Volgens een studie van Castro en collega's van de Vall d'Hebron CVS-onderzoeksgroep

onderscheiden ME/CVS- en fibromyalgie-patiënten zich van gezonde mensen

op basis van verhoogde oxidatieve stress en verminderde ATP- en Q10-nivo's.

Deze studie bevestigt de bevindingen van Myhill en collega's in ME/CVS (zie hier en hier).

Recent toonde Gerdle met zijn collega's mitochondriale dysfunctie aan in de vierhoofdige dijbeenspieren en een relatie met verminderde spierkracht aan in fibromyalgie (zie hier).

Bij fibromyalgie-patiënten is, maar niet bij ME/CVS-patiënten, is er tevens sprake van

lagere citraatsynthase actviteit, kleinere mitochondriale "omvang" en

verminderde genexpressie van de mitochondrium-gerelateerde genen PGC-1α en TFAM.

Could mitochondrial dysfunction be a differentiating marker

between Chronic Fatigue Syndrome and Fibromyalgia?

Antioxid Redox Signal. 2013 Apr 22. doi:10.1089/ars.2013.5346.

Castro-Marrero J, Cordero MD, Saez-Francas N, Jimenez-Gutiérrez C,

Aguilar-Montilla FJ, Aliste L, Alegre-Martin J.

Abstract

Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

are complex and serious illnesses.

It is estimated to affects

up to 2.5% and 5% of the general population worldwide, respectively.

The aetiology is unknown;

however, recent studies suggest that

mitochondrial dysfunction has been involved in the pathophysiology of both conditions.

We have investigated

the possible association between mitochondrial biogenesis and oxidative stress

in patients with CFS and FM.

We studied 23 CFS patients, 20 FM patients and 15 healthy controls.

Peripheral blood mononuclear cells (PBMC) showed

decreased levels of CoQ10

from CFS patients (p<0.001 compared to controls) and

FM subjects (p<0.001 compared to controls) and

ATP levels

for CFS patients (p<0.001 compared to controls) and

for FM subjects (p<0.001 compared to controls).

On the contrary,

CFS/FM patients had

significantly increased levels of lipid peroxidation,

respectively (p<0.001 for both CFS and FM patients respect to controls)

indicative of oxidative stress-induced damage.

Mitochondrial citrate synthase activity

was significantly lower in FM patients (p<0.001)

and however, in CFS resulted in similar levels than controls.

Mitochondrial DNA content (mtDNA/gDNA ratio)

was normal in CFS and reduced in FM patients

vs. healthy controls, respectively (p<0.001).

Expression levels of PGC-1α and TFAM by immunoblotting showed

significantly lower in FM patients (p<0.001) and

were normal in CFS subjects compared to healthy controls.

These data lead to the hypothesis that

mitochondrial dysfunction-dependent events

could be a marker of differentiation

between CFS and FM

indicating the mitochondria

as a new potential therapeutic target for these conditions.

PMID: 23600892