A to,że zabiegi udrażniania żył pomagają to niezaprzeczalny fakt!Teoretyczna przyczyna SM (MS) - C.C.S.V.I.
Moderator: Beata:)
A propos Stanford, to juz jakis czas temu natknelam sie na ktoryms z anglojezycznych forów, ze byl juz podobny przypadek.
Profesor prowadzacy badania na jednym z amerykanskich uniwersytetow zostal zmuszony do zakonczenia swoich badan. Zakazano mu jednak wypowiadania sie wogole na ten temat, w tym z jakich powodow zaprzestal on swojej dzialalnosci.
Jak znajde jeszcze raz te informacje to podziele sie linkiem.
Moje prywatne odczucie jest takie, iz informacja udzielona przez doktora Jeffrey Dunn, a przytoczona na stronie PTSR jest jakas strasznie subiektywna i pokretna. “Jeśli mogę cokolwiek zrobić aby ochronić pacjentów z SM przed potencjalnie niebezpiecznymi skutkami złudnych nadziei lub ryzykiem inwazyjnego i nieudowodnionego leczenia, to jestem zadowolony jeśli mogę to zrobić”.
Dlaczego sugeruje, ze nadzieje sa zludne i niebezpieczne? Dobrze, ze dodal choc potencjalnie niebezpieczne
A co do ryzyka nieudowodnionego leczenia, to czy stara sie tez chronic pacjentow z SM przed chocby np. mitoksantonem? Przeciez tez jest potencjalnie niebezpieczny a jego skutecznosc jest nieudowodniona. Zwiazane z nim nadzieje tez zatem moznaby uznac za zludne, a zawiedzenie sie tez moze prowadzic w tym przypadku do potencjalnie niebezpiecznych skutkow! Domagam sie zatem zamkniecia BIGFARMY i zakazania jej dalszej niebezpiecznej dla ludzkosci dzialalnosci!
Naczyniowcy wysuneli sie przed szereg i trzeba im bylo utrzec nosa...Czy bezczelna BIGFARMA ma ludzi za debili? Moze chorzy i ich rodziny nie maja takiej sily przebicia jak ONA, ale myslec tez umieja.
Tak wiec niech sobie BIGFARMA wyprawia co chce w Stanach, byleby nie u nas!
Poza tym,
pozdrawiam Was wszystkich.
Profesor prowadzacy badania na jednym z amerykanskich uniwersytetow zostal zmuszony do zakonczenia swoich badan. Zakazano mu jednak wypowiadania sie wogole na ten temat, w tym z jakich powodow zaprzestal on swojej dzialalnosci.
Jak znajde jeszcze raz te informacje to podziele sie linkiem.
Moje prywatne odczucie jest takie, iz informacja udzielona przez doktora Jeffrey Dunn, a przytoczona na stronie PTSR jest jakas strasznie subiektywna i pokretna. “Jeśli mogę cokolwiek zrobić aby ochronić pacjentów z SM przed potencjalnie niebezpiecznymi skutkami złudnych nadziei lub ryzykiem inwazyjnego i nieudowodnionego leczenia, to jestem zadowolony jeśli mogę to zrobić”.
Dlaczego sugeruje, ze nadzieje sa zludne i niebezpieczne? Dobrze, ze dodal choc potencjalnie niebezpieczne
A co do ryzyka nieudowodnionego leczenia, to czy stara sie tez chronic pacjentow z SM przed chocby np. mitoksantonem? Przeciez tez jest potencjalnie niebezpieczny a jego skutecznosc jest nieudowodniona. Zwiazane z nim nadzieje tez zatem moznaby uznac za zludne, a zawiedzenie sie tez moze prowadzic w tym przypadku do potencjalnie niebezpiecznych skutkow! Domagam sie zatem zamkniecia BIGFARMY i zakazania jej dalszej niebezpiecznej dla ludzkosci dzialalnosci!
Naczyniowcy wysuneli sie przed szereg i trzeba im bylo utrzec nosa...Czy bezczelna BIGFARMA ma ludzi za debili? Moze chorzy i ich rodziny nie maja takiej sily przebicia jak ONA, ale myslec tez umieja.
Tak wiec niech sobie BIGFARMA wyprawia co chce w Stanach, byleby nie u nas!
Poza tym,
pozdrawiam Was wszystkich.
