Gout

Key points:

1. Gout is the most common inflammatory arthritis with a prevalence of about 2% in Australasia.
2. Key steps in the development of gout are 1)chronic hyperuricemia 2) monosodium rate monohydrate 3)interaction between the crystals and the inflammatory system, which is primarily responsible for the clinical features. 
3. Definition of hyperuricemia: serum rate level > 0.42
4. Hyperuricemia is caused by medications and genetic predisposition
5. Only 20% of patients with hyperuricemia develop gout 
6. Definite diagnosis can only be achieved via synovial fluid analysis. This needs to be done before recommending hypouricemic drug therapy.
7. Management of acute gout:
   
   8. There is an increase risk of gout when the patient is started on rate lowering therapy. Patients can be started on low dose colchicine 0.5 mg daily or daily NSAID or 5mg prednisolone. Usually prophylaxis is required for around 3-6 months.
   
   
   9. Serum rate target is less than 0.36 mmol/L, however for patients with a large rate crystal load (as reflected by the presence of tophi) erosions or chronic joint deformity due to gout, the target is a serum rate of less than 0.3 mol/L
   
   
   10. Diet and lifestyle modification alone usually is inadequate to lower serum urate level.
   
   
   11. Allopurinal hypersensitivity syndrome occurs with greater frequency in the setting of renal insufficiency, advanced age, HLA B58:01 positivity and higher initial doses but can occur in their absence. The syndrome usually occurs in the first 12 weeks of exposure, and thus the development of rash during this period should prompt immediate cessation of allopurinol, assessment of liver and renal function, and for the possibility of hypersensitivity. 
   
   
   12.Probenecid is another agent which can be used as rate lowering agent. But the patient needs to have renal function > 30-40ml/min. Because of the marked increase in urinary uric acid in the early phase of treatment, good hydration and urinary alkalisation are appropriate.