2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis

Khanna, Dinesh; Khanna, Puja P.; Fitzgerald, John; Singh, Manjit; Bae, Sangmee; Neogi, Tuhina; Pillinger, Michael H.; Merill, Joan; Lee, Susan; Prakash, Shraddha; Kaldas, Marian; Gogia, Maneesh; Pérez-Ruiz, Fernando; Taylor, William J.; Lioté, Frédéric; Choi, Hyon K.; Singh, Jasvinder A; Dalbeth, Nicola; Kaplan, Sanford; Niyyar, Vandana Dua; Jones, Danielle; Yarows, Steven A.; Roessler, Blake J.; Kerr, Gail S.; King, Charles M.; Levy, Gerald; Fürst, Daniel E.; Edwards, N. Lawrence; Mandell, Brian F.; Schumacher, H. Ralph; Robbins, Mark L.; Wenger, Neil S.; Terkeltaub, Robert

doi:10.1002/acr.21773

Cited by 642 publications

(586 citation statements)

References 57 publications

(100 reference statements)

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“…Os antinflamatórios não esteroides são a terapêutica de primeira linha para a maioria dos doentes, desde que não haja Revista Interdisciplinar em Ciências da Saúde e Biológicas, 2017; 1(1)52-64 contraindicação 23,24 . O principal mecanismo de ação dos AINEs ocorre através da inibição específica da COX e consequente redução da conversão do ácido aracdônico ou araquidônico (AA) em prostaglandinas.…”

Section: Diagnósticounclassified

“…Entre os principais AINES utilizados no tratamento de crises agudas da gota estão: Indometacina, Piroxicam, Naproxeno e Sulindaco. O ácido acetilsalicílico, apesar de ser um anti-inflamatório não esteroidal deve ser evitado sempre que possível, pois reduz a excreção de ácido úrico pelos rins 22,24,25 . Os inibidores específicos da ciclooxigenase-2 (Coxibes -Refecoxib, Celecoxib) apesar de serem fármacos eficientes nas crises de gota, seu uso não é aconselhável em pacientes com crises de gota associadas a doença cardiovascular e/ou cerebrovascular estabelecidas 24 .…”

Section: Diagnósticounclassified

“…O medicamento não apresenta efeito algum sobre a concentração de urato sérico, a excreção urinária do ácido úrico ou a solubilidade do urato no plasma. Apresenta, contudo, efeitos adversos frequentes, dose-dependentes, como vômitos, diarreia, dor abdominal e mais raramente hepatite, supressão medular, neuropatia e insuficiência cardíaca 3,24,26 .…”

Section: Diagnósticounclassified

“…Os corticosteroides podem ser usados via oral, intravenosa, intramuscular e intra-articular, e são indicados caso não seja possível o uso de AINES ou colchicina (24). Por serem lipofílicos, os corticosteróides ultrapassam rapidamente a membrana celular e entram no citoplasma, onde se ligam ao receptor específico e, desta forma, atingem o núcleo celular, interagindo com o DNA e regulando a ativação e supressão de diferentes genes de alguns mediadores da inflamação como as citocinas, de enzimas indutíveis durante o processo inflamatório como a COX-2 e de moléculas de adesão (que recrutam células inflamatórias como neutrófilos, eosinófilos e linfócitos T da circulação, para os locais da inflamação) 16 .…”

Section: Diagnósticounclassified

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Gota: uma revisão da literatura.

Heckler

Wust

Libardoni

et al. 2017

RICSB

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RESUMOA Gota ou também chamada de artrite gotosa é uma artropatia inflamatória desencadeada pelo excesso de ácido úrico que acaba se depositando, na forma de cristal de urato monossódico, na articulação. O ácido úrico é o produto final do metabolismo das purinas, que deve dissolver-se no sangue e ser eliminado através da urina. Quantidades excessivas de acido úrico podem surgir devido a erros inatos do metabolismo das purinas seja pela superprodução e/ou insuficiência na excreção renal de ácido úrico ou pode estar relacionado a condições ou enfermidades que elevam seus níveis séricos. O presente estudo baseou-se numa revisão da literatura que teve como objetivo salientar aspectos recentes da gota relacionados a patogenia, além de características clínicas, diagnóstico, prevenção e tratamento. Para a realização desta revisão, foram selecionados artigos científicos publicados em bancos de dados. Foram utilizados artigos publicados nos últimos 15 anos, nos idiomas português, espanhol e inglês. A Gota pode ser dividida em quatro fases: hiperuricemia assintomática, crise aguda, períodos intercríticos e gota crônica que podem evoluir para urolitíase e nefropatia úrica. A gravidade da doença é proporcional à frequência das crises agudas e a repetição desses quadros indica progressão do processo patológico. Descritores: Artrite gotosa; Gota; Ácido úrico. ABSTRACTGout or also called gouty arthritis is an inflammatory joint disease triggered by excessive uric acid that ends up depositing in the form of monosodium urate crystal, within the joint. Uric acid is the final product of purine metabolism, which must dissolve in blood and should eliminated through the urine. Excessive amounts of uric acid may arise due to inborn errors of metabolism of purines or by over-production and / or impaired kidney excretion of uric acid or may be related to conditions or diseases that raise serum levels. The present study was based on a review of the literature that aimed to highlight recent aspects of gout related to pathogenesis, clinical features, diagnosis, prevention and treatment. For a performance of this review, scientific papers published in databases were selected. We used articles published in the last 15 years, in the languages, Spanish and English. Gout can divided into four phases: asymptomatic hyperuricemia, acute crisis, intercritical periods, chronic gout that may progress to urolithiasis and uric nephropathy. Disease severity is proportional to the frequency of acute attacks and repetition these conditions indicates progression of the pathological process.

