Cortisol biomarker bij ME/CVS?

[marlène]

Een interessant artikel van Prof Pall (voorlopig in het engels)

Chronic Fatigue Syndrome—Where Should We Search for a Specific Biomarker?

Searching for specific biomarkers for specific multisystem illnesses should focus, according to the NO/ONOO- cycle model, on the effects of the impact of that cycle on whatever tissue impact is most characteristic of a particular illness. In the case of MCS, FM and PTSD, the issue of specificity is readily apparent because the most characteristic symptoms or signs of illness are readily apparent. In the case of CFS, they are not. However the recent deliberations on CFS have focussed on the symptom of post-exertional malaise as the most characteristic symptom (21) and it is there that we should focus our search for a specific biomarker, in my view.
Post-exertional malaise is a phenomenon where exercise in CFS patients produces an exacerbation of their entire spectrum of symptoms, an exacerbation that the NO/ONOO- cycle model predicts is likely to be due to up-regulation of NO/ONOO- cycle biochemistry. The view that excessive exercise in CFS may up-regulate the basic causal mechanism is supported by some of the pioneering observations of Dr. Melvin Ramsay. Ramsay observed that CFS sufferers who continued to work longest before collapse had a much poorer prognosis than those who were diagnosed early and underwent prolonged bed rest (22).
How might one use the phenomenon of post-exertional malaise to develop a specific biomarker for MCS? When I discussed this issue with Dr. Paul Cheney, suggesting that this is where we should focus our efforts to develop a specific biomarker for CFS, he told me that his CFS patients show a characteristic difference from normal controls—whereas normal controls show an increase in corticol levels after exercise, his CFS patients do not. The notion that changes in cortisol response may cause post-exertional malaise in an attractive one. Cortisol (and other glucocorticoids) is known to lower the induction of the inducible nitric oxide synthase and may have a substantial role, therefore, in controlling nitric oxide levels. A deficient cortisol response to exercise may lead, therefore, to increased nitric oxide levels after exercise in CFS patients vs. controls, leading, in turn, to up-regulation of the NO/ONOO- cycle.


Others have expressed views similar to those I write here. Torpy (27) described CFS patients with “altered dynamic responses to stress, especially cortisol to stimuli.” Neeck and Crofford reported “abnormalities of central components of the HPA axis” in CFS.
The prediction, then, is that exercise, acting in part or in whole through aberrent cortisol control, will act in CFS patients to up-regulate NO/ONOO- cycle biochemistry in a response that will not be seen in normal controls . Is there any evidence for this? Jammes et al (29) reported large increases in markers of oxidative stress in CFS patients after exercise, whereas only small increases were seen in controls. LaManca et al (30) reported much larger cognitive deficits after exercise in CFS patients compared with controls, consistent with such cognitive deficits being caused by NO/ONOO- cycle biochemistry.
Even the major changes in cardiac function found in CFS patients by Peckerman et al (31,32) and by Cheney (33 and personal communication) may be caused by lowered cortisol levels because cardiac dysfunction in humans and animals can be caused by lowered cortisol levels (reviewed in ref 8, chapter 5).
The notion that dysfunctional cortisol control in response to exercise is behind the phenomenon of post-exertional malaise in CFS should allow one to use exercise control of almost any easily measurable NO/ONOO- cycle element to develop a specific biomarker for CFS. In addition, almost any easily measureable symptom or sign of CFS might also be used. My own prejudice is that we should use markers of nitric oxide production before and after exercise, but no doubt others may have other parameters they may prefer to measure.

...

CFS is chronic because of the action of the NO/ONOO- cycle mechanism. We can explain the generation of both non-specific and specific symptoms and signs of CFS, the latter discussed here and the former in my book (8). We can explain its comorbidity with other multisystem illnesses and of other well-accepted diseases such as migraine and asthma as being due to each of these illnesses having similar causal mechanisms.
We can explain the action of certain agents and entire treatment protocols which appear to be effective in the treatment of CFS, some discussed above and others discussed on my main web page and in my book (8). Indeed it is the great promise of this mechanism as a predictor of therapeutic approaches that is its most important feature for the many who suffer from CFS and related illnesses.
We can explain the stunning variation, both quantitative and qualitative in the symptoms and signs of illness among CFS patients and, indeed, among patients of the whole group of multisystem illnesses.
It has been the many previously unexplained features of CFS and these multisystem illnesses that has led others to argue we needed a new paradigm of human of disease in order to explain them. That is exactly what we have.

References:
1. Pall ML. 2000 Elevated, sustained peroxynitrite levels as the cause of chronic fatigue syndrome. Med Hypoth 54:115-125.

[luxor]

Interessant... dit leunt zeer sterk aan bij de ziekte van Addison... en laat dat nu net iets zijn waar mijn moeder al 25 patient van is...

Hoezo niet erfelijk ... ?

[mamoes]

Even vraagje, mijn engels is namelijk schrikbarend slecht op dit niveau
Gaat dit over cortisolwaarde in bloed of middels een cortisolspeekseltest ?

Bij 3 van onze dochters kwam uit een cortisolspeekseltest namelijk dat dit veel te laag is maar in het bloed is het niet aantoonbaar. Zij zijn extreem moe, concentratiestoornis, geluidsgevoelig, pijn in gewrichten en spieren, enz.
Helaas geen diagnose dus het zijn lichamelijk onbegrepen klachten.
Het zit tussen de oren.
Ik moet zelf altijd goed mijn grenzen stellen en mijn broer is al zo'n 16 jaar ziek.
Waarvan de laatste 5 jaar aan het opknappen via homeopaat naar aanleiding van medicatie op uitslag cortisolspeekseltest.

Addison symptonen, hoezo erfelijk ?

[nijntje]

bij mij waren de bloedwaarden van cortisol ontzettend laag,
ik heb een tijd hydrocortisone geslikt en voelde me daar beter mee.
De laatste maanden is mijn waarde verbetert... uit zichzelf...
en ja, ik voel me ook wat beter.
Of het een biomarker kan worden, weet ik niet (cfr idem resultaten bij addisson), maar ik denk wel dat het een marker is die aanduidt hoe goed/slecht het met je gaat,
wat denken jullie?

[greta]

ik heb niet officieel ME maar wel interstitele cysttis met daarbij behorende zware vermoeidheid (fatique)
mijn cortisolspeekseltest was ook niet goed
Eind van de ochtend en eind van de avond was mn cortisol veel te laag
Die ochtenddip voelde ik erg goed
Nu met LDn is dat stukken minder

in December ga ik de cortisoltest herhalen
ben benieuwd of de lDN daar invloed op heeft