GoutPal Interactive

I have read more than one article correllating high uric acid with high intelligence. It's nice to know that something GOOD goes along with whatever gene it is that makes us handle uric acid improperly.

Hi, its the first time I have used a forum. I am 37, had my first gout attack 3 weeks ago, now its back, doc says my UA is high but gave me  500mg naproxen to be taken twice a day. It is helping, I have cut back on food and beer intake. But what more can I do to help myself.

For example, how long does it take to reduce the UA in the body? Week? Month?

If I do have a wild weekend of wrong food and lots of beer, will this bring on attack, if so, how much time afterwards? I am lost to all this stuff and doctors are not always helpful. Would like some feed back please.

JT

Post edited 12:04 pm – May 16, 2009 by GoutPal

Aviator said:

Interesting article on Uric acid function in the body…

“this molecule may have that property because it communicates that there's been tissue injury and danger, and what happens in gout patients is that they have an exaggeration of what is a normal reaction.”

http://www.urotoday.com/browse…..amage.html

Uric acid is obviously beneficial and necessary.  Is it only we gout sufferers that exhibit an almost 'allergic' reaction to the crystals?  In asymptomatic hyperuricmea, does Uric acid precipitate out of solution into crystals but they aren't attacked by the immune system?  Rather than treating the inflamation with anti-imflammatories and in effect, combating the effects of immune response, might the response itself be moderated through some sort of vaccine, medication or other as yet undiscovered treatment?

Here is more along those lines:

http://ndt.oxfordjournals.org/…..21/11/3046

“In an acute gouty flare, UA crystals incite a tremendous inflammatory response in the synovial space. The UA crystals directly activate fibroblasts and monocytes present in the articular tissues. These cells then elaborate IL-8, a proinflammatory cytokine responsible for attracting neutrophils to the synovial space. From Martinon and colleagues’ exciting article, we now know another mechanism by which UA can stimulate inflammation, the inflammasome. If the inflammasome production of IL-1ß drives the initiation of inflammation in gouty flares, then in the future, we may be able to treat gouty flares with IL-1ß antagonists.”

Great articles, Aviator. Thank you

There are a number of trials taking place at the moment of an IL1 blocker – rilonacept (marketed as Arcalyst). The ones that I found (clinicaltrials.gov) are:

• Study Utilizing Rilonacept in Gout Exacerbations (SURGE) – to determine the efficacy and safety of an experimental drug called rilonacept in subjects with an acute gout attack. Subjects will participate in in this study for 30 days. Rilonacept alone is being compared with indomethacin alone and the combination of rilonacept plus indomethacin in treating acute gout flares.
• PREventative Study Against URate-Lowering Drug-Induced Gout Exacerbations 1 (PRE-SURGE 1) – to determine the safety and effectiveness of an experimental drug called rilonacept in subjects with gout who are beginning allopurinol treatment for gout. Subjects will participate in this study for approximately 22 weeks. Rilonacept is being studied for use in preventing allopurinol-induced gout flares.
• Review of Safety Using Rilonacept in Preventing Gout Exacerbations (RE-SURGE) – to determine the safety and effectiveness of an experimental drug called rilonacept in subjects with gout who are on urate-lowering therapy. Subjects will participate in this study for approximately 20 weeks. Rilonacept is being studied for use in preventing gout flares in subjects on urate-lowering therapy.

Very nice. With a bit of intensive study on that (it's the same study in two different formats for anyone wondering why  we're talking in the singular), I might just begin to understand how the gout immune system response works. Thank you slavekp. Keep 'em coming.