Gout: Why Is This Curable Disease So Seldom Cured?
Gout: Why Is This Curable Disease So Seldom Cured?
Gout is the most common inflammatory arthritis and one in which pathogenesis and risk factors are best understood. One of the treatment objectives in current guidelines is 'cure'. However, audits show that only a minority of patients with gout receive adequate advice and treatment. Suboptimal care and outcomes reflect inappropriately negative perceptions of the disease, both in patients and providers. Historically, gout has been portrayed as a benign and even comical condition that is self-inflicted through overeating and alcohol excess. Doctors often focus on managing acute attacks rather than viewing gout as a chronic progressive crystal deposition disease. Urate-lowering treatment is underprescribed and often underdosed. Appropriate education of patients and doctors, catalysed by recent introduction of new urate-lowering treatments after many years with no drug development in the field, may help to overcome these barriers and improve management of this easily diagnosed and curable form of potentially severe arthritis.
Gout is now the most common kind of inflammatory arthritis in men and an increasingly frequent cause of inflammatory joint disease in women, with a prevalence exceeding that of rheumatoid arthritis. Overall, 1–2% of European adults and 3.9% of US adults are affected, but this rises with age to 7% of men over the age of 65 and to 3% of women aged over 85 years. The disease is strongly heritable, with other risk factors including metabolic syndrome (obesity, hypertension, hyperlipidaemia and hyperglycaemia), chronic renal impairment and certain drug treatments, including diuretics.
Of all forms of chronic arthropathy, gout is the one we understand the best. It is a true crystal deposition disease caused by persistent elevation of serum urate (sUA) levels above the saturation point for monosodium urate (MSU) crystal formation (approximately 404 μmol/l). An initial period of asymptomatic hyperuricaemia is associated with silent formation of sodium urate crystals in and around peripheral joints. Eventually, however, this ongoing crystal deposition results in symptomatic clinical problems. Usually, though not exclusively, the first presentation is acute, self-limiting 'attacks' of extremely painful synovitis that result from shedding of crystals into the joint space from the articular cartilage where they form. Importantly, however, subclinical chronic crystal-induced inflammation and the mechanical effects of densely packed crystals ('tophi') on articular cartilage and bone may result in irreversible joint damage and associated symptoms, a condition referred to as 'chronic tophaceous gout'.
In general, a confident diagnosis of typical acute attacks of gout (eg, podagra) is possible from the clinical features alone, although less typical presentations require confirmation of crystal presence in joint or tophus aspirates—the 'gold standard' for definitive diagnosis—or demonstration of the double contour sign on joint ultrasonography. Diagnosis and management in most cases is straightforward and can be undertaken in primary care, although in patients with significant comorbidity, especially renal impairment, or intolerance to allopurinol, secondary specialist referral may be required. Effective treatment strategies to reduce sUA levels sufficiently to prevent further crystal formation and to dissolve existing urate crystals, thus eliminating the causative agent and effectively 'curing' the disease, have been available for many years. In addition to symptomatic treatment of acute attacks and lifestyle modification to address modifiable risk factors, nearly all patients require long-term treatment with urate-lowering treatment (ULT). There is available support from current evidence-based management guidelines to aid diagnosis and to guide clinical decision-making.
Regrettably, however, studies show that only a minority of gout patients receive effective lifestyle advice and ULT, the majority continuing to have recurrent attacks and being at risk of further joint damage and other complications. When questioned about the adequacy of gout management and treatment, patients' and practitioners' responses differ, with practitioners often feeling that management was adequate and patients expressing concerns about ineffective medication and reporting discontinuation of treatment and the need for more information.
Several epidemiological and other studies demonstrate an increase in the severity and prevalence of gout. Although this may be partly attributed to increased longevity and consequent comorbidity (renal impairment, hypertension and treatment with diuretics) and to the continuing increase in prevalence of obesity and metabolic syndrome, there is also evidence that suboptimal management of gout contributes to the problem.
Why, then, despite the possibility of early and accurate diagnosis, the availability of effective treatment and our insight into the severity and consequences of the disease, is gout managed so ineffectively? Perhaps it is time to reappraise our approach to gout in order to identify and address the shortcomings in the way this curable joint disease is managed.