Ostatnio zmieniony 2010-03-05, 15:11 przez Stokrotka, łącznie zmieniany 1 raz.
Meil do dr Kosteckiego: kosteckj@op.pl
tu jest bardzo dobra odpowiedź dr Ashton Embry na zarzuty neurologów, że metoda niebezpieczna i nieznana.
Chronic cerebrospinal venous insufficiency (CCSVI) and multiple sclerosis - counter arguments
Chronic cerebrospinal venous insufficiency and multiple sclerosis
Omar Khan, MD 1 *, Massimo Filippi, MD 2, Mark S. Freedman, MD, FRCPC 3, Frederik Barkhof, MD, PhD 4, Paula Dore-Duffy, PhD 1, Hans Lassman, MD 5, Bruce Trapp, PhD 6, Amit Bar-Or, MD, FRCPC 7, Imad Zak, MD 8, Marilyn J. Siegel, MD, FACR 9, Robert Lisak, MD, FRCP 1
1Multiple Sclerosis Center, Department of Neurology, Wayne State University School of Medicine, Detroit
2Neuroimaging Research Unit, Scientific Institute and University Hospital San Raffaele, Milan
3Multiple Sclerosis Research Unit, The Ottawa Hospital General Campus, University of Ottawa, Ottawa
4Department of Radiology and Amsterdam MS Center; VU University Medical Center, Amsterdam
5Centre for Brain Research, Medical University of Vienna, Vienna
6Department of Neurosciences; Lerner Research Institute, Cleveland Clinic, Cleveland
7Montreal Neurological Institute, McGill University, Montreal
8Department of Radiology; Wayne State University School of Medicine, Detroit
9Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis
*Correspondence to Omar Khan, Multiple Sclerosis Center & Image Analysis Laboratory, Department of Neurology, Wayne State University School of Medicine 4201 St Antoine, 8A-UHC, Detroit, Michigan 48323
Ph: (313) 745-4280; Fax: (313) 966-9271
Abstract
A chronic state of impaired venous drainage from the central nervous system, termed as chronic cerebrospinal venous insufficiency (CCSVI), is claimed to be a pathologic phenomenon exclusively seen in multiple sclerosis (MS).
This has invigorated the causal debate of MS and generated immense interest in the patient and scientific communities.
A potential shift in the treatment paradigm of MS involving endovascular balloon angioplasty or venous stent placement has been proposed as well as conducted in small patient series.
In some cases, it may have resulted in serious injury.
In this Point of View, we discuss the recent investigations that led to the description of CCSVI as well as the conceptual and technical shortcomings that challenge the potential relationship of this phenomenon to MS.
The need for conducting carefully designed and rigorously controlled studies to investigate CCVSI has been recognized by the scientific bodies engaged in MS research.
Several scientific endeavors examining the presence of CCSVI in MS are being undertaken.
At present, invasive and potentially dangerous endovascular procedures as a therapy for patients with MS should be discouraged until such studies have been completed, analyzed, and debated in the scientific arena.
Annals Of Neurology © 1999-2010 John Wiley & Sons, Inc.
An Open Letter to the Authors of Chronic Cerebrospinal
Venous Insufficiency and Multiple Sclerosis (Khan et al,
2010, Annals of Neurology)
Ashton Embry, Direct-MS
Background: A week ago a “Point of View” article on Chronic Cerebrospinal
Venous Insufficiency and Multiple Sclerosis was made available online at the
website of Annals of Neurology.
It was written by 11 authors, with both
neurologists and radiologists being represented. Notably 7 of 11 authors
(including the first four, senior authors) disclosed significant financial interests
with pharmaceutical companies which produce drugs for MS (see Appendix).
In their opinion piece, the authors discussed Dr Zamboni’s published work on
CCSVI and concluded it should be considered “preliminary”. To my knowledge
no one has ever considered it to be otherwise. Most of the article consisted of
points and arguments that suggest it is not reasonable to consider CCSVI to be
the main cause of the MS disease process. Such a discussion has some value
although I must point out few are claiming CCSVI is the main driver of MS. Dr
Zamboni has been very clear on this and simply says CCSVI may be a significant
contributor to MS onset and progression. Thus, in their Point of View, the authors
essentially put up a straw man and then spend most of the article taking it apart.
