Why does IVIG work so fast?
AnonymousJuly 6, 2010 at 8:12 pm
I am wondering if anyone has any insights as to why IVIG works so fast (at least, for me).
The first time I had IVIG, I was basically unable to walk, let along climb stairs. After three treatments, I was back on my feet, and able to climb a few stairs without too much difficulty. A similar result happened another time when I let myself get too rundown, and had to be hospitalized again. For the last few months, I have been on a regular schedule of having IVIG every four weeks. I no longer get so rundown, but I still feel an improvement very quickly after the treatments.
Now, my understanding of the mechanism of CIDP is that the immune system attacks and degrades the myelin sheath on the outside of the nerves, so they no longer fire properly. If this is the case, how can the IVIG cause such a quick improvement? Can the myelin really grow back that quickly? Or maybe the damage is really very slight, so it doesn’t take much repair to show an improvement?
I know it won’t really affect my treatment, but I am very curious about how the IVIG actually works.
Thanks for any feedback.
AnonymousJuly 7, 2010 at 7:52 am
I’m not sure even the doctors know how/why IVIg works so well for some people but I can tell you the same thing is true for me on subcutaneous Ig. My sessions are three times a week and last two hours each – after the first hour of the infusion I am already starting to feel better. It makes no sense to me that it would work so fast so I assumed it was psychological until my husband and I started playing the “how long has it been” game. Without knowing how much of my infusion has passed I can predict to within 5 minutes how long it has been just based on how much better I feel. After my infusion I start to get a few side effects but my legs are no longer shaking, I can grip things again and all those things that slowed down before the infusion (digestion, kidney’s etc) pick up speed and return to normal within a couple of hours.
My GUESS is that it’s the inflammation of the nerves that interferes with the function as much as it is the actual damage so introducing replacement Igs would tell your body to stop sending your Igs to attack and thus reduce the inflammation at, on, or near your nerves. That’s just a guess and Ive never gotten a straight answer from any of my healthcare providers. If anybody wants to rip apart my theory and replace it with a better one please feel free…
AnonymousJuly 7, 2010 at 12:27 pm
I’ve read enough posts on this forum to reckon that almost nobody has the same disease manifestations nor do they have identical response to IVIG.
The JAMA (The Journal of the American Medical Association) which has strict “Conditions of Use” and “Copyright” restrictions has a good article about this dated 2004. They do not allow posting their data to an electronic bulletin board.
“[U]Intravenous Immunoglobulin in Autoimmune Neuromuscular Diseases
[/U] Marinos C. Dalakas, MD JAMA. 2004;291:2367-2375.”
Bring your brain, and a cup of coffee, when you read this article.
I’d like to direct your attention to Figure 1 and the details in the blue boxes. In particular see boxes C, D & E. So, it seems, you might have one, more, or all of these problems.
The article is here: [url]http://jama.ama-assn.org/cgi/content/full/291/19/2367[/url]
p.s. I’m still reading this one….
AnonymousJuly 7, 2010 at 7:13 pm
I have printed out the JAMA paper, and will try to digest it. I think I will probably give a copy to my doctor, too.
I also like Julie’s theory. To me, it makes a lot more sense that inflammation could be reduced quickly, rather than myelin regrow quickly.
If this is the case, it means you should really be treated quickly when you start to experience symptoms (or, in my case, the ever-present symptoms get worse).
AnonymousJuly 7, 2010 at 11:52 pm
I think we tend to forget how important the inflammatory part of our disease really is. When I was first diagnosed, Solumedrol gave me back a great deal of my function, in less than 24 hours. It is highly unlikely that Solumedrol had any significant immunosuppressant effect so quickly, so I have to think that there was a substantial reduction in inflammation.
The “P” in CIDP is usually an abbreviation for “polyneuropathy.” However, it is also, and probably more precisely, an abbreviation for poly(radiculo)neuropathy. Poly(radiculo)neuropathy not only include the peripheral nerves, but also the nerve roots at the spine. My guess is that if the nerve roots are significantly inflamed, there is a large reduction in function, no matter how good the nerves further out are; rather like a kinked hose near the faucet. A good anti-inflammatory, such as a steroid or IVIg, would make a big difference, by unkinking the hose.
As a guess, the balance between inflammation and demyelination, which of course are inter-related, might help explain some of the variation in the disease course.
AnonymousJuly 8, 2010 at 6:20 am
That’s interesting Mark.
The paper mentioned the importance of IVIG during the early inflammatory phase of CIDP and how patients were seeing improvements relatively quickly. In my case treatment was delayed for years, so it fits with me being past the early inflammatory part and having to deal more with demyelination and slow growing nerves.
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