More Testing that may be Abnormal

Specific correlations between muscle oxidative stress and chronic
fatigue syndrome: a working hypothesis.

Journal: J Muscle Res Cell Motil. 2008 Feb 15 [Epub ahead of print]

Authors: Fulle S, Pietrangelo T, Mancinelli R, Saggini R, Fanò G.

Affiliation: Ce.S.I.Center for Research on Ageing, Università "G.
d'Annunzio", Chieti-Pescara, Italy.

NLM Citation: PMID: 18274865


Chronic fatigue syndrome (CFS) is a relatively common disorder
defined as a status of severe persistent disabling fatigue and
subjective unwellness. While the biological basis of the pathology of
this disease has recently been confirmed, its pathophysiology remains
to be elucidated. Moreover, since the causes of CFS have not been
identified, treatment programs are directed at symptom relief, with
the ultimate goal of the patient regaining some level of pre-existing
function and well-being.

Several studies have examined whether CFS is associated with: (i) a
range of infectious agents and or immune disturbance; (ii) specific
changes of activity in the central or peripheral nervous systems; and
(iii) elevated stress periods, which may be associated with the
pathology via genetic mechanisms. The role of oxidative stress in CFS
is an emerging focus of research due to evidence of its association
with some pathological features of this syndrome.

New data collectively support the presence of specific critical
points in the muscle that are affected by free radicals and in view
of these considerations, the possible role of skeletal muscle
oxidative imbalance in the genesis of CFS is discussed.

 

Intracellular immune dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome: state of the art and therapeutic implications.

Journal: Expert Opin Ther Targets. 2008 Mar;12(3):281-9.

Authors: Nijs J, Frémont M.

Affiliation: Vrije Universiteit Brussel, Faculty of Physical
Education & Physiotherapy, Department of Human Physiology, Building
L, Pleinlaan 2, 1050 Brussels, Belgium. Jo.Nijs@vub.ac.be

NLM Citation: PMID: 18269338


BACKGROUND: Evidence in support of intracellular immune dysfunctions in people with myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) is accumulating, but few studies have addressed
intracellular immunity as a potential therapeutic target.

OBJECTIVE: To provide an overview of our present understanding of
intracellular immunity in ME/CFS, to relate the intracellular immune
dysfunctions to other aspects of the illness like decreased natural
killer cell function, the presence of infections and poor exercise
performance, and to point to potential therapeutic targets.

METHODS: An in-depth review of the scientific literature of
intracellular immunity in people with ME/CFS was performed.

RESULTS/CONCLUSION: From the scientific literature it is concluded
that proteolytic cleavage of the native RNase L enzyme is
characteristic of the dysregulation of intracellular immunity in
people with ME/CFS, but the origin of the dysregulation is
speculative. There is increasing evidence for immune cell apoptosis
and upregulation of various aspects of the 2'-5' oligoadenylate
(2-5A) synthetase/RNase L pathway in ME/CFS. This review provides the
theoretical rationale for conducting studies examining the
effectiveness of direct or indirect drug targeting of the 2-5A
synthetase/RNase L pathway in ME/CFS patients.