Abstract and Introduction
Abstract
Gout is the most common inflammatory arthritis and one in which pathogenesis and risk factors are best understood. One of the treatment objectives in current guidelines is 'cure'. However, audits show that only a minority of patients with gout receive adequate advice and treatment. Suboptimal care and outcomes reflect inappropriately negative perceptions of the disease, both in patients and providers. Historically, gout has been portrayed as a benign and even comical condition that is self-inflicted through overeating and alcohol excess. Doctors often focus on managing acute attacks rather than viewing gout as a chronic progressive crystal deposition disease. Urate-lowering treatment is underprescribed and often underdosed. Appropriate education of patients and doctors, catalysed by recent introduction of new urate-lowering treatments after many years with no drug development in the field, may help to overcome these barriers and improve management of this easily diagnosed and curable form of potentially severe arthritis.
Introduction
Gout is now the most common kind of inflammatory arthritis in men and an increasingly frequent cause of inflammatory joint disease in women, with a prevalence exceeding that of rheumatoid arthritis. Overall, 1–2% of European adults and 3.9% of US adults are affected, but this rises with age to 7% of men over the age of 65 and to 3% of women aged over 85 years. The disease is strongly heritable, with other risk factors including metabolic syndrome (obesity, hypertension, hyperlipidaemia and hyperglycaemia), chronic renal impairment and certain drug treatments, including diuretics.
Of all forms of chronic arthropathy, gout is the one we understand the best. It is a true crystal deposition disease caused by persistent elevation of serum urate (sUA) levels above the saturation point for monosodium urate (MSU) crystal formation (approximately 404 μmol/l). An initial period of asymptomatic hyperuricaemia is associated with silent formation of sodium urate crystals in and around peripheral joints. Eventually, however, this ongoing crystal deposition results in symptomatic clinical problems. Usually, though not exclusively, the first presentation is acute, self-limiting 'attacks' of extremely painful synovitis that result from shedding of crystals into the joint space from the articular cartilage where they form. Importantly, however, subclinical chronic crystal-induced inflammation and the mechanical effects of densely packed crystals ('tophi') on articular cartilage and bone may result in irreversible joint damage and associated symptoms, a condition referred to as 'chronic tophaceous gout'.
In general, a confident diagnosis of typical acute attacks of gout (eg, podagra) is possible from the clinical features alone, although less typical presentations require confirmation of crystal presence in joint or tophus aspirates—the 'gold standard' for definitive diagnosis—or demonstration of the double contour sign on joint ultrasonography. Diagnosis and management in most cases is straightforward and can be undertaken in primary care, although in patients with significant comorbidity, especially renal impairment, or intolerance to allopurinol, secondary specialist referral may be required. Effective treatment strategies to reduce sUA levels sufficiently to prevent further crystal formation and to dissolve existing urate crystals, thus eliminating the causative agent and effectively 'curing' the disease, have been available for many years. In addition to symptomatic treatment of acute attacks and lifestyle modification to address modifiable risk factors, nearly all patients require long-term treatment with urate-lowering treatment (ULT). There is available support from current evidence-based management guidelines to aid diagnosis and to guide clinical decision-making.
Regrettably, however, studies show that only a minority of gout patients receive effective lifestyle advice and ULT, the majority continuing to have recurrent attacks and being at risk of further joint damage and other complications. When questioned about the adequacy of gout management and treatment, patients' and practitioners' responses differ, with practitioners often feeling that management was adequate and patients expressing concerns about ineffective medication and reporting discontinuation of treatment and the need for more information.
Several epidemiological and other studies demonstrate an increase in the severity and prevalence of gout. Although this may be partly attributed to increased longevity and consequent comorbidity (renal impairment, hypertension and treatment with diuretics) and to the continuing increase in prevalence of obesity and metabolic syndrome, there is also evidence that suboptimal management of gout contributes to the problem.
Why, then, despite the possibility of early and accurate diagnosis, the availability of effective treatment and our insight into the severity and consequences of the disease, is gout managed so ineffectively? Perhaps it is time to reappraise our approach to gout in order to identify and address the shortcomings in the way this curable joint disease is managed.