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Already the most common cause of inflammatory arthritis, it may be more common than you think😉  We’re all familiar with the typical Gout attack: sudden red hot swelling in and around a joint, peaking within a day, resolving within a week.  That is if there is disturbance of the Gout crystals deposited within a joint or just under the skin.  If the crystals are within tendons, it may well cause constant mechanical pain.

A multi-institutional study led by a Massachusetts General Hospital investigator finds significant racial disparities in the risk that patients being treated for gout will…

Allopurinol is commonly prescribed to treat Gout, but it is known to cause life-threatening Allopurinol Hypersensitivity Syndrome involving Stevens-Johnson Syndrome and liver failure. The risk is much higher among those carrying the HLA-B5801 gene. This gene is more prevalent among Han Chinese.

Allopurinol is also not as effective as the uricosuric agents like Probenecid and Benzbromarone (and soon to be available, Lesinurad) in achieving treatment target of SUA <5mg/dL (300 umol/L) for most patients.  This can be due to:

  1. the overwhelming majority of Gout patients (up to 95%) are underexcretors (either renal over-reabsorbers, or intestinal underexcretors with renal compensatory under-reabsorption);
  2. the fear of adverse reaction, especially in the renally-impaired susceptible patients (Han Chinese, Thai, Japanese), often limits the dose of Allopurinol prescribed.  By starting low and going slow, the dose can be pushed up to 800mg daily to achieve treatment target.

Besides being the most “unsafe” drug in Gout treatment, and despite being far less effective, Allopurinol remains the mainstay of treatment in both family and hospital practice.  It’s time for a mindset (and practice) change.  Perhaps I should embark on an educational roadshow.