FWD:RSD World News- cytokine research
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FWD:RSD World News- cytokine research
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From: byrd45 (Original Message) Sent: 8/6/2006 8:40 PM
My Groups | RSD-WorldNews Main Page
Deformation of nerve roots, neuritis (and other immunogenic nervous system challenges), and frank injury to nervous structures can set in motion the production of cytokines (proinflammatory endogenous substances). The interleukins (IL-1beta, IL-6) and tumor necrosis factor (TNF)-alpha are the most common. The cascade of mediators of the inflammatory cycle set in motion by the release of these cytokines forms the basis of what we currently think are the mechanisms of neuropathic pain. As a result, the use of cytokine-directed therapies is an area of active research.
Gordon Irving, MD,[41] gave an interesting presentation on clinical work being done on targeting cytokine inhibitory therapy. Two examples discussed during his presentations were (1) a study in which TNF-alpha inhibitors were applied on porcine cauda equine after irritation from nucleus pulposus in a human trial (N = 10), normalization in nerve conduction velocities was observed[42]; and (2) a study in which a single infusion of infliximab decreased sciatic pain by 49% within an hour, all patients returned to work within 1 month, and none required surgery. In addition, results from a pilot study investigating the treatment of acute, severe sciatica with etanercept showed that better results were observed with etanercept than with intravenous steroids.[43] Thalidomide, which inhibits IL-1beta, TNF-alpha, IL-6, and IL-8 and other cytokines, reduces pain and frequency of pain in interstitial cystitis, as well as pain in CRPS I.
Recommend Delete Message 1 of 1 in Discussion
From: byrd45 (Original Message) Sent: 8/6/2006 8:40 PM
My Groups | RSD-WorldNews Main Page
Deformation of nerve roots, neuritis (and other immunogenic nervous system challenges), and frank injury to nervous structures can set in motion the production of cytokines (proinflammatory endogenous substances). The interleukins (IL-1beta, IL-6) and tumor necrosis factor (TNF)-alpha are the most common. The cascade of mediators of the inflammatory cycle set in motion by the release of these cytokines forms the basis of what we currently think are the mechanisms of neuropathic pain. As a result, the use of cytokine-directed therapies is an area of active research.
Gordon Irving, MD,[41] gave an interesting presentation on clinical work being done on targeting cytokine inhibitory therapy. Two examples discussed during his presentations were (1) a study in which TNF-alpha inhibitors were applied on porcine cauda equine after irritation from nucleus pulposus in a human trial (N = 10), normalization in nerve conduction velocities was observed[42]; and (2) a study in which a single infusion of infliximab decreased sciatic pain by 49% within an hour, all patients returned to work within 1 month, and none required surgery. In addition, results from a pilot study investigating the treatment of acute, severe sciatica with etanercept showed that better results were observed with etanercept than with intravenous steroids.[43] Thalidomide, which inhibits IL-1beta, TNF-alpha, IL-6, and IL-8 and other cytokines, reduces pain and frequency of pain in interstitial cystitis, as well as pain in CRPS I.
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