Commonly misconstrued as nerve pain from the physical presence of sharp crystals in the joints, gout pain is actually caused by the immune system reacting with crystals, similar to the way it attacks a virus such as flu.
Much recent gout research has been concerned with understanding how this pain mechanism works.
Though the ultimate gout cure relies on stopping uric acid excess in the first place, better pain relief can at least cure the pain until uric acid crystals can be dissolved.
In fact, inflammatory processes are at the heart of many diseases, and so advances in one area of arthritis research can often help gout sufferers.
This is certainly the case in a new drug called canakinumab, code named ACZ885.
In your body, a protein called IL-1 (Interleukin-1) plays an important part in inflammation, and how we feel pain from the inflammatory process. Drugs that block this reaction go a long way to relieving pain in rheumatoid arthritis and related inflammatory diseases.
ACZ885 was found to inhibit IL-1ß mediated joint inflammation in preclinical models. It was well tolerated in this firstproof-of-concept study in RA patients...Further studies are warranted to confirm these initial results, [and] to identify those patients who will profit most from blocking IL-1ß
Since we know that this inflammatory process is what ultimately causes most gout pain, it makes sense to investigate the role of canakinumab in gout.
There are now several trials of this drug for gout sufferers. See the gout cure forum for announcements of new trials.
Canakinumab Page Created: 10th February 2009 - Last Reviewed: 10th February 2009