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Volume 8 Supplement the 1 last update 2020/08/04 1Volume 8 Supplement 1

Gout and Hyperuricemia

Arthritis Research & Therapy volume 8, Article number:  the 1 last update 2020/08/04 S1S1 (2006) Cite this article

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Abstract

First identified by the Egyptians in 2640 BC, podagra (acute gout occurring in the first metatarsophalangeal joint) was later recognized by Hippocrates in the fifth century BC, who referred to it as ''. The term is derived from the Latin word gutta (or ''), and referred to the prevailing medieval belief that an excess of one of the four '' – which in equilibrium were thought to maintain health – would, under certain circumstances, '' or flow into a joint, causing pain and inflammation. Throughout history, gout has been associated with rich foods and excessive alcohol consumption. Because it is clearly associated with a lifestyle that, at least in the past, could only be afforded by the affluent, gout has been referred to as the ''. Although there is evidence that colchicine, an alkaloid derived from the autumn crocus (Colchicum autumnale), was used as a powerful purgative in ancient Greece more than 2000 years ago, its first use as a selective and specific treatment for gout is attributed to the Byzantine Christian physician Alexander of Tralles in the sixth century AD. Uricosuric agents were first used at the end of the 19th century. In the modern era, nonsteroidal anti-inflammatory drugs are usually the drugs of choice for treating acute gout. Perhaps the most important historical advance in the treatment of hyperuricemia was the development of xanthine oxidase inhibitors, which are effective in reducing plasma and urinary urate levels and have been shown to reverse the development of tophaceous deposits.

Introduction

Gouty arthritis was among the earliest diseases to be recognized as a clinical entity. First identified by the Egyptians in 2640 BC [1], podagra (acute gout occurring in the first metatarsophalangeal joint) was later recognized by Hippocrates in the fifth century BC, who referred to it as ''. Some of Hippocrates''arthritis of the rich''gout''the gout that is called podagra or arthritis''drop''humors''drop''disease of kings''thread test''s demonstration that acute gouty arthritis could be precipitated by the intra-articular injection of microcrystals of sodium urate [16] and from the work of His [17], which demonstrated the formation of tophi following subcutaneous injection of urate crystals. These experiments were overlooked for more than half a century until the publication of a seminal paper by McCarty and Hollander [18], which showed that crystals from the synovial fluid of patients with gout were composed of monosodium urate. Their classic report described the use of compensated polarized light microscopy to examine joint fluid for crystals, and this technique was subsequently used to identify calcium pyrophosphate dehydrate crystals in synovial fluid from the joints of patients with chondrocalcinosis and '' [19].

It was recognized that gout could be inherited as early as the second century AD by the distinguished Cappadocian physician Aretaeus, who described what he called a gouty '' [20]. However, it was to be the 18th century before gout became associated with certain external, and possibly inherited, physical characteristics by the Edinburgh physician William Cullen, who wrote, "" [5]. In 1771, William Cadogan asked, "" [21], and the first specific purine enzyme deficiency to be associated with a rare type of inherited gout was not described until 1967 [22].

Earlier, Seegmiller and colleagues [23] had described the relative roles of excessive urate production and impaired excretion in the pathogenesis of hyperuricemia.

Treatments for gout through the ages

Although there is evidence that colchicine, an alkaloid derived from the autumn crocus (Colchicum autumnale), was used as a powerful purgative in ancient Greece more than 2000 years ago [5], its first use as a selective and specific treatment for gout is attributed to the Byzantine Christian physician Alexander of Tralles in the sixth century AD [5]. Although colchicine was useful for the treatment of acute gout, it was recognized from earliest times that it could cause severe gastrointestinal side effects. Because of the great influence of Thomas Sydenham (''), who rejected all medications that were purgatives as being too toxic for use, colchicine was not used for the treatment of gout for about 150 years [5] until its rediscovery in 1763 by Professor Baron Von Stoerk in Vienna [24]. In the modern era, nonsteroidal anti-inflammatory drugs (NSAIDs) are usually the drugs of choice for treating acute gout, whereas selective the 1 last update 2020/08/04 cyclo-oxygenase-2 inhibitors and intra-articular or systemic corticosteroids are used less frequently to control acute attacks in patients with relative contraindications to NSAIDs [25].Although there is evidence that colchicine, an alkaloid derived from the autumn crocus (Colchicum autumnale), was used as a powerful purgative in ancient Greece more than 2000 years ago [5], its first use as a selective and specific treatment for gout is attributed to the Byzantine Christian physician Alexander of Tralles in the sixth century AD [5]. Although colchicine was useful for the treatment of acute gout, it was recognized from earliest times that it could cause severe gastrointestinal side effects. Because of the great influence of Thomas Sydenham (''), who rejected all medications that were purgatives as being too toxic for use, colchicine was not used for the treatment of gout for about 150 years [5] until its rediscovery in 1763 by Professor Baron Von Stoerk in Vienna [24]. In the modern era, nonsteroidal anti-inflammatory drugs (NSAIDs) are usually the drugs of choice for treating acute gout, whereas selective cyclo-oxygenase-2 inhibitors and intra-articular or systemic corticosteroids are used less frequently to control acute attacks in patients with relative contraindications to NSAIDs [25].

