GoutPal Interactive

Xanthine oxidase reduction by quercetin fascinates me.

Xanthine Oxide Reducing Insect

Can tea, onions, apples and other foods hold the secret for natural gout cures? Lots of scientists are looking, but extracting the active ingredients is hard.

This is really bugging me! But, could bugs be the answer?

Quercetin is a member of the flavonoid group of compounds. These compounds occur naturally in plants, and have been shown to have properties that are beneficial to health.

Quercetin has been studied in several recent investigations to assess it’s ability to inhibit xanthine oxidase (XO). Both allopurinol and febuxostat work by XO inhibition.

Unfortunately, the quercetin studies are largely confined to laboratory experiments with occasional animal tests. Animal tests so far have not shown success, and this appears to be down to solubility of quercetin.

Just as I thought I had finished reviewing relevant research, I spotted a mention of quercetin buried deep in a study of large cabbage white caterpillars. So deep, that I cannot assess if quercetin is actually relevant, but it does not matter – the abstract is fascinating.

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Allopurinol intolerant gout sufferers in the USA moved one step closer to an alternative gout fixer yesterday.

Though this does not bind the FDA to issuing approval for febuxostat, it represents a highly positive outcome and bodes well for a new treatment sometime in the next few months.

In this part of the approval process, evidence is considered by the committee. I’ll present some of the evidence in detail over the next few weeks. To set the scene, here is the summary, from “Briefing Document for Febuxostat” by Takeda Pharmaceuticals North America, Inc.

Summary and Conclusions

Febuxostat is a potent, nonpurine, selective inhibitor of Xanthine Oxidase (XO), which has been shown to be effective in reducing and maintaining serum uric acid (sUA) <6.0 mg/dL at doses of 40 mg and 80 mg. Maintaining these sUA levels is associated with the clinical benefits of tophi resolution and reduction in gout flare.

Febuxostat 40 mg and 80 mg provide an effective treatment option for patients with hyperuricemia and gout. Based on the clinical data, 40 mg and 80 mg are effective doses with 80 mg providing added benefit for patients with more severe disease.

Febuxostat also provides benefit in this patient population with comorbid conditions and has an advantage over allopurinol of not requiring dose adjustment in patients with mild to moderate renal impairment.

Febuxostat doses of 40 mg and 80 mg are well tolerated and have a similar safety profile as the currently marketed allopurinol. The rates of cardio-vascular (CV) events observed in the febuxostat clinical program were low. The potential CV risk was prospectively evaluated in the CONFIRMS Study and no difference in the rate of CV events was observed between febuxostat 80 mg and allopurinol; whereas, with its known risk of AHS, the risk in terms of severe rash is greater with allopurinol.

Febuxostat 40 mg and 80 mg doses are both recommended for approval to allow clinicians individualized dosing options. The 80 mg dose is more effective than 40 mg, especially in subjects with more severe disease as defined by the presence of tophi or higher sUA levels.

Overall, the benefits of febuxostat 40 mg and 80 mg clearly outweigh the risks and support approval of febuxostat for the treatment of hyperuricemia in patients with gout.