Chronic Fatigue Syndrome Support Group
Chronic Fatigue Syndrome (ME/CFS) describes a sense of exhaustion and post-exertion malaise, even when you have gotten enough rest and sleep. The disease is characterized by six months of incapacitating fatigue experienced as profound exhaustion and extremely poor stamina, and problems with concentration and short-term memory. The cause is unknown, but it is a...
This is a new research paper about the researchers accidently finding a possible treatment for at least a subset of CFS.
abstract- http://www.biomedcentral.com/1471-2377/9/28
Full article-
http://www.biomedcentral.com/content/pdf/1471-2377-9-28.pdf
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'Clinical impact of B-cell depletion with the anti-CD20 antibody rituximab in chronic fatigue syndrome: a preliminary case series'
Oystein Fluge and Olav Mella
BMC Neurology 2009, 9:28doi:10.1186/1471-2377-9-28
Published: 1 July 2009
Abstract (provisional)
Background Chronic fatigue syndrome (CFS) is a disease of unknown aetiology. A patient with CFS had unexpected, marked recovery of CFS symptoms lasting for five months during and after cytotoxic chemotherapy for Hodgkin's disease. We reasoned that the transient CFS recovery was related to methotrexate treatment, which induces immunomodulation in part through B-cell depletion.
Methods In a case series, this patient and two additional CFS patients were B-cell depleted by infusion of the monoclonal anti-CD20 antibody rituximab.
Results All three had improvement of all CFS symptoms. Patients 1 and 2 had major amelioration from 6 weeks after intervention, patient 3 slight improvement from the same time, but then improved markedly from 26 weeks after intervention. The symptomatic effect lasted until weeks 16, 18 and 44, respectively. At relapse, all were retreated with a single (patient 1) or double rituximab infusion (patients 2 and 3). Again, all three had marked symptom improvement, mimicking their first response. After new symptom recurrence, patients 1 and 2 were given weekly oral methotrexate, patient 1 having effect also from this agent. Patients 1 and 2 were again treated for a third rituximab infusion after new relapse, again with a marked clinical benefit. No unexpected toxicity was seen.
Conclusion These observations suggest that B-lymphocytes are involved in CFS pathogenesis for a subset of patients. Benefit for all CFS symptoms, the delayed symptom relief following B-cell depletion, the kinetics of relapses, and the effect also from methotrexate treatment, provide suggestive evidence that B-cells play a significant role in the ongoing clinical features, and that CFS may be amenable to therapeutic interventions aimed at modifying B-cell number and function. More systematic investigations of this therapeutic strategy, and of its biological basis, are now needed.
abstract- http://www.biomedcentral.com/1471-2377/9/28
Full article-
http://www.biomedcentral.com/content/pdf/1471-2377-9-28.pdf
*************************
'Clinical impact of B-cell depletion with the anti-CD20 antibody rituximab in chronic fatigue syndrome: a preliminary case series'
Oystein Fluge and Olav Mella
BMC Neurology 2009, 9:28doi:10.1186/1471-2377-9-28
Published: 1 July 2009
Abstract (provisional)
Background Chronic fatigue syndrome (CFS) is a disease of unknown aetiology. A patient with CFS had unexpected, marked recovery of CFS symptoms lasting for five months during and after cytotoxic chemotherapy for Hodgkin's disease. We reasoned that the transient CFS recovery was related to methotrexate treatment, which induces immunomodulation in part through B-cell depletion.
Methods In a case series, this patient and two additional CFS patients were B-cell depleted by infusion of the monoclonal anti-CD20 antibody rituximab.
Results All three had improvement of all CFS symptoms. Patients 1 and 2 had major amelioration from 6 weeks after intervention, patient 3 slight improvement from the same time, but then improved markedly from 26 weeks after intervention. The symptomatic effect lasted until weeks 16, 18 and 44, respectively. At relapse, all were retreated with a single (patient 1) or double rituximab infusion (patients 2 and 3). Again, all three had marked symptom improvement, mimicking their first response. After new symptom recurrence, patients 1 and 2 were given weekly oral methotrexate, patient 1 having effect also from this agent. Patients 1 and 2 were again treated for a third rituximab infusion after new relapse, again with a marked clinical benefit. No unexpected toxicity was seen.
Conclusion These observations suggest that B-lymphocytes are involved in CFS pathogenesis for a subset of patients. Benefit for all CFS symptoms, the delayed symptom relief following B-cell depletion, the kinetics of relapses, and the effect also from methotrexate treatment, provide suggestive evidence that B-cells play a significant role in the ongoing clinical features, and that CFS may be amenable to therapeutic interventions aimed at modifying B-cell number and function. More systematic investigations of this therapeutic strategy, and of its biological basis, are now needed.
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My 6mo twin DD's are EBF and just started rice cereal on the first. Everything has been going fine except this morning one of them had a diaper rash (lots of redness around her anus). I read this as one of the signs of an allergy. BUT I did just buy a different brand diaper yesterday (which they have used randomly before w/no issues). Do you think its the cereal or the diaper? Im ready to start...
From a quick read of wikipedia, here's part of what it says about Rituximab, the drug in question- "The antibody binds to the cluster of differentiation 20 (CD20). CD20 is widely expressed on B cells, from early pre-B cells to later in differentiation, but it is absent on terminally differentiated plasma cells. CD20 does not shed, modulate or internalise. ***Although the function of CD20 is unknown, it may play a role in Ca2+ influx across plasma membranes, maintaining intracellular Ca2+ concentration and allowing activation of B cells***."
http://en.wikipedia.org/wiki/Rituximab
The reason this is interesting is that Calcium ion activity and channelopathies have long been suspected in CFS, with Vernon et al even finding direct evidence of such a channelopathy. From their paper 'Exercise responsive genes measured in peripheral blood of women with Chronic Fatigue Syndrome and matched control subjects'- "Differences in ion transport and ion channel activity were evident at baseline and were exaggerated after exercise, as evidenced by greater numbers of differentially expressed genes in these molecular functions."
http://www.biomedcentral.com/1472-6793/5/5
I don't know much about all this, but I think channelopathies have to do with the intracellular ions that circulate in the body. Sodium, potassium, calcium, magnesium, etc. They all have positive or negative charges, which draw or expel fluids and such into and out of cells through specific gates in the cell membrane. So if you have a channelopathy, that means that one or more of these gates are stuck open or closed, and if that happens, it means that lots of ions go into the cell and lots of fluid follows, which blows up the cell. It's a normal bodily process called apoptosis, or cell death, but if it happens all the time then the person is screwed. And as we all know, our bodies are fairly screwed!
So it seems to fit with what is known about CFS, at least in a subset, as always is the case. And I could be wrong about any of the above, it's just my understanding of it at the moment.