Gout and its comorbidities: implications for therapy

Abstract

Gout is a common form of arthritis. It is associated with a number of comorbidities, including hypertension, cardiovascular disease, renal impairment, diabetes, obesity, hyperlipidaemia and frequently in a combination known as the metabolic syndrome. These comorbidities and their treatment may have an effect on the development of gout and on the choice of therapeutic agent. Treatment of acute gout with short-term corticosteroids may be a safer option than either NSAIDs or colchicine in patients with significant renal and/or cardiac impairment. Sustained reduction of serum urate <0.36 mmol/l is required for long-term management of gout. The optimal dosing regimen for patients with renal impairment is the subject of on-going investigation. There is less experience with newer urate-lowering therapies. This review will consider the relationship between comorbidities and gout with a particular focus on the treatment of gout and the potential interactions between drugs used for gout and those for comorbid conditions.

Gout characteristics associate with depression, but not anxiety, in primary care: Baseline findings from a prospective cohort study

“…Comorbidity is common in people with gout [4] and whilst the association with physical conditions has been widely investigated [5][6][7], research into the potential association between gout and psychological comorbidity (including anxiety and depression) remains limited. In particular there is sparse information on the prevalence of either anxiety or depression in gout patients in primary care, the setting where the majority of gout patients are managed and treated [8].…”

Patient awareness, knowledge and use of colchicine: an exploratory qualitative study in the Counties Manukau region, Auckland, New Zealand

“…8 The combination of colchicine and a statin poses a theoretical increased risk of myopathy and rhabdomyolysis. 18,19 Some participants in this study were taking this drug combination, and although clinicians are expected to regularly monitor creatinine kinase, another NZ study claimed that a quarter of all patients with renal impairment who are at high risk of colchicineinduced myopathy did not actually receive adequate safety monitoring. 37 Other drugs of concern taken by the participants in this study were thiazide diuretics and low dose aspirin, both known to elevate serum urate levels and increase the risk of an acute gouty attack.…”

“…8,33,34 Current co-morbidities affect or limit the choice of therapeutic agents. 18 Several participants reported one or more co-morbidities such as hypertension, cardiovascular disease, diabetes and/or renal impairment, all known risk factors for exacerbating gout and increasing the risk of tophi development. 18,35 Healthcare professionals need to be mindful of medication safety aspects in complex patients.…”

“…14 Unintentional overdoses are most likely attributed to interacting medicines, as reported by study in a US hospital where 46% of colchicine fatalities were attributed to a likely interaction. 15 Interactions occur most often with clarithromycin, [15][16][17][18] and statins [19][20][21] which requires routine creatinine kinase levels to gauge the incidence and severity of these rare complications.…”

Genetic variations in the CLNK gene and ZNF518B gene are associated with gout in case–control sample sets

“…An elevated concentration of SUA, or hyperuricemia (HUA), is a pivotal "danger signal" for gout and may also be a risk factor for a number of comorbidities including cardiovascular disease and mortality, hypertension, diabetes, obesity, hyperlipidemia, and metabolic syndrome [7][8][9]. In addition, elevated SUA levels can result in chronic kidney disease, by triggering chronic interstitial nephritis and the formation of urinary tract stones composed of uric acid [10].…”