title: CaseBook challenges: Managing gout, hyperuricemia and comorbidities -- dialogue with the experts.
abstract: The prevalence of gout and hyperuricemia are on the rise in the United States corresponding with an increase in risk factors for these conditions, such as obesity, metabolic syndrome, and the use of diuretics. A progressive disorder, untreated gout can be debilitating and result in tophi, chronic arthropathy, and recurrent kidney stones. Although joint aspiration is needed for a definitive diagnosis, the majority of patients are diagnosed presumptively based on medical history and presentation with characteristic signs and symptoms. Patients with gout also often have multiple comorbidities, and there is an increasing body of evidence that shows hyperuricemia is associated with incidence hypertension, diabetes, chronic kidney disease, and heart failure. Clinical strategies for the management of gout and hyperuricemia must include considerations for these and other common cardiometabolic and renal conditions. In addition to acute flare therapy and prophylaxis, the treatment of gout involves lowering serum uric acid (SUA) levels with the urate-lowering therapies (ULTs) allopurinol or febuxostat. Once begun, treatment with ULT is lifelong. However, inadequate dosing and patient nonadherence or intolerance to therapy often lead to treatment failure. Recent guidelines from the American College of Rheumatology stress tailoring therapy and target SUA level (traditionally <6 mg/dL, but lower levels may be needed for certain patients) based on gout severity and the presence of comorbid conditions. Because painful acute gout flares may result in trips to the emergency department and because the majority of gout cases are managed in primary care, it is important for clinicians practicing in these settings to be able to diagnose and treat this condition and communicate with patients to improve their understanding of the disease process and adherence to treatment.
authors.affiliation: ASH Comprehensive Hypertension Center, The University of Chicago Medicine, Chicago, IL. Electronic address: gbakris@gmail.com.
authors.forename: George L
authors.initials: GL
authors.lastname: Bakris
authors.affiliation: Collegeville Family Practice, Ursinus College, Collegeville, PA. Electronic address: pdoghramji@comcast.net.
authors.forename: Paul P
authors.initials: PP
authors.lastname: Doghramji
authors.affiliation: Division of Rheumatology and Immunology, Duke University School of Medicine, Durham, NC. Electronic address: robert.keenan@duke.edu.
authors.forename: Robert T
authors.initials: RT
authors.lastname: Keenan
authors.affiliation: New York Methodist Hospital, Weill Medical College of Cornell University, New York, NY. Electronic address: sts9005@nyp.org.
authors.forename: Steven H
authors.initials: SH
authors.lastname: Silber
mesh_terms: D000493:Allopurinol / Q000627:therapeutic use; D015897:Comorbidity; D019468:Disease Management; D004334:Drug Administration Schedule; D000069465:Febuxostat; D006073:Gout / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology / Q000628:therapy; D006074:Gout Suppressants / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D033461:Hyperuricemia / Q000097:blood / Q000453:epidemiology / Q000628:therapy; D055118:Medication Adherence; D011320:Primary Health Care / Q000592:standards; D012307:Risk Factors; D012720:Severity of Illness Index; D013844:Thiazoles / Q000627:therapeutic use; D014481:United States / Q000453:epidemiology; D014527:Uric Acid / Q000097:blood*
chemical_list: D006074:Gout Suppressants; D013844:Thiazoles; D000069465:Febuxostat; D014527:Uric Acid; D000493:Allopurinol