Gout can be triggered by a number of gluttonous habits:
Now some people are worse off because they have to take medications that cause hyperuricemia. Amongst them are transplant patients depending on immunosuppressants and diuretics, for example a heart transplant patient whom I recently saw in clinic.
Diuretics:HCTZ is a common trigger of gout attacks but all other diuretics also do. Rising serum uric acid with diuretic use occurs with low doses and increases dose-dependently. Volume depletion stimulates a marked increase in proximal tubular reabsorption of urate. The mechanisms involved in the regulation of urate reabsorption by extracellular volume status are however unclear. Furosemide can induce hyperlacticacidemia sufficient to suppress tubular excretion of urate . Diuretics have also been shown to interfere directly with uric acid handling by the kidney. Loop diuretics and thiazides have been shown to directly inhibit NPT4-mediated urate secretion and furosemide can inhibit urate uptake by URAT1.
Management is aimed at lowering serum uric acid levels with Allopurinol or Febuxostat. Febuxostat is an alternative to allopurinol in patients with allopurinol intolerance or hypersensitivity. In my (limited) experience uricosuric drugs such as Probenecid are rarely used in practice anymore and the teaching is that they actually can trigger acute gout attacks by initially decreasing excretion. Pegloticase, a pegylated recombinant porcine-like uricase, can be given in severe cases when Allopurinol or Febuxostat are not effective. The drug needs to be given IV but thanks to its long half-life only every 2-4 weeks.
Posted by Florian Toegel