TNF-a inhibitor, Etanercept

[Guest guest]

Has anyone here tried Etanercept, a TNF-a inhibitor?

Marti

http://phoenix-cfs.org/IACFS07II%20BrainGenes.htm

<http://phoenix-cfs.org/IACFS07II%20BrainGenes.htm>

CONFERENCE HIGHLIGHT

Kerr: Gene Session Summary

GENETICS/PROTEOMICS WITH A CFS PERSPECTIVE

All eyes were on Dr. Kerr as he began his summary. Dr. Kerr is engaged

in the largest and most important gene expression study yet done on CFS.

Thus far CFS gene expression studies have, for the most part, failed the

test of replication; while they have had the same general results

(immune, nervous system, mitochondrial genes, etc.) none have

highlighted the same genes to a convincing degree.

Dr. Kerr believes that the failure of most gene expression studies to

rigorously double-check their results has been one cause of this

disturbing heterogeneity. There are surely other reasons as well;

different methodologies used, different sets of genes examined, possibly

inaccurate gene data bases, different kinds of CFS patients taking part,

etc. By examining the entire genome and rigorously double-checking his

results, Dr. Kerr is accounting for many of these. If any gene

expression study will `work', i.e. can be replicated one would

think it would be his.

I was, therefore, kind of holding my breath during Dr. Kerr's

presentation. He stated that his analysis of 100 CFS patients is almost

complete. His gene expression studies are finding three main

abnormalities in CFS patients that involve the immune system,

mitochondrial function and G-protein signaling and, yes, he is

validating his original gene expression results. (What a relief!) He

mentioned three genes, in particular; gelsolin – which is involved

in apoptosis and amyloidosis, another that is upregulated by

organophosphate pesticides, and EIF – a mitochondrial gene involved

in the demyelination of nerves, and may be implicated in viral activity.

He next indicated that while hereditary factors are at work in CFS that

he doesn't believe they play a really major role. He then singled

out the powerful pro-inflammatory cytokine TNF-a, which has not only

been found elevated in CFS patients but has a mutation that is

associated with fatigue. Dr. Kerr is currently engaged in a trial of the

TNF-a inhibitor, Etanercept, in a select number of CFS patients.

Dr. Kerr then noted several intersections between his gene expression

results and other findings. Both that his gene expression and Dr.

Baraniuk's cerebral spinal fluid proteome results have highlighted

gelsolin - a possible marker of amyloidosis. Likewise the Nestad study

suggested that mitochondrial problems caused the increased lactate brain

levels found.