HPE Grunenthal handbook - Page 3

Introduction Understanding gout: Not just acute joint attacks Understanding gout, and consequently managing it, has always been demanding for clinicians but greater knowledge of disease pathogenesis, more sophisticated diagnostic modalities, and an increasing array of therapeutic options is diminishing this challenge Frédéric Lioté MD PhD Professor of Rheumatology, University Paris Diderot; Rheumatology Department, Viggo Petersen Centre, Lariboisière Hospital, Paris, France Gout is one of the most common human joint diseases, 3–10-times more frequent than rheumatoid arthritis. It is one of the few chronic diseases that when properly treated with a hypouricaemic drug, can easily lead to a ‘cure under treatment’. The difficulty lies in the clinical inertia of the attending physician and the patient’s compliance. Most patients are treated on an outpatient basis, but they often come to hospital emergency rooms for gout attacks, which is a great place to get the patient back in control. What is gout? It is a disease of overload of the body with uric acid salts – urates – that form microcrystals in and around joints, or even in the skin or other structures. These microcrystals can lead to very characteristic acute arthritis. Gout is not just acute joint attacks. 1 How are urate microcrystals formed? The main cause is hyperuricaemia, that is, an excess of serum uric acid (sUA) in the blood. The upper value of normal uricaemia in both sexes is 360µmol/l or 6.0mg/dl. Above this level, in about one in ten patients, the excess sUA/hyperuricaemia precipitates as microcrystals. This phenomenon is reversible, which is reassuring for the patient, the doctor and the pharmacist: if the uricaemia is reduced below 6.0mg/dl (300µmol/l), the crystals dissolve. How is hyperuricemia established? It is simple: gout is mainly of genetic origin. 2 The excess uric acid is a result of reduced urinary elimination and enhanced intestinal absorption. Uric acid is filtered through the glomerulus and partially reabsorbed through the renal tubule, before being secreted and eliminated in the urine. Uric acid transporters, such as URAT1 in the renal tubule and ABG2 in the intestine and renal tubule, are involved. They can have abnormal activity and reabsorb too much, for example, for URAT1. The uric acid ‘bathtub’ then overflows and leads to crystallisation of the uric acid. Are there other factors besides the genetic component? Environmental/dietary factors are often involved: high purine foods (meat, seafood, etc), purines from other sources, such as beer with or without alcohol, and excess fructose (for example, from sweetened carbonated drinks). 3 Comorbidities and their treatment reduce uric acid elimination including: chronic kidney failure hospitalpharmacyeurope.com | 2018 | 3