Diacerein is a drug used in the treatment of osteoarthritis. It works by inhibiting interleukin-1. At therapeutically useful concentrations, it counteracts the effects of cytockines on newly secreted proteins, metalloproteinase activity and nitric oxide production. However, nitric oxide blockers alone are inneffective, implicating that a specific gene program is turned on in cytokine-stimulated chondrocytes, and diacerein may prevent metabolic alterations caused by cytokine exposure in chondrocytes.
http://www.cochrane.org/reviews/en/ab005117.html
This study took 2000 people with hip or knee osteoarthritis, and compared their improvements with patients taking placebo's or NSAIDS. Results showed small, consistent benefit in improvement in pain, and benefitted more than placebo or NSAIDS patients.
http://ebm.bmj.com/cgi/content/full/12/3/74 Had a similar study, but their conclusions were that diacerein is comprobably to NSAIDS during treatment of osteoarthritis. However, post-treatment showed diacerein reduced pain more than placebo or NSAIDs and improved function more than NSAIDs
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6 comments:
I haven't been able to find evidence of a mechanism for this compound. How does it inhibit IL-1, if that is what it does? Does anyone have a reference? And is it a drug, or a "nutraceutical"? Thanks.
In paragraph 2 I think you meant osteoarthritis rather than osteoporosis.
All I can find at the moment is that diacerin is an anthraquinone derivative, which inhibits IL-1 beta, and is classified as a symptomatic slow acting drug in OA (SYSADOA).
Moldovan F. et al. Diacerhein and rhein reduce the ICE-induced IL-1beta and IL-18 activation in human osteroarthritic cartilage. Osteroarthritis Cartilage 2000;8:186-96
wouldn't the inhibition of IL-1 be detrimental to the other effects it has as far as benefiting other immunities?
I agree, inhibiting IL-1 for long periods of time could have an impact on the ability to fight off infections. I'm guessing that this is one of those issues where all sides of the therapy need to be looked at closely. A sort of pro v. con thing.
As an aside, there is a newer class of NSAIDs: NO-releasing NSAIDs. I'm assuming that they weren't used in this study (if iNOS was a suspect mediator of disease), but they are currently being developed as a more "mucosal-friendly" alternative, and have somewhat increased anti-tumorigenic activity.
Rigas, B. and Williams, JL. Int. J. Oncol. 2002; 20:5, pp 885-90
Would these then worsen osteoarthritis progression?
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