The prevalence of gout is increasing, despite good treatment options available. Under diagnosis, late diagnosis, undertreatment and discontinuation of treatment contribute to the rising incidence. These data were presented during an Outcome Science Session at the EULAR Annual Congress 2016 in London.
‘Gout is a disease for which we understand the mechanism, we know how to diagnose it, and we have had good treatment options for at least 50 years’, said Dr. Lennard Jacobsson (University of Gothenburg). ‘However, the prevalence of gout is increasing. In Europe the prevalence is 1.7% to 2.5%; in the U.S. the prevalence is almost 4%. Gout is becoming epidemic.’
Several factors contribute to the rising of the prevalence of gout, Dr. Jacobsson explained. ‘Risk factors such as aging of the population, rising body mass index and growing physical inactivity contribute to a rise in the incidence of gout. In addition, underdiagnosis, late diagnosis, undertreatment and discontinuation of treatment contribute to the rise in prevalence of gout.’ Dr. Jacobsson spurred rheumatologists and other physicians to diagnose and treat cases promptly and better explain the treatment process to their patients.
‘Urate crystals can build up over as much as a decade before a person experiences a first gout attack. It can take 3 to 5 years of effective treatment to get rid of these urate crystal masses. Over that time., especially at the beginning, patients may still have gout attacks. They often misinterpret these attacks as side effects of the medication or treatment failure. If patients are not educated properly about the disease and its treatment, this can easily lead to discontinuation.’
Once considered a disease of the wealthy, gout now is predominantly associated with lower income and low socio-economic class, as is the case for many chronic diseases. In addition, gout is interrelated with several metabolic syndromes such as obesity, hypertension and diabetes. ‘If you have renal disease, you have higher uric acid levels and can more easily get gout. But, the other way round, from high uric aced levels you may get decreased renal function.’
Urate lowering drugs form the heart of the treatment, stressed Dr. Jacobsson. ‘These drug should be described from the first flare’, agreed Dr. Pascal Richette (Hôpital Lariboisière, Paris) in his presentation during a How to Treat/Manage Session. ‘Delaying urate lowering therapy will expose patients to a higher crystal load, difficulties in dissolution and longstanding hyperuricemia which is deleterious for the cardiovascular system and the kidneys. In addition, cessation of hyperuricemia-inducing drugs is recommended as well as diet and more exercise.’
Several drugs can be used to lower urate, e.g. XO-inhibitors (allopurinol, febuxostat), uricosurics (lesinurad, benzbromarone, probenecid) and pegloticase. ‘It’s important to treat to target: 300 – 360 µmol/l’, stressed Richette. ‘And remember: patient education is necessary to obtain compliance!’
ASCO Annual Meeting 2016