Tue, 23 Mar 1999

Hi,
In Oktober 1998 I had a conversation with Prof. Dr. Kenny De
Meirleir from the "Vrije Universiteit Brussel". I was there, 
because of the lab. test for the Low Molecular Weight
RNase-L enzym. I am a PWC for 18 years. The outcome of my
test was 4,3. Dr. De Meileir said to me: "The number of the
score don't say anything about the severity of CFS, but it says
more about the duration. When you have this illness for 18
years, I would expect a small peak, but not as high as yours;
this is rather high".

We talked about CFS, RNase-L, Ampligen, etcetera and later
on he said: "The RNase-L interferes with the
protein-metabolism of the cell and this can cause all kinds of
symptoms: fatigue and a bad recuperation are some of them.
We now do understand the immunologic basis mechanism of
CFS. Because of your RNase-L test, it is for sure, that your
illness has a viral origin".

Than I asked him, if this means, that CFS is infectious between
people in normal daily life. Dr. De Meirleir: "I don't think
so. But BLOOD PRODUCTS CAN TRANSMIT IT; WE ARE SURE OF THAT. WE
HAVE A RATHER LARGE NUMBER OF CFS PATIENTS, WHO BECAME ILL
IMMEDIATELY AFTER TRANSFUSION...."

On February 26th last he made this alarming message public.
Below is an abstract, which you can find on Ted Shaw's
excellent web side:

http://www.networx.com.au/mall/cfs/Abstra99.htm

With tulips from Amsterdam,
Jan van Roijen <access@SPEED.A2000.NL>


**************************************************
Sydney February 1999 CFS Conference

Abstract:

BLOOD TRANSFUSION AND CHRONIC FATIQUE SYNDROME

K. De Meirleir, P. De Becker, I. Campine. Human Physiology
and Medicine, Vrije Universiteit Brussel, Brussels, Belgium

We analysed the data of 1210 consecutive patients complaining
of chronic fatigue who visited our fatigue clinic at the Vrije
Universiteit Brussel.

In this group, 752 patients fulfilled the CDC criteria for CFS
(Fuduka, 1994). Of those CFS patients, 34 (4.5%) have a
common factor in their past medical history that immediately
preceded the onset of their CFS. These patients had received a
blood transfusion a few days to a week prior to developing a
'flu-like syndrome that later proved to be the acute onset of
their CFS. Another 8 patients also received a blood
transfusion but their illness only started at least 2 months
later, so that we cannot take these patients into our calculations.

None of these post-transfusion patients developed hepatitis C
or other types of viral hepatitis. Some have antibodies (IgG)
against CMV or EBV, but the development of these antibodies
in time relationship to the blood transfusion could not be
determined. In 9 of 34 patients the LMW RNaseL test was
performed; in all 9 patients the low molecular RnaseL
accounts for the upregulation of the total RNaseL enzyme
activity. This 2-5A synthetase RNaseL pathway is activated in
viral disorders.

THESE FINDINGS POINT TOWARDS A TRANSMITTABLE CAUSE IN THIS
SUBSET OF CFS PATIENTS IN WHICH ACUTE ONSET WAS TEMPORALLY
LINKED TO BLOOD TRANSFUSION. AS VIRUSES AND POSSIBLY OTHER
MICRO-ORGANISMS SEEM TO BE ABLE TO TRIGGER AN ACUTE ONSET
OF CFS AND THE FACT THAT RNASE L DYSFUNCTION SEEMS TO BE
PREFERENTIALLY RELATED TO CFS, IT COMES AS NO REAL SURPRISE
THAT RECEIVERS OF A BLOOD TRANSFUSION, OFTEN BEING IN A
WEAKENED STATUS, CAN DEVELOP CFS.

WE THEREFORE WOULD ADVISE CFS PATIENTS NOT TO BE BLOOD
DONORS AND SECONDLY THAT THE ADMINISTRATION OF BLOOD
TRANSFUSIONS HAS TO BE VERY CAREFULLY CONSIDERED AND ONLY
BE GIVEN WHEN STRICTLY NECESSARY AND NOT AS A STANDARD
PROCEDURE AFTER E.G. THE DELIVERY OF A BABY.