Altered neuroendocrine control and association to clinical symptoms in adolescent CFS

[Kati]

http://translational-medicine.biomedcentral.com/articles/10.1186/s12967-016-0873-1
Open access, from Norway

Altered neuroendocrine control and association to clinical symptoms in adolescent chronic fatigue syndrome: a cross-sectional study

• Vegard Bruun Wyller, Valieria Vitelli, Dag Sulheim, Even Fagermoen, Anette Winger, Kristin Godang and Jens Bollerslev

Journal of Translational Medicine201614:121
DOI: 10.1186/s12967-016-0873-1

© Wyller et al. 2016

Received: 3 December 2015
Accepted: 20 April 2016
Published: 5 May 2016

Abstract

Background
Chronic fatigue syndrome (CFS) is a common and disabling disorder, and a major threat against adolescent health. The pathophysiology is unknown, but alteration of neuroendocrine control systems might be a central element, resulting in attenuation of the hypothalamus–pituitary–adrenalin (HPA) axis and enhancement of the sympathetic/adrenal medulla (SAM) system. This study explored differences in neuroendocrine control mechanisms between adolescent CFS patients and healthy controls, and whether characteristics of the control mechanisms are associated with important clinical variables within the CFS group.

Methods
CFS patients 12–18 years of age were recruited nation-wide to a single referral center as part of the NorCAPITAL project. A broad case definition of CFS was applied. A comparable group of healthy controls were recruited from local schools. A total of nine hormones were assayed and subjected to network analyses using the ARACNE algorithm. Symptoms were charted by a questionnaire, and daily physical activity was recorded by an accelerometer.

Results
A total of 120 CFS patients and 68 healthy controls were included. CFS patients had significantly higher levels of plasma norepinephrine, plasma epinephrine and plasma FT4, and significantly lower levels of urine cortisol/creatinine ratio. Subgrouping according to other case definitions as well as adjusting for confounding factors did not alter the results. Multivariate linear regression models as well as network analyses revealed different interrelations between hormones of the HPA axis, the SAM system, and the thyroid system in CFS patients and healthy controls. Also, single hormone degree centrality was associated with clinical markers within the CFS group.

Conclusion
This study reveals different interrelation between hormones of the HPA axis, the SAM system, and the thyroid system in CFS patients and healthy controls, and an association between hormone control characteristics and important clinical variables in the CFS group. These results add to the growing insight of CFS disease mechanisms.

Trial registration Clinical Trials NCT01040429

 

[Kati]

Quotes from the paper:

After completion of baseline assessment, the CFS patients were subjected to a randomized controlled trial of low-dose clonidine featuring follow-up controls at week 8 and week 30 [10]; this paper, however, report baseline result only

Clonidine (trade names Catapres, Kapvay, Nexiclon, Clophelin, and others) is a medication used to treat high blood pressure, attention deficit hyperactivity disorder, anxiety disorders, withdrawal (from either alcohol, opioids, or smoking), migraine, menopausal flushing, diarrhea, and certain pain conditions.[4] It is classified as a centrally acting α2adrenergic agonistand imidazoline receptor agonist that has been in clinical use for over 40 years.[5]

 

[JaimeS]

Quotes from the paper:



Clonidine (trade names Catapres, Kapvay, Nexiclon, Clophelin, and others) is a medication used to treat high blood pressure, attention deficit hyperactivity disorder, anxiety disorders, withdrawal (from either alcohol, opioids, or smoking), migraine, menopausal flushing, diarrhea, and certain pain conditions.[4] It is classified as a centrally acting α2adrenergic agonistand imidazoline receptor agonist that has been in clinical use for over 40 years.[5]

This may be referring to their other paper that showed that, despite the fact that norepi and epi are elevated in adolescents with CFS, clonidine made them more fatigued, as measured by a significantly decreased number of steps per day. That is, the epi and norepi are compensatory measures the body uses to try and replace...

...something.

-J

 

[M Paine]

I wonder how much microglial activation, and CNS inflammation in general terms may be the source of HPA dysfunction... as interesting as it is to see that there is HPA and endocrine related pathology, I get the feeling that an endocrine disorder is not suspected by most to be at the heart of this issue. Would be interested to know more, my understanding is that there is little evidence that this is an endocrine disorder . Although I don't mean to diminish this as unimportant. I'm sure that putting the breaks on the Endocrine related symptoms would improve the lives of many.

 

[JaimeS]

I wonder how much microglial activation, and CNS inflammation in general terms may be the source of HPA dysfunction... as interesting as it is to see that there is HPA and endocrine related pathology, I get the feeling that an endocrine disorder is not suspected by most to be at the heart of this issue. Would be interested to know more, my understanding is that there is little evidence that this is an endocrine disorder . Although I don't mean to diminish this as unimportant. I'm sure that putting the breaks on the Endocrine related symptoms would improve the lives of many.

I think endocrine issues are actually a pretty big deal in ME/CFS, but I agree that isn't the widespread notion. I got some pretty sophisticated testing because the endocrine system was the first potential culprit in profound fatigue without a noticeable infectious onset. They uncovered some weird pathology my endo had trouble even explaining.

But to be fair, my epi and norepi pee levels were normal.

-J