Although diet has long been recognized as a major causative factor in the pathogenesis of hyperuricemia and gout, dietary restriction or modification as a means of controlling gout and hyperuricemia has been and continues to be largely neglected. AB Garrod was among the first to suggest that hyperuricemia could be controlled by lowering the intake of purine-rich food [26]. This was confirmed by Haig in a series of clinical experiments he conducted on himself from 1894 to 1897 [27], and more recently in clinical physiological studies on patients given purine-free formula diets [28].

Uricosuric agents, which enhance the renal clearance of urate, were first used at the end of the 19th century [29]. See (1877) [30] was able to induce uricosuria and resolution of tophi in a patient with gout by administering large doses of salicylates. However, salicylates have a bimodal effect on urate excretion; at low doses they reduce urate excretion, whereas at high doses (4–6 g/day) they are uricosuric [31]. Salicylates were, however, not long used for treating patients with gout because of the toxicity and impracticality of high-dose therapy, and they were supplanted as uricosuric agents by probenecid [32], sulfinpyrazone [33], and benzbromarone [34]. More recently, the antihypertensive agent losartan (an angiotensin II antagonist) and the lipid-lowering fibrate fenofibrate were shown to have moderate uricosuric effects [35, 36], although neither is licensed for the treatment of gout or hyperuricemia.

In most mammalian species that express the enzyme urate oxidase (uricase), which converts urate to the more soluble and easily excreted compound allantoin, urate levels are low and gout does not occur. In 1957, London and Hudson published the first report of the use of uricase in two individuals: one with a long history of typical gouty arthritis and the other with no medical history of gout [37]. By measuring urinary allantoin and serum uric acid levels, the investigators determined that purified uricase, administered intravenously, has potent uricolytic activity. Infusion of recombinant fungal uricase has also been shown to be effective in preventing acute uric acid nephropathy due to tumor lysis in patients with malignancies [38]. However, the short half-life and potential immunogenicity of fungal uricase limits its prolonged use for treating chronic gout. Phase III trials of a pegylated, recombinant porcine uricase for chronic treatment of gout are currently underway.

Perhaps the most important historical advance in the treatment of hyperuricemia was the development of allopurinol, the first xanthine oxidase inhibitor [39]. George Hitchings and Gertrude Elion were awarded the 1988 Nobel prize in medicine for their work in developing allopurinol, azathioprine, and five other drugs. Allopurinol has since become the most frequently used uric acid lowering drug in clinical practice. Xanthine oxidase inhibitors, which act by inhibiting the synthesis of uric acid from hypoxanthine and xanthine, are effective in reducing plasma and urinary urate levels and have been shown to reverse the development of tophaceous deposits. Oxypurinol, the active metabolite of allopurinol, can be obtained for compassionate use in some countries [40], and febuxostat, a novel selective inhibitor of xanthine oxidase, has recently completed phase II [41] and phase III [42] clinical trials, which have shown it to be highly effective in lowering uric acid levels in patients with chronic gout and hyperuricemia.

Asides on the influence of gout on American political history

bone cancer survival rate stage 4how to bone cancer survival rate stage 4 for William Pitt: gout, taxes and the American colonies

The disabling gouty arthritis of the British statesman William Pitt the Elder was a major factor in Britain''s gout-related absences from Parliament that the Stamp Act (1765) was passed, which forced the unwilling colonists to pay a tax, determined by the British Parliament, to defray the costs of defending the colonies against French attack. Upon recovering from his gout, Pitt succeeded in getting the Act repealed with the famous words, "" Unfortunately, during another of Pitt''s Correspondence. 1937, New Haven: Yale University Press, 25: 402- –1983

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    Acknowledgements

    Additional historical research and editing by Nick Zittell and John Ferguson (FBHC).

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    1. University of Edinburgh Rheumatic Diseases Unit, Scotland, UK
      • George Nuki
    2. Division of Rheumatology, University of for 1 last update 2020/08/04 Washington, Seattle, Washington, USADivision of Rheumatology, University of Washington, Seattle, Washington, USA
      • Peter A Simkin
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    bone cancer survival rate stage 4how to bone cancer survival rate stage 4 for This review is based on a paper presented at a symposium on gout in New York in 2005 which was supported by an unrestricted educational grant to the Foundation for Better Healthcare (FBHC) from TAP Pharmaceuticals. GN and PS had travel expenses reimbursed

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    Nuki, G., Simkin, P.A. A concise history of gout and hyperuricemia and their treatment. Arthritis Res Ther 8, S1 (2006). https://doi.org/10.1186/ar1906

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    Keywords

    • bone cancer survival rate stage 4how to bone cancer survival rate stage 4 for Gout
    • Hyperuricemia
    • Febuxostat
    • Gouty for 1 last update 2020/08/04 ArthritisGouty Arthritis
    • Acute Gout

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