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        New Message Board Archives >> Medications, Treatments, Therapies 2004 >> drap
        
(Message started by: drap on Apr 5^th, 2004, 10:01am)

Title: drap
Post by drap on Apr 5^th, 2004, 10:01am

has anybody heard anything about using vioxx for CH.

drap

Title: Re: drap
Post by pubgirl on Apr 5^th, 2004, 11:01am

Sorry Drap, have never heard of anyone taking it for anything other than menstrual pain or arthritis and can't imagine why any doctor would think a non steroidal anti-inflammatory drug would be one of choice for CH [smiley=huh.gif]

Wendy

Title: Re: drap
Post by Tom on Apr 5^th, 2004, 4:37pm

VIOXX® = rofecoxib = one of the NSAID

The mechanism of action of VIOXX is believed to be due to inhibition of prostaglandin synthesis, via inhibition of cyclooxygenase- 2 (COX- 2).

Another drug from the same chemical group is Celebrex® = celecoxib, sometimes used successfully in the treatment of PPH/CPH as (probably better tolerated) alternative to indomethacin.

Neither rofecoxib nor celecoxib or indomethacin help CH, but it's always worth to give one of them a try, in case it could be PPH or CPH.

Thomas

Title: Re: drap
Post by pubgirl on Apr 6^th, 2004, 2:11am

Thomas

Interesting about the use of prostaglandin inhibitors for PH, especially as quite a few people find indomethacin messes up their insides too badly. I shall log that one in my brain for the future.

I take a prostaglandin inhibitor (mefenamic acid) on a regular basis for a different problem, and I can confirm it certainly does absolutely nothing to help my clusters.

W

Title: Vioxx Curcumin
Post by floridian on Apr 6^th, 2004, 8:41am

At lower doses, vioxx decreases cox-2 but can increase nitric oxide production -- nitric oxide is one of the inflammatory mediators close to the pain in cluster headaches and too much NO is not good. At very high doses, vioxx decreases NO, but toxicity becomes a problem.

Tea flavonoids sponge up nitric oxide. Curcumin (from turmeric) also inhibits cox-2, nitric oxide, phospholipase, lipooxygenase, leukotrienes, thromboxane, prostaglandins, collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1 (MCP-1), interferon-inducible protein, tumor necrosis factor (TNF), and interleukin-12 (IL-12) .

Quote:

J Pharmacol Exp Ther. 2003 Mar;304(3):1153-60.
Opposite effects of rofecoxib on nuclear factor-kappaB and activating protein-1 activation.

Niederberger E, Tegeder I, Schafer C, Seegel M, Grosch S, Geisslinger G.

Pharmazentrum frankfurt, Klinikum der Johann Wolfgang Goethe-Universitat Frankfurt, Frankfurt am Main, Germany. e.niederberger@em.uni-frankfurt.de

Rofecoxib is a selective cyclooxygenase (COX)-2 inhibitor approved for the treatment of pain and inflammation in rheumatoid and osteoarthritis. Daily doses between 12.5 and 50 mg were found to reduce pain and inflammation, however, without a clear dose-effect relationship. Interestingly, rofecoxib treatment is associated with an unexpected incidence of renal adverse events compared with other COX inhibitors. Here, the effects of rofecoxib on the transcription factors nuclear factor-kappaB (NF-kappaB) and activating protein-1 (AP-1) were analyzed to find out whether transcriptional changes might explain the lack of clear dose dependency and the occurrence of renal side effects. In vitro, rofecoxib dose dependently inhibited DNA binding capacity of NF-kappaB at doses of 10 to 100 microM, whereas the binding activity of AP-1 was considerably increased at 100 microM. In vivo, the anti-inflammatory effect of rofecoxib was equal at 1 and 10 mg/kg, whereas 50 mg/kg caused a significant further reduction of a zymosan-induced paw edema. This was associated with a clear decrease of inducible nitric oxide synthase (iNOS) protein expression in the spinal cord at this dose. At 1 and 10 mg/kg, however, iNOS was increased but COX-2 was decreased. Thus, the expression of proinflammatory proteins was similarly inconsistent as transcription factor regulation. In conclusion, the opposite effects of rofecoxib on AP-1 and NF-kappaB may explain the lack of clear dose dependency with rofecoxib in clinical studies or animal experiments. The effects on AP-1 may possibly affect renal sodium transport because certain renal sodium channels are regulated through AP-1. Transcription factor regulation might therefore influence both wanted and unwanted effects of rofecoxib.