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I had my
12th injection of Amevive last Friday and I was PASI scored to see if
there was any improvement but my score was higher than when I originally
started, indicating my P was more wide spread.
I have been
told that unless there is some improvement in the next 4 weeks (no
treatment) that it would be a waste of time waiting for the next course of
12 injections and, in fact, 5 days since my last injection my skin is
worse than ever. Will probably
have to go back on cyclosporine until the next drug hits Australia.
I must admit
I am very disappointed, I have been following the progress of this drug
via the internet for a few years now and was so hopeful. –Pat O.
Response: I'm sorry, too, Pat.
For whatever it's worth, after my failed 6 months on Enbrel I
returned to reliable cyclosporine and started to see clearance in 10 days!
I've been back on cyclo now for about 5 months and have one active
lesion (on top of the knee that suffers the worst psoriatic arthritis).
I felt so good about being mostly cleared again that I shaved off
my beard and mustache. Some of
my grandkids didn't recognize me.
to start Amevive in January and will probably try it.
There just doesn't seem to be any rhyme or reason behind who
benefits and who doesn't.
doesn’t work for me I’m going to have to do some serious research
about the biologics before I move forward to Raptiva.
These drugs are simply too expensive to be so “ify.”
When you read the pharmaceutical company presentations about their
drugs, the efficacy comes off pretty cut’n’dried.
They work because blah blah blah; or they don’t work because blah
blah. What we remember most is
the “not working because of adverse reactions.”
In other words, it’s not that the drug didn’t work so much as
that it did something else that precluded its continuation.
We don’t hear much about — or quickly forget — the incidences
of “nothing happened, neither bad nor good,” which is close to what
you experienced with Amevive and I’ve experienced with Enbrel.
If, in fact,
the biochemistry at work in these biologics successfully “turns off” a
process that results in the formation of lesions, what is happening when
the lesions don’t go away? Is
there something in us that is inhibiting the action of the biologic?
Is there something about our lesions that doesn’t care whether or
not this particular process is “turned off?”
Until questions like these are answered, we really don’t
understand the disease OR the medicine.
Stay in touch. -Ed