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Section: Diagnósticounclassified

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Gota: uma revisão da literatura.

Heckler

Wust

Libardoni

et al. 2017

RICSB

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“…In this setting the recent publication of the American College of Rheumatology (ACR) guidelines for the management of gout are a welcome addition to the resources at the disposal of practicing clinicians to assist in the management of this group of potentially complex patients 4,5 . The ACR guidelines recommend probenecid as an alternative first-line pharmacological urate-lowering therapy for those with a history of contraindication or intolerance to a xanthine oxidase inhibitor and with a creatinine clearance of 50 ml/min or more 4 .…”

Section: The Real World Of Goutmentioning

confidence: 99%

The Real World of Gout

Conway

2013

J Rheumatol

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Management of Gout

Shmerling

2012

JAMA

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Mr R is a 57-year old man with a history of podagra (acute first metatarsal-phalangeal joint pain and swelling), hyperuricemia, and mild chronic kidney disease. An immigrant from Eastern Europe, Mr R worked as an engineer and is now retired. He lives with his wife and has several children. For many years, he has been a patient at a hospital-based primary care practice. He has a 60-packyear history of smoking but does not abuse alcohol or other drugs. He has no family history of gout, but his grandfather and father had renal disease of uncertain etiology.In 1993, Mr R experienced his first episode of podagra and was treated with indomethacin and an "injection into my toe." Five years later, his first measurement of uric acid was 7.7 mg/dL. Over the next 10 years, recurrent episodes of podagra were accompanied by uric acid levels as high as 9 mg/dL. Treatment with colchicine caused diarrhea without pain relief. He has adamantly refused further colchicine treatment. A consulting rheumatologist recommended that he use ibuprofen as his principal medication during acute episodes. In 2006, his serum creatinine level was first elevated to 1.3 mg/dL (with an estimated glomerular filtration rate of 57 mL/min/1.73 m 2 ); it later increased to 1.5 mg/dL but stabilized more recently at 1.3 mg/dL. He has had microalbuminuria, most recently with an albumincreatinine ratio of 442 mg/g (normal range, Ͻ30 mg/g). Aside from the presence of 2 cysts, kidney size and architecture were unremarkable on ultrasound and computed tomography.At the time of the elevation in creatinine, Mr R started therapy with allopurinol, 100 mg/d, which he continues. His uric acid levels range between 6 and 7 mg/dL. He has never had physical stigmata of gout other than intermittent swelling, redness, and pain in his great toe. He has not had recurrent symptoms since initiating allopurinol. Mr R has long-standing obesity. His height is 68 in (173 cm); weight, 258 lb (116 kg); and body mass index (calculated as weight in kilograms divided by height in meters squared), 39.2. His blood pressure has been mildly elevated. He has a long history of hyperlipidemia. Currently, his low-density lipoprotein cholesterol level is 172 mg/dL (ideal range, Ͻ129 mg/dL). He currently takes rosuvasta- CME available online at www.jamaarchivescme.com and questions on p 2154.Gout is an ancient disease. Despite significant advances in the understanding of its risk factors, etiology, pathogenesis, prevention, and treatment, millions of people with gout experience repeated attacks of acute arthritis and other complications. The incidence of gout is increasing, most likely reflecting increasing rates of obesity and other lifestyle factors, including diet. Comorbid conditions that often accompany gout, including chronic kidney disease and diabetes mellitus, present challenges for the management of gout. Using the case of Mr R, a 57-year-old man with a history of podagra, hyperuricemia, and mild renal insufficiency, the diagnosis and treatment of gout are discussed. For those with mode...

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2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis

Cited by 642 publications

References 57 publications

Gota: uma revisão da literatura.

Gota: uma revisão da literatura.

The Real World of Gout

Management of Gout

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