Discussion in 'Latest ME/CFS Research' started by Daffodil, Jul 5, 2011.
Thanks daffodil - hope someone can sum it up for us not up to reading it
I'm really a total layman, but i can give it a try
It's about a substance called alpha-1-antitrypsin. It seems they want to protect a method or methods of how to produce a drug using that substance (alpha-1-antitrypsin) and how to treat ME/CFS with that drug.
A bit further down they say about alpha-1-antitrypsin
Here they say what they think AAT can do
I wonder why we haven't heard more about it if it worked so well. There are so many people with ME/CFS in Barcelona, i'm sure there would be enough people willing to try it.
Also read what Dr. Enlander said at the bottom of the page.
Thank you eric. So we'll have to wait for proper trials of this drug, looks interesting , but Fukuda criteria and only 1 patient ??
Im not sure how they will patent this, it is already in use as a therapy to treat lung disease caused by alpha-1-antitrypsin deficiency which can cause emphysema and other lung disorders (it is a genetic defect whereby the person does not produce enough alpha 1 antytrypsin to stop lung inflammation) so far it has not been linked with any other inflammatory disorders.
I was tested for this because i have a chronic lung problem, my results came back on the border of normal and low, dont know what that means. and despite continuing lung issues i have not been offered it as a therapy.
Daffodil, thanks for posting this thread. I have been interested in A1AT deficiency since I found out I have one defective gene (type MZ). A1AT cleaves elastase. My elastase results from VIPdx were over 2000. Elastase cleaves RNaseL. I also express the LMW RNaseL. Although the gene is not the cause of our illness, it is probably worse in those with A1AD.
@ Justy, check out the alpha-1 foundation website for free, confidential A1AT phenotyping from the ACT program at MUSC.
Does anyone think it would be helpful to put up a survey?
Dr. Blanco has done a number of A1AT studies and a few regarding fibromyalgia; a quick pubmed search will bring them up.
Am I reading that wrong? In the results listed, the single patient in this unblinded, uncontrolled study showed an improvement in her maximum work output on one test. No significant improvement in oxygen consumption, no improvement in maximum heart rate, no improvement in cognitive function. That she returned to work is great. The rest I don't know if it is an assumption on the part of the writer or quantifiable: "clear clinical improvement, ..., experienced less fatigue and exhibited improved tolerance of physical exercise and slightly reduced cognitive dysfunction." In any case, there are lots of things that have helped one person, or several people, some of which are absurd and have no scientific justification. Without more studies, I don't see what's so exciting about this. I certainly don't think this statement is supported: "It is therefore demonstrated that by means of the present invention, patients [note plural] with CFS can be effectively treated with drugs prepared on the basis of AAT". It showed that one person got better after a rather dramatic, exciting intervention (it's new, gots lots of science behind it, it's IV, done with lots of hard tests...). Unless I'm missing something.
You can also try a Google Site Search
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