Wednesday, November 2, 2011

University of Hawaii: theoretical justification for using Rituximab in ME and CFS

DrSpeedy replied to jvandermeer on 02 Nov 2011 at 12:59 GMT:
Most of the issues raised by Van der Meer and colleagues have been kindly addressed by Prof Jonathan Edwards and Prof Olav Mella.

There is however one thing I would like to add.

Van der Meer and colleagues start off by saying that "The finding of Fluge et al [1] that B lymphocyte depletion the anti-CD20 monoclonal antibody, Rituximab (RTX) has beneficial effects in patients with chronic fatigue syndrome is astonishing, particularly since they do not present any theoretical justification for using RTX."

As we all know, many discoveries in medicine are actually made by accident. We are treating one problem, and by accident, find out that the treatment works for something else. A famous example is the discovery that Viagra didn't work very well for hypertension but works really well for erectile dysfunction. As Prof Mella has described, they were treating a patient with lymphoma with Rituximab and then discovered that it works very well for chronic fatigue syndrome or Myalgic Encephalomyelitis as well. With these sort of accidental findings, the theoretical justification can only be sought afterwards obviously.

People who are familiar with ME or CFS as some want to call it, know that there are almost 5000 research papers showing all sorts of physical abnormalities in this very disabling disease. Most of these abnormalities centre around the mitochondria, immune dysfunction and ongoing viral infections.

A recent study by Yabusaki and colleagues from the University of Hawaii showed that 95% of ME/CFS Patients have Anticardiolipin Antibodies, suggesting that ME/CFS may be an autoimmune condition. And they continued by giving the following theoretical justification for using Rituximab in ME/CFS:

"As a possible autoimmune disease, CFS patients may be treated by suppression of the ACA or by diminishing the antigen CL in serum. Previous studies have shown that treatment with monoclonal antibodies to B cells reduces ACA levels to normal in patients with autoimmune disease, leading to clinical improvements.

Specifically, Rituximab, a chimeric monoclonal CD20 antibody, has been shown to normalize high ACA serum titers of patients with autoimmune systemic lupus erythematosus, rheumatoid arthritis, autoimmune thrombocytopenia, and autoimmune hemolytic anemia.
Rituximab may serve as an effective therapeutic agent for ameliorating the symptoms of CFS." (1).

(1) Y. Hokama, C. Empey Campora, C. Hara, T. Kuribayashi,
D. Le Huynh, and K. Yabusaki, Anticardiolipin Antibodies in the Sera of Patients with Diagnosed
Chronic Fatigue Syndrome, Journal of Clinical Laboratory Analysis 23 : 210–212 (2009)

Competing interests declared: I am a Family Physician or GP as it is called in Australia or the UK. I am also an ME patient unfortunately. Bedbound that is. So at the moment I’m in private practice so to speak.

I have the following conflict of interest: I would like to get better and see that the wasting of public money on CBT (talk therapy for a neurological disease, really helpful) and other silly therapies for ME stops, and will be used in better ways.


~SerendipityCat~ said...

Go Speedy!!! <3

CJD said...

I so much appreciate your blog. It's helpful to have someone put all the medical mumbo-jumbo into plain English. And, because you have ME, you can totally understand the patient's view, not just an MD view....Prayers & Blessings.

Anonymous said...

thank you for putting this together for us
hope they clarify the research subjects carefully so we know whether it applies to ME, or just to CFS.

Ohdeudeu said...

Anyone can tell me why in this study only 7% of ME/CFS patients have Anticardiolipin Antibodies (IGm) ?

Ohdeudeu said...

The correct link:

Ohdeudeu said...

Sorry I need to headhache the URL:

Anonymous said...

This work was funded for years by the National CFIDS Foundation. Big thanks to them!


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