RNAse-L en PKR enzyme als een mogelijke verklaring

voor een abnormale reaktie bij inspanning



Chronic fatigue syndrome intracellular immune deregula­tions

as a possible etiology for abnormal exercise response


Jo Nijs, Kenny De Meirleir, Mira Meeus, Neil R. McGregor and Patrick Englebienne

Received 1 October 2003;  Accepted 9 November 2003; Available online 20 February 2004.



The exacerbation of symptoms after exercise differentiates Chronic fatigue syndrome (CFS) from several other fatigue-associated disorders. Research da­ta point to an abnormal response to exercise in patients with CFS compa­red to healthy sedentary controls, and to an increasing amount of evidence poin­ting to severe intracellular immune deregulations in CFS patients. This manu­script explores the hypothetical interactions between these two sepa­ra­tely re­ported observations. First, it is explained that the deregula-tion of the 2-5A synthetase/RNase L pathway may be related to a channelopathy, capable of initiating both intracellular hypomagnesaemia in skeletal muscles and tran­sient hypoglycemia. This might explain muscle weakness and the reduction of maximal oxygen uptake, as typically seen in CFS patients. Second, the activation of the protein kinase R (PKR) enzyme, a characteristic feature in at least subsets of CFS patients, might account for the observed excessive nitric oxide (NO) production in patients with CFS. Elevated NO is known to induce vasodilation, which may limit CFS patients to increase blood flow during exercise, and may even cause and enhanced post-exercise hypotension. Finally, it is explored how several types of infections, frequently identified in CFS patients, fit into these hypothetical pathophysiological interactions.


Opmerking: PKR en RNAse-L worden geproduceerd na blootstelling aan chemicalien of infekties, FT!!