Verslag New Horizons-konferentie 2008


Dr. Rosemund Vallings






Op 6 mei 2008 vond in Cambridge een internationale ME/CVS-konferentie plaats.

De organisatie van de konferentie was in handen van ME Research UK n the Irish ME Trust.


Voor meer informatie over het programma etc. klik hier.


Dr. R. Vallings bezocht namens de Associated New Zealand ME Society (ANZMES) de bijeenkomst en maakte daarvan een verslag: klik op onderstaand logo voor het verslag.






Enkele fragmenten uit het verslag:



prof. Nancy Klimas


She explained how we needed to get away from clinical case definitions towards biomedical subgrouping and described the Canadian definition as more clinical by including autonomic, neuroendocrine and immune dysfunction.


She feels "the most important symptom of all is post-exertional relapse.


In this illness there is an immune cascade leading to chronic immune activation, with a shift from Th1 to Th2 dominance. The immune activation leads to functional defects. The level of severity depends on the pro-inflammatory cytokines.


There are many symptoms of autonomic dysfunction. These occur as a result of parasympathetic dysfunction with sympathetic over activation. Neurally mediated hypotension, orthostatic hypotension, slow gastric emptying, heart rate variability, haemodynamic instability (shown on tilt table), decline in cognitive function after treadmill, abnormal perfusion in cerebellum, reduced perfusion in mid cerebral region, and a drop in blood pressure causing relapse are among the many effects.



dr. Byron Hyde


In another study in 2008, he found that Hepatitis B vaccination led to 22% of cases of ME.



dr. Daniel Peterson


Oxidative impairment is evident in ME/CFS and there is a need to demonstrate this to insurers. Exercise tolerance testing with expired gas exchange is widely recommended, but paired tests are needed as performance is significantly decreased on the second test over a 2-day interval.



dr. Faisel Khan


ME/CFS patients have significantly enhanced vascular responses to acetylcholine (ACh) compared with control subjects. This may be a consequence of free radical attack on acetylcholinesterase expression on the vascular endothelium, giving rise to a reduced expression of the enzyme, resulting in the prolongation of the ACh response.


Arterial stiffness is also significantly elevated in ME/CFS compared to controls, and this is associated with elevation of CRP, pointing to low grade inflammation and oxidative stress.


Isoprostane is a marker for oxidative stress, and in ME/CFS this goes up with exercise intolerance. Oxidative stress can lead to endothelial damage.



prof. Brigitte Evengard


Alpha and beta Estrogen (ERα and ERβ) receptors are implicated in several diseases. There was reduced expression of ERβ in patients consistent with immune mediated pathogenesis in CFS.