundred years before that. The narrow therapeutic window (gastrointestinal toxicity at doses near the therapeutic) and the substantial | The acute-gout medicines have all been used for centuries in some form. Colchicine, extracted from the autumn crocus ''[[wikipedia:Colchicum autumnale|Colchicum autumnale]]'' by [[wikipedia:Pierre Joseph Pelletier|Pelletier]] and [[wikipedia:Joseph Bienaimé Caventou|Caventou]] in 1820, has been used for acute gout in some form since the Byzantine era (Alexander of Tralles in the sixth century described the use of ''Colchicum''). Colchicine's antigout mechanism (microtubule disruption that inhibits neutrophil chemotaxis and crystal-driven inflammasome activation) was elucidated in the twentieth century, but the medicine had been used effectively for fifteen hundred years before that. The narrow therapeutic window (gastrointestinal toxicity at doses near the therapeutic) and the substantial interaction profile (CYP3A4 substrate; severe toxicity with concurrent clarithromycin or grapefruit) shape its contemporary use. The 2010 FDA approval of branded colchicine (Colcrys, URL Pharma) at much higher cost than the unbranded preparation was a controversial regulatory episode; the medicine returned to generic competition in 2014. | ||
The non-steroidal anti-inflammatory medicines (described under [[:Category:NSAIDs|NSAIDs]] and [[:Category:Non-opioid_analgesics|non-opioid analgesics]]) became standard first-line treatment for acute gout in the post-1971 (Vane prostaglandin-mechanism) era; indomethacin, naproxen, ibuprofen, and the COX-2-selective celecoxib are all effective at full anti-inflammatory doses for 5 to 7 days. Systemic corticosteroids (oral prednisone 30-40 mg daily for 5-7 days; intraarticular triamcinolone or methylprednisolone) provide equivalent efficacy with a different adverse-effect profile and are first-line for patients in whom NSAIDs or colchicine are contraindicated. The IL-1 antagonists (anakinra, canakinumab, rilonacept) are reserved for refractory cases or patients in whom all of the above are contraindicated, on the basis of the central role of the NLRP3 inflammasome and IL-1β in crystal-driven gout inflammation. | The non-steroidal anti-inflammatory medicines (described under [[:Category:NSAIDs|NSAIDs]] and [[:Category:Non-opioid_analgesics|non-opioid analgesics]]) became standard first-line treatment for acute gout in the post-1971 (Vane prostaglandin-mechanism) era; indomethacin, naproxen, ibuprofen, and the COX-2-selective celecoxib are all effective at full anti-inflammatory doses for 5 to 7 days. Systemic corticosteroids (oral prednisone 30-40 mg daily for 5-7 days; intraarticular triamcinolone or methylprednisolone) provide equivalent efficacy with a different adverse-effect profile and are first-line for patients in whom NSAIDs or colchicine are contraindicated. The IL-1 antagonists (anakinra, canakinumab, rilonacept) are reserved for refractory cases or patients in whom all of the above are contraindicated, on the basis of the central role of the NLRP3 inflammasome and IL-1β in crystal-driven gout inflammation. | ||