Monday, November 16, 2009

More evidence of inflammation in (ME)CFS

Margaret Williams 14th November 2009

http://www.meactionuk.org.uk/More-evidence-of-inflammation-in-


In his presentation in Bergen on 20th November 2009, Professor Peter White's
power point slides state about (ME)CFS that maintaining factors include
illness beliefs, the search for legitimacy, being on benefits, and the
diagnostic label, and that immune or viral measures are NOT involved in the
maintenance of the disorder

( http://www.unifobhelse.no/upload/Bergen%20What%20is%20CFS%202009.pdf ).

White's assertion that immune or viral measures are not involved in the
maintenance of the disorder would seem to be a direct denial of the evidence
of two of the world's leading immunologists who specialise in ME/CFS,
Professors Mary Ann Fletcher and Nancy Klimas, who recently published yet
more confirmatory evidence of immune dysfunction in the maintenance of the
disorder (Journal of Translational Medicine 2009:7:96:
doi:10.1186/1479-5876-7-96). Their peer reviewed article was published
immediately upon acceptance.

Fletcher and Klimas et al are clear that cytokine abnormalities are common
in (ME)CFS and that the cytokine changes observed are more likely to be
indicative of immune activation and inflammation, rather than specific for
(ME)CFS, as people with fibromyalgia, Gulf War Illness, rheumatological
disorders and multiple sclerosis may also have similar cytokine patterns.
...."The elevations in LTa, IL-1a, IL1b and IL-6 indicate inflammation, likely
to be accompanied by autoantibody production, inappropriate fatigue, myalgia
and arthralgia, as well as changes in mood and sleep patterns.

"This study is among the first in the (ME)CFS literature to report the
plasma profiles of a reasonably large panel of cytokines assessed
simultaneously by multiplex technique.

"Cytokine abnormalities appear to be common in (ME)CFS. The changes from the
normal position indicate immune activation and inflammation.

"The results imply a disorganised regulatory pattern of TH1 function,
critical to antiviral defence.

"The results from this study support a TH2 shift, pro-inflammatory cytokine
up-regulation and down-regulation of important mediators of cytotoxic cell
function".

Since it is now unequivocal that people with (ME)CFS show markers of
inflammation, what will be the impact on the Wessely School's MRC PACE Trial
that is predicated on the assumptions of deconditioning, on the "perception"
of effort and on aberrant illness beliefs and whose participants are
instructed about "sleep hygiene"?

No comments: