Back to the Dark Ages. Blood letting and doping

Créange A, Lefaucheur JP, Balleyguier MO, Galactéros F. Iron depletion induced by bloodletting and followed by rhEPO administration as a therapeutic strategy in progressive multiple sclerosis: A pilot, open-label study with neurophysiological measurements. Neurophysiol Clin. 201343(5-6):303-12. doi: 10.1016/j.neucli.2013.09.004


OBJECTIVES:To evaluate the concept that iron depletion (ID) induced by bloodletting and followed by recombinant human erythropoietin (rhEPO) administration could be a therapeutic strategy in progressive multiple sclerosis (PMS) and that it could be assessed by neurophysiological measurements.
PATIENTS AND METHODS:In four patients with PMS, bloodletting was performed until ID was induced, and then rhEPO was administered (300UI/kg/week). The changes induced by the treatment were assessed by clinical scores, biological tests, and neurophysiological study of cortical excitability using transcranial magnetic stimulation techniques.
RESULTS:The treatment was well tolerated except for muscle cramps and one popliteal vein thrombosis in a patient confined to chair. ID was obtained within 28 weeks and was associated with endogenous production of EPO. No bloodletting was further required during a six-month period after introduction of rhEPO. At the end of the follow-up (up to one year), fatigue and walking capacities tended to improve in two patients. Neurophysiological changes were characterized by an increased cortical excitability, including a decrease of motor thresholds and an enhancement of intracortical facilitation and cerebellothalamocortical inhibition.
CONCLUSIONS:The combined ID-rhEPO therapy could authorize a prolonged administration of rhEPO in PMS patients, able to modify cortical excitability of the glutamatergic and gabaergic circuits. These preliminary data are encouraging to design a larger, controlled therapeutical trial to assess the value of such a strategy to improve functional symptoms in PMS patients, and maybe to prevent axonal degeneration. Neurophysiological measurements based on cortical excitability studies could provide sensitive parameters to evaluate treatment-induced changes in this context.
It is accepted that there is iron accumulation in MS lesions. Iron is found in haemoglobin in red blood cells and EPO can increase the production of cells, which helps athletes get more oxygen and get better performance. This is why cyclists used it to cheat, e.g Lance Armstrong. This study bled people with MS and then gave them EPO. Erythropoietin, independent of the haematopoietic effects can promote neuroprotective effects. I am afraid n=4 tells us nothing and this is not enough evidence to suggest do nothing.

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