In de mei-uitgave van Discover wordt aandacht besteed aan de rol van B-cellen in ME/CVS,
mede naar aanleiding van de rituximab/B cel-depletie-studies van Fluge en Melle (klik hier).
Are B-Cells to Blame for Chronic Fatigue Syndrome?
The ravages of chronic fatigue syndrome may be the result of
an overlooked but essential part of the body's own immune system.
FROM THE MAY 2013 ISSUE
Wednesday, April 03, 2013
Myalgic encephalomyelitis, or chronic fatigue syndrome,
is a perplexing disorder that may seem more like a voodoo hex than an illness.
Patients might lie bedridden in dark rooms, in chronic pain,
often with multiple neurological symptoms like muscle pain, sweating and dizziness.
Doctors have targeted various causes,
from herpes viruses to retroviruses to depression.
But a surprising new explanation suggests that
the disorder is an autoimmune disease of the nervous system
caused by overactive B-cells,
which are normally responsible for churning out pathogen-killing antibodies.
In 2011, two Norwegian oncologists,
Oystein Fluge and Olav Mella of Haukeland University Hospital in Bergen,
along with colleagues, studied 30 people diagnosed with
chronic fatigue immune dysfunction syndrome (CFIDS).
Each received either a placebo or
a highly specialized chemotherapy drug called rituximab,
which rapidly and selectively depletes B-cells.
After 12 months, 10 of 15 patients on the drug significantly improved;
only two of 15 on the placebo improved.
Fluge and Mella, the Norwegian oncologists,
credit Edwards with inspiring their work.
They also think their results suggest that an unknown antibody
- probably an antibody against self, targeting the body’s own healthy tissue -
is triggering chronic fatigue syndrome.
That's because despite rapid B-cell depletion, improvement lagged.
Patients who responded to the treatment
took two to eight months to show a response.
Fluge and Mella are now working on a multicenter study and
monitoring their original patients as they receive booster treatments,
to try and determine optimal treatments for CFIDS.
So far, their results are in line with their previous hypothesis,
though only two-thirds of patients respond to these treatments.
That suggests there might be a second mechanism
that could independently lead to CFIDS.
Met dan aan Manja, die me attendeerde op bovenstaand artikel.