Overall, most of their arguments against CCSVI as the main cause of MS are
readily dismissed once MS is seen as an autoimmune disease often exacerbated
by the presence of CCSVI.
The only truly offensive part of the article was the authors’ attempt to rationalize
their self-serving desire that no one with MS should be tested for CCSVI. They
emphasized the very rare occurrence of a serious adverse event associated with
endovascular treatment and totally neglected to discuss the risks of not being
tested and treated for CCSVI. Such a one-sided rationalization which is nullified
by a blatant conflict of interest of most of the authors cannot be taken seriously.
Below is an open letter to the authors.
Dear Dr Khan and fellow authors,
I recently read your opinion piece on CCSVI which was made available online in
Annals of Neurology (Khan et al, 2010) last week. I see it as part of “MS Wars:
Part II – The Medical Empire Strikes Back”. Overall, I enjoyed reading your article
because I always find it useful to read the arguments of those who hold a
different opinion than me on an important subject. I was also pleased that you
restrained yourselves and did not follow Mark Freedman’s infamous lead and call
Dr Zamboni’s work “a hoax”. The only part of the article I found distasteful was
your advice for persons with MS to not get tested for CCSVI for at least 5-10
years (while further research is being done). I discuss this point in detail later.
For a more up to date and more objective opinion piece on MS and CCSVI, I
direct you to my recent article “CCSVI and Multiple Sclerosis: Integrating New
Data to Help Guide Actions” which can be downloaded at http://tinyurl.com/yf36ege.
This article interprets the relationship between the
CCSVI and MS in light of the recently available results from CCSVI-related
studies at the universities of Buffalo and Georgetown. Given you must have
known this critical information would be available in early 2010, I am surprised
you rushed into print before such crucial data were available. This made your
“Point of View” hopelessly outdated on the day it became available. I can only
surmise you did not want any solid data from the Buffalo and Georgetown studies
to cause problems for your critique.
In my article I also address the question of whether persons with MS should get
tested and treated for CCSVI as soon as possible or should wait 5-10 years until
major clinical trials are completed and analyzed. A reasonable answer to this
question depends on the major new data from the universities of Buffalo and
Georgetown. Your analysis of this same question without the benefit of these
crucial data is sadly premature and poorly supported. As I will discuss later, my
advice on this key question is the opposite of yours and, unlike yours, mine is
supported by the new data and is not hopelessly compromised by unacceptable
and major conflicts of interest.
To me, given the robust results of the University of Buffalo Phase 1 study and the
findings of hundreds of endovascular procedures which have already been done
to relieve CCSVI (almost all have found major blockages in the veins draining the
brain), there can be little doubt that CCSVI is associated with MS. And, as I
argue in my article, because the vascular malformations which constitute CCSVI
are mainly congenital (Georgetown data), there can be little doubt that CCSVI is
an important factor in the MS disease process in many cases (definitely not all
cases). Of course, without this new data, you could not offer any worthwhile
opinions on whether or not CCSVI is part of MS.
Furthermore, any claim that the established, robust association of CCSVI and
MS is purely coincidental cannot be taken seriously although I am sure such an
implausible thought will be offered by some. In my article, I interpret MS as an
autoimmune disease which, in many cases, is exacerbated by the co-occurrence
of CCSVI (in 25% of the healthy population and perhaps up to 60% of persons
with MS according to the University of Buffalo work). I find the “either it’s
autoimmune or it’s CCSVI” polarity which dominates your article to be overly
simplistic. An integration of the two phenomena is the most reasonable model
because both have very strong evidence supporting their involvement in MS. Of
course, the new data were required for such an integrated model to become
obvious.
Another key question which you could not evaluate without the new data is
whether or not CCSVI contributes to MS progression. The University of Buffalo
results nicely show that the higher the disability, the higher the chance that
CCSVI is involved. The congenital origin of the vascular malformations dictates
that such results mean that CCSVI is an adjuvant to the MS disease process. If
one has MS and CCSVI they have a much higher chance of progressing to a
higher disability level than a person with MS but no CCSVI. Given the potential
adverse effects of CCSVI on the CNS vascular system, such an empiricallysupported
association is certainly rational and plausible.
The argument that this relationship is due to MS causing CCSVI, an argument
you mentioned in your article, is ruled out by the data although once again I am
sure such an illogical interpretation will continue to be put forth. Many of you
have experience with EAE, the animal model for MS as an autoimmune disease.
I suggest you try to see the relationship of CCSVI and MS as being similar to the
addition of tetanus toxin (opens BBB) to the myelin/adjuvant mix which drives
autoimmunity in EAE.
Given the above, if one has MS, they would be wise to get tested for CCSVI and,
if necessary, treated for it. This is based on the logical reasoning (precautionary
principle) that the chance of harm associated with doing nothing (i.e. progressing
more rapidly and farther if CCSVI is present) is substantially greater than the
chance of harm associated with having endovascular surgery to relieve CCSVI
(extremely rare, serious side effects). As Mark “It’s a Hoax” Freedman correctly
and perhaps prophetically said, “Time is Brain” (Freedman, 2009). With this, and
the apparent role of CCSVI as an accelerant of the MS disease process, in mind,
persons with MS do not have the luxury to follow your self-serving, time table and
wait 5-10 years for what you see as required research to be completed.
Of course, most people with MS realize the obvious and are desperately seeking
such testing and treatment. Who wouldn’t if they had MS and were progressing
(the current drugs really don’t do much for most in the long run). Notably, most
neurologists are unable to understand or empathize with such a logical decision
to want to get CCSVI treated if present. The advice in your opinion piece of not to
get treated for CCSVI for at least 5 -10 years from now is both irresponsible and
dangerous. And this brings us to the topic of the serious lack of objectivity of
such advice.
One big problem with you saying not to get treated for CCSVI is that almost all of
you are closely aligned with the pharmaceutical industry and thus have a major
conflict of interest when you offer such advice. Should we heed the advice of
scientists closely allied with the petroleum industry when it comes how to
address the potential problems of global warming? Of course not! We do not
heed it because they have a blatant conflict of interest so we just don’t know if
they are pulling a fast one or not. One thing we know for sure, it is highly unlikely
their advice will be objective.
Like it or not, the long list of drug company associations for most of the authors
(see appendix below) disqualifies your “Point of View” as being a credible source
when it comes to advice on what to do about a non-drug treatment like CCSVI. I
would stress, you can’t have it both ways. You can’t take money from drug
companies and then turn around and offer advice on a treatment which
potentially would harm the drug companies. Naturally your advice is going to be
“Don’t use the non-drug treatment. Use only the drugs”. How can it be otherwise
and that is why advice from those with obvious conflicts of interest is self-serving
and worthless. It is too bad that most neurologists aren’t like George Ebers of
Oxford University and rise above the temptation to take the easy money from the
drug companies and thus escape a barefaced conflict of interest.
In summary, your Point of View is completely out of date and your advice
regarding CCSVI testing and treatment is totally compromised and of no value. It
is also potentially very harmful for persons with MS. Five to ten years is a very
long time to have to wait for testing and treatment of CCSVI and such a long time
represents a huge amount of lost brain (Time is Brain). I can only suggest you try
hard to take a patient-centred, evidence-based approach and do everything you
can to make testing and treatment of CCSVI available as soon as possible.
Sincerely,
Dr Ashton Embry
President, Direct-MS
Appendix- Financial Disclosures of the Authors
Dr Khan has received research support from the National MS Society (NMSS),
the National Institutes of Health (NIH), Teva Neuroscience, Genzyme Corporation, Biogen Idec,
Novartis Pharmaceuticals, and Acorda Therapeutics; consultancy and speaking honoraria from
Teva Neuroscience, Biogen Idec, Novartis Pharmaceuticals, and Bayer Healthcare.
Dr. Filippi has received research support from Bayer-Schering Pharma, Biogen-
Dompé AG, Genmab A/S, Merck Serono, Teva Pharmaceutical Industries Ltd.,
Fondazione Italiana Sclerosi Multipla (FISM), and Fondazione Mariani; consultancy and speaking
honoraria from Bayer Schering Pharma, Biogen-Dompé AG, Genmab A/S, Merck Serono, Teva
Pharmaceutical Industries Ltd.
Dr. Freedman has received research support from the Canadian MS Society, EMD Merck-
Serono, Genzyme, and Bayer Schering Pharma; consultancy and speaking honoraria from Teva
Neuroscience, Bayer Healthcare, and EMD Merck-Serono.
Dr Barkhof has received research support from the Dutch MS Research Foundation and Merck-
Serono; consultancy and speaking honoraria from EMD Merck-Serono, Bayer-Schering Pharma,
Biogen-Idec, UBC, Sanofi-Aventis, Novo-Nordisk.
Dr Dore-Duffy has received research support from the NMSS and the NIH.
Dr Trapp has received research support from the NIH, NMSS, Canadian MS Society, Ohio Third
Frontier, Vertex, and EMD Merck-Serono; consultancy and speaking honoraria from Teva
Neuroscience, Biogen Idec and Pfizer.
Dr. Bar-Or has received research support from the MS Society of Canada (MSSC) and the MSSC
Research Foundation, The Canadian Institutes of Health Research, the FRSQ, Bayhill
Therapeutics, Biogen Idec, Bio MS, Genentech, and Teva Neuroscience; consultancy and
speaking honoraria from Biogen Idec, Eli Lilly, Genentech, MerckSerono, Novartis, Roche and
Teva Neuroscience.
Dr Lisak has received research support from the NMSS, NIH, Teva Neuroscience, and Questcor;
consultancyand speaking honoraria from Teva Neuroscience and Bayer Healthcare.
Drs Siegel, Lassmann, and Zak have nothing to disclose.
Chronic cerebrospinal venous insufficiency (CCSVI) and multiple sclerosis - counter arguments
Chronic cerebrospinal venous insufficiency and multiple sclerosis
Omar Khan, MD 1 *, Massimo Filippi, MD 2, Mark S. Freedman, MD, FRCPC 3, Frederik Barkhof, MD, PhD 4, Paula Dore-Duffy, PhD 1, Hans Lassman, MD 5, Bruce Trapp, PhD 6, Amit Bar-Or, MD, FRCPC 7, Imad Zak, MD 8, Marilyn J. Siegel, MD, FACR 9, Robert Lisak, MD, FRCP 1
1Multiple Sclerosis Center, Department of Neurology, Wayne State University School of Medicine, Detroit
2Neuroimaging Research Unit, Scientific Institute and University Hospital San Raffaele, Milan
3Multiple Sclerosis Research Unit, The Ottawa Hospital General Campus, University of Ottawa, Ottawa
4Department of Radiology and Amsterdam MS Center; VU University Medical Center, Amsterdam
5Centre for Brain Research, Medical University of Vienna, Vienna
6Department of Neurosciences; Lerner Research Institute, Cleveland Clinic, Cleveland
7Montreal Neurological Institute, McGill University, Montreal
8Department of Radiology; Wayne State University School of Medicine, Detroit
9Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis
*Correspondence to Omar Khan, Multiple Sclerosis Center & Image Analysis Laboratory, Department of Neurology, Wayne State University School of Medicine 4201 St Antoine, 8A-UHC, Detroit, Michigan 48323
Ph: (313) 745-4280; Fax: (313) 966-9271
Abstract
A chronic state of impaired venous drainage from the central nervous system, termed as chronic cerebrospinal venous insufficiency (CCSVI), is claimed to be a pathologic phenomenon exclusively seen in multiple sclerosis (MS).
This has invigorated the causal debate of MS and generated immense interest in the patient and scientific communities.
A potential shift in the treatment paradigm of MS involving endovascular balloon angioplasty or venous stent placement has been proposed as well as conducted in small patient series.
In some cases, it may have resulted in serious injury.
In this Point of View, we discuss the recent investigations that led to the description of CCSVI as well as the conceptual and technical shortcomings that challenge the potential relationship of this phenomenon to MS.
The need for conducting carefully designed and rigorously controlled studies to investigate CCVSI has been recognized by the scientific bodies engaged in MS research.
Several scientific endeavors examining the presence of CCSVI in MS are being undertaken.
At present, invasive and potentially dangerous endovascular procedures as a therapy for patients with MS should be discouraged until such studies have been completed, analyzed, and debated in the scientific arena.
Annals Of Neurology © 1999-2010 John Wiley & Sons, Inc.
An Open Letter to the Authors of Chronic Cerebrospinal
Venous Insufficiency and Multiple Sclerosis (Khan et al,
2010, Annals of Neurology)
Ashton Embry, Direct-MS
Background: A week ago a “Point of View” article on Chronic Cerebrospinal
Venous Insufficiency and Multiple Sclerosis was made available online at the
website of Annals of Neurology.
It was written by 11 authors, with both
neurologists and radiologists being represented. Notably 7 of 11 authors
(including the first four, senior authors) disclosed significant financial interests
with pharmaceutical companies which produce drugs for MS (see Appendix).
In their opinion piece, the authors discussed Dr Zamboni’s published work on
CCSVI and concluded it should be considered “preliminary”. To my knowledge
no one has ever considered it to be otherwise. Most of the article consisted of
points and arguments that suggest it is not reasonable to consider CCSVI to be
the main cause of the MS disease process. Such a discussion has some value
although I must point out few are claiming CCSVI is the main driver of MS. Dr
Zamboni has been very clear on this and simply says CCSVI may be a significant
contributor to MS onset and progression. Thus, in their Point of View, the authors
essentially put up a straw man and then spend most of the article taking it apart.
Overall, most of their arguments against CCSVI as the main cause of MS are
readily dismissed once MS is seen as an autoimmune disease often exacerbated
by the presence of CCSVI.
The only truly offensive part of the article was the authors’ attempt to rationalize
their self-serving desire that no one with MS should be tested for CCSVI. They
emphasized the very rare occurrence of a serious adverse event associated with
endovascular treatment and totally neglected to discuss the risks of not being
tested and treated for CCSVI. Such a one-sided rationalization which is nullified
by a blatant conflict of interest of most of the authors cannot be taken seriously.
Below is an open letter to the authors.
Dear Dr Khan and fellow authors,
I recently read your opinion piece on CCSVI which was made available online in
Annals of Neurology (Khan et al, 2010) last week. I see it as part of “MS Wars:
Part II – The Medical Empire Strikes Back”. Overall, I enjoyed reading your article
because I always find it useful to read the arguments of those who hold a
different opinion than me on an important subject. I was also pleased that you
restrained yourselves and did not follow Mark Freedman’s infamous lead and call
Dr Zamboni’s work “a hoax”. The only part of the article I found distasteful was
your advice for persons with MS to not get tested for CCSVI for at least 5-10
years (while further research is being done). I discuss this point in detail later.
For a more up to date and more objective opinion piece on MS and CCSVI, I
direct you to my recent article “CCSVI and Multiple Sclerosis: Integrating New
Data to Help Guide Actions” which can be downloaded at http://tinyurl.com/yf36ege.
This article interprets the relationship between the
CCSVI and MS in light of the recently available results from CCSVI-related
studies at the universities of Buffalo and Georgetown. Given you must have
known this critical information would be available in early 2010, I am surprised
you rushed into print before such crucial data were available. This made your
“Point of View” hopelessly outdated on the day it became available. I can only
surmise you did not want any solid data from the Buffalo and Georgetown studies
to cause problems for your critique.
In my article I also address the question of whether persons with MS should get
tested and treated for CCSVI as soon as possible or should wait 5-10 years until
major clinical trials are completed and analyzed. A reasonable answer to this
question depends on the major new data from the universities of Buffalo and
Georgetown. Your analysis of this same question without the benefit of these
crucial data is sadly premature and poorly supported. As I will discuss later, my
advice on this key question is the opposite of yours and, unlike yours, mine is
supported by the new data and is not hopelessly compromised by unacceptable
and major conflicts of interest.
To me, given the robust results of the University of Buffalo Phase 1 study and the
findings of hundreds of endovascular procedures which have already been done
to relieve CCSVI (almost all have found major blockages in the veins draining the
brain), there can be little doubt that CCSVI is associated with MS. And, as I
argue in my article, because the vascular malformations which constitute CCSVI
are mainly congenital (Georgetown data), there can be little doubt that CCSVI is
an important factor in the MS disease process in many cases (definitely not all
cases). Of course, without this new data, you could not offer any worthwhile
opinions on whether or not CCSVI is part of MS.
Furthermore, any claim that the established, robust association of CCSVI and
MS is purely coincidental cannot be taken seriously although I am sure such an
implausible thought will be offered by some. In my article, I interpret MS as an
autoimmune disease which, in many cases, is exacerbated by the co-occurrence
of CCSVI (in 25% of the healthy population and perhaps up to 60% of persons
with MS according to the University of Buffalo work). I find the “either it’s
autoimmune or it’s CCSVI” polarity which dominates your article to be overly
simplistic. An integration of the two phenomena is the most reasonable model
because both have very strong evidence supporting their involvement in MS. Of
course, the new data were required for such an integrated model to become
obvious.
Another key question which you could not evaluate without the new data is
whether or not CCSVI contributes to MS progression. The University of Buffalo
results nicely show that the higher the disability, the higher the chance that
CCSVI is involved. The congenital origin of the vascular malformations dictates
that such results mean that CCSVI is an adjuvant to the MS disease process. If
one has MS and CCSVI they have a much higher chance of progressing to a
higher disability level than a person with MS but no CCSVI. Given the potential
adverse effects of CCSVI on the CNS vascular system, such an empiricallysupported
association is certainly rational and plausible.
The argument that this relationship is due to MS causing CCSVI, an argument
you mentioned in your article, is ruled out by the data although once again I am
sure such an illogical interpretation will continue to be put forth. Many of you
have experience with EAE, the animal model for MS as an autoimmune disease.
I suggest you try to see the relationship of CCSVI and MS as being similar to the
addition of tetanus toxin (opens BBB) to the myelin/adjuvant mix which drives
autoimmunity in EAE.
Given the above, if one has MS, they would be wise to get tested for CCSVI and,
if necessary, treated for it. This is based on the logical reasoning (precautionary
principle) that the chance of harm associated with doing nothing (i.e. progressing
more rapidly and farther if CCSVI is present) is substantially greater than the
chance of harm associated with having endovascular surgery to relieve CCSVI
(extremely rare, serious side effects). As Mark “It’s a Hoax” Freedman correctly
and perhaps prophetically said, “Time is Brain” (Freedman, 2009). With this, and
the apparent role of CCSVI as an accelerant of the MS disease process, in mind,
persons with MS do not have the luxury to follow your self-serving, time table and
wait 5-10 years for what you see as required research to be completed.
Of course, most people with MS realize the obvious and are desperately seeking
such testing and treatment. Who wouldn’t if they had MS and were progressing
(the current drugs really don’t do much for most in the long run). Notably, most
neurologists are unable to understand or empathize with such a logical decision
to want to get CCSVI treated if present. The advice in your opinion piece of not to
get treated for CCSVI for at least 5 -10 years from now is both irresponsible and
dangerous. And this brings us to the topic of the serious lack of objectivity of
such advice.
One big problem with you saying not to get treated for CCSVI is that almost all of
you are closely aligned with the pharmaceutical industry and thus have a major
conflict of interest when you offer such advice. Should we heed the advice of
scientists closely allied with the petroleum industry when it comes how to
address the potential problems of global warming? Of course not! We do not
heed it because they have a blatant conflict of interest so we just don’t know if
they are pulling a fast one or not. One thing we know for sure, it is highly unlikely
their advice will be objective.
Like it or not, the long list of drug company associations for most of the authors
(see appendix below) disqualifies your “Point of View” as being a credible source
when it comes to advice on what to do about a non-drug treatment like CCSVI. I
would stress, you can’t have it both ways. You can’t take money from drug
companies and then turn around and offer advice on a treatment which
potentially would harm the drug companies. Naturally your advice is going to be
“Don’t use the non-drug treatment. Use only the drugs”. How can it be otherwise
and that is why advice from those with obvious conflicts of interest is self-serving
and worthless. It is too bad that most neurologists aren’t like George Ebers of
Oxford University and rise above the temptation to take the easy money from the
drug companies and thus escape a barefaced conflict of interest.
In summary, your Point of View is completely out of date and your advice
regarding CCSVI testing and treatment is totally compromised and of no value. It
is also potentially very harmful for persons with MS. Five to ten years is a very
long time to have to wait for testing and treatment of CCSVI and such a long time
represents a huge amount of lost brain (Time is Brain). I can only suggest you try
hard to take a patient-centred, evidence-based approach and do everything you
can to make testing and treatment of CCSVI available as soon as possible.
Sincerely,
Dr Ashton Embry
President, Direct-MS
Appendix- Financial Disclosures of the Authors
Dr Khan has received research support from the National MS Society (NMSS),
the National Institutes of Health (NIH), Teva Neuroscience, Genzyme Corporation, Biogen Idec,
Novartis Pharmaceuticals, and Acorda Therapeutics; consultancy and speaking honoraria from
Teva Neuroscience, Biogