Effects of colchicine on risk of cardiovascular events among patients with gout: as evidence accrues, is it time for a randomised trial?
This is a commentary on a multivariate analysis I posted on 8 Dec '15, which showed a link between colchicine usage in gout and halving of cardiovascular risk (hazard ratio 0.51).
The only way to prove this relationship is to conduct a randomised clinical trial.
It can be done, since withholding colchicine in gout prophylaxis is not unethica...l. However, no pharma will bankroll the trial since colchicine is long off patent (but it can commercially viable in USA: consider the case of Colcrys).
It should be done, since the ability (if proven) of a relatively safe and cheap medication to halve cardiovascular risk is very clinically relevant.
Till then, gout patients may be better off staying on colchicine prophylaxis (if well tolerated) than off it.
There are clues that uric acid may not be all that bad and useless:
1) humans lack uricase to break it down;
2) our kidneys actively reabsorb the uric acid filtered through;
3) it is a powerful antioxidant.
Perhaps its release and concentration at sites of massive cell death and Inflammation is to mop up collateral oxidative damage....
This article drawing a link between Gout and lower Alzheimer risk makes for an interesting read, as are other articles drawing similar protective links to Dementia and Parkinson's disease. Like the previous post, such links are derived from multivariate analysis of epidemiological data, which I roundly derided yesterday. But today's posts demonstrate 2 good things that can follow on: the first is to engender proper randomised controlled clinical trials to either prove or disprove the link; the second to engender rational postulates to explain the observed link, possibly leading to further investigational experiments.
This is a great educational app on Gout. I would like to highlight 3 points:
1) Only a third of our daily uric acid production is externally derived (ie food), so don't fret so much about what foods may be causing your Gout. Just keep well hydrated, take your medicines, and enjoy life (in moderation);
2) Gout, like other inflammatory diseases, should be treated to target, to prevent joint & kidney damage, and to reduce cardiovascular risk. The target is <6mg/dL, and <5.5mg/dL if tophaceous;
3) 85-90% of Gout patients are under-excretors rather than over-producers of uric acid, so a uricosuric agent is more likely to work better. It is also safer than Allopurinol, which carries a small but potentially fatal risk of hypersensitivity reaction.