Well, TNF blockade is a completely different drug class than the IgE antibody drugs like Tanox/Xolair:
http://www.nature.com/jidsp/journal/v12/n1/full/5650029a.htmlDifferent mechanism, I mean.
What I find most appalling-- but
highly instructive-- about the story of Embrel is that the drug was brought to market almost entirely EMPIRICALLY.
This is exactly the same kind of design paradigm which is being followed for atopic disorders (including the clinical work into desensitization and suppression of anaphylaxis) via drugs, desensitization protocols, and herbal treatments. Nobody KNOWS
why some of it works... just THAT it seems to.Personally, that's something that makes me very very wary. Because it often comes with a pricetag that you can't see when you sign on-- a pricetag that NOBODY knows at the time, more to the point. Nobody knows enough about the underlying mechanism of how severe atopy happens to start with-- so treatments are tinkering with an engine using a timing light, basically, without knowing what makes the pistons move, or that without lubrication, the entire thing will eventually just seize. (This isn't a perfect analogy, but it's as good as I've got today)
The herbal treatment is the one that looks the most promising (overall) at this point-- but the problem is that nobody has any idea what the mechanism is.
Just like with Embrel when it was first marketed. It worked-- and it seemed to be unlike anything ELSE, mechanistically (which can be tested without knowing HOW it is different, by the way). It worked when nothing else would.
Nobody stopped to consider that maybe the "Yeah, but HOW does it work?" might be important down the line in terms of side-effects. Because it never occurred to anyone on the clinical side that it might matter (much). Clinicians aren't (generally) people that have a good grasp on the underlying biochemistry here. Not that they should, mind you-- they are physicians, not scientists. But the problem is that there is so much pressure to do SOMETHING for patients that there are probably a lot of areas where the clinical trials and treatment protocols are running out ahead of the basic understanding of the system.
I
so wish that treatment design were being driven by better basic science. <sigh> At least with straight up immunotherapy, there is a considerable amount of empirical history so support the understanding of HOW it works.
I also don't judge anyone for wanting to participate-- even if the risks are largely unknown right now-- because I am
extremely sympathetic to how hard MFA/LTFA can be, in terms of quality of life. I'm in that boat with y'all, and I know (bitterly) how high the cost is to a family to live with merely having 'avoidance' as your toolkit. We're living it, too.
Autoimmune disorders are some scary, scary stuff, though-- and that is one grab bag that most people
should think twice about reaching for. Knowing how to turn things ON in that system (via external pressors) isn't the same thing as knowing how to shut them back off again. Researchers
know how to produce an anaphylaxis model in mice. What they do NOT know is how to "undo" that transformation. The same thing is true in a variety of other autoimmune disorders, from RA to MS to TypeI diabetes. Heck,
cancer is ALWAYS on the table when you tinker with things.
Start turning knobs in
that system in the hopes that {improvement in autoimmune disorder} will happen... and you never know what you might end up with alongside that improvement. That would be okay if we understood completely how to UNDO changes that we do, or if it were clearer what down-stream effects each change would make. But that isn't where the science is right now. KWIM? So the benefit to an individual would have to be VERY large to justify the risks-- at least right now. For some people, that is almost certainly true. (R's son clearly benefitted a great deal from his Xolair treatment, and I know one other person who has, as well.) But for someone like Ark's DS1, yeah-- I wouldn't have signed on for it, either.
We refused Embrel for DD's eczema, too. Unknown mechanism meant that for her eczema, no way was the *unknown* risk worth the benefit.