Friday, December 22, 2017

The Use of CMV-IVIG in Chronic Fatigue Syndrome

Two failed trials for intravenous immunoglobulins exist within the compendium of CFS history, at separate dosage intervals. Sporadic accounts of improvements with higher dosing regimens and frequency are available, as one of the criticisms was the dosing was too low. In practicality, since no insurance company will cover this without co-morbidity, the treatment then costs tens of thousands in the United States.

Evidence suggests that CFS patients have a 70% infectious onset, assume half of those conservatively are EBV-mediated (influenza, parvovirus, rhinovirus, mycoplasma, HIV, lyme as clinically experienced remainders), with an additional 5% (conservative) CMV-mediated.

An alternative to these ambiguous and un-targeted enhancement of the B-cell milieu would be a pilot trial of CytoGam. This drug is not really used in transplants frequently because from a pharmacoeconomic standpoint, it is more efficient to simply use higher amounts of immunoglobulins. Under the current conceptual framework of CFS, this extra IgG is not helpful and may be deleterious, common wisdom (if it is correct) dictates CFS is an issue of defective T-cell and NK cell subset dysregulation.

Loebel et al. 2014 says that both T- and B-cell subsets are defective in chronic fatigue syndrome, and they did not even isolate post-viral onset categories.

I still think Autologous t-cell transplantation is a better modality, but perhaps this one is more palatable in the current climate. 

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