Dan Kaufmann , Nathorn Chaiyakunapruk , Naomi Schlesinger
{"title":"优化痛风治疗:当前和新出现的尿尿疗法的综合综述。","authors":"Dan Kaufmann , Nathorn Chaiyakunapruk , Naomi Schlesinger","doi":"10.1016/j.jbspin.2024.105826","DOIUrl":null,"url":null,"abstract":"<div><div>Gout is the most common inflammatory arthritis, affecting approximately 5.1% of adults in the United States (US) population. Gout is a metabolic and autoinflammatory disease. Elevated uric acid pools lead to the precipitation of monosodium urate (MSU) crystals in and around joints, as well as other tissues, and the subsequent autoinflammatory response. Since elevated serum urate (SU) levels (hyperuricemia) correspond with gout severity, urate-lowering therapies (ULTs) are the cornerstone of gout treatment. ULTs include xanthine oxidoreductase inhibitors, uricosurics, less commonly used in the US but widely used in Europe and Asia, including benzbromarone, dotinurad, and probenecid (the only US Food and Drug Administration (FDA) approved uricosuric in the US), and uricases, including rasburicase and pegloticase (available only in the US). Over 90% of the daily load of uric acid filtered by the kidneys is reabsorbed through renal transporters. These urate transporters include uric acid transporter 1 (URAT1), glucose transporter 9, and organic anion transporters 1, 3, and 4 (OAT1, OAT3, OAT4). They are the target of approved and in-the-pipeline uricosurics. Any drug that increases renal excretion of uric acid, independently of the mechanism through which it exerts its effect, may be considered a uricosuric drug. This review discusses drugs that increase renal excretion of uric acid, either approved or in development, as well as off-label drugs with uricosuric properties.</div></div>","PeriodicalId":54902,"journal":{"name":"Joint Bone Spine","volume":"92 2","pages":"Article 105826"},"PeriodicalIF":3.8000,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Optimizing gout treatment: A comprehensive review of current and emerging uricosurics\",\"authors\":\"Dan Kaufmann , Nathorn Chaiyakunapruk , Naomi Schlesinger\",\"doi\":\"10.1016/j.jbspin.2024.105826\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Gout is the most common inflammatory arthritis, affecting approximately 5.1% of adults in the United States (US) population. Gout is a metabolic and autoinflammatory disease. Elevated uric acid pools lead to the precipitation of monosodium urate (MSU) crystals in and around joints, as well as other tissues, and the subsequent autoinflammatory response. Since elevated serum urate (SU) levels (hyperuricemia) correspond with gout severity, urate-lowering therapies (ULTs) are the cornerstone of gout treatment. ULTs include xanthine oxidoreductase inhibitors, uricosurics, less commonly used in the US but widely used in Europe and Asia, including benzbromarone, dotinurad, and probenecid (the only US Food and Drug Administration (FDA) approved uricosuric in the US), and uricases, including rasburicase and pegloticase (available only in the US). Over 90% of the daily load of uric acid filtered by the kidneys is reabsorbed through renal transporters. These urate transporters include uric acid transporter 1 (URAT1), glucose transporter 9, and organic anion transporters 1, 3, and 4 (OAT1, OAT3, OAT4). They are the target of approved and in-the-pipeline uricosurics. Any drug that increases renal excretion of uric acid, independently of the mechanism through which it exerts its effect, may be considered a uricosuric drug. This review discusses drugs that increase renal excretion of uric acid, either approved or in development, as well as off-label drugs with uricosuric properties.</div></div>\",\"PeriodicalId\":54902,\"journal\":{\"name\":\"Joint Bone Spine\",\"volume\":\"92 2\",\"pages\":\"Article 105826\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2024-11-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Joint Bone Spine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1297319X24001374\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"RHEUMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Joint Bone Spine","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1297319X24001374","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
Optimizing gout treatment: A comprehensive review of current and emerging uricosurics
Gout is the most common inflammatory arthritis, affecting approximately 5.1% of adults in the United States (US) population. Gout is a metabolic and autoinflammatory disease. Elevated uric acid pools lead to the precipitation of monosodium urate (MSU) crystals in and around joints, as well as other tissues, and the subsequent autoinflammatory response. Since elevated serum urate (SU) levels (hyperuricemia) correspond with gout severity, urate-lowering therapies (ULTs) are the cornerstone of gout treatment. ULTs include xanthine oxidoreductase inhibitors, uricosurics, less commonly used in the US but widely used in Europe and Asia, including benzbromarone, dotinurad, and probenecid (the only US Food and Drug Administration (FDA) approved uricosuric in the US), and uricases, including rasburicase and pegloticase (available only in the US). Over 90% of the daily load of uric acid filtered by the kidneys is reabsorbed through renal transporters. These urate transporters include uric acid transporter 1 (URAT1), glucose transporter 9, and organic anion transporters 1, 3, and 4 (OAT1, OAT3, OAT4). They are the target of approved and in-the-pipeline uricosurics. Any drug that increases renal excretion of uric acid, independently of the mechanism through which it exerts its effect, may be considered a uricosuric drug. This review discusses drugs that increase renal excretion of uric acid, either approved or in development, as well as off-label drugs with uricosuric properties.
期刊介绍:
Bimonthly e-only international journal, Joint Bone Spine publishes in English original research articles and all the latest advances that deal with disorders affecting the joints, bones, and spine and, more generally, the entire field of rheumatology.
All submitted manuscripts to the journal are subjected to rigorous peer review by international experts: under no circumstances does the journal guarantee publication before the editorial board makes its final decision. (Surgical techniques and work focusing specifically on orthopedic surgery are not within the scope of the journal.)Joint Bone Spine is indexed in the main international databases and is accessible worldwide through the ScienceDirect and ClinicalKey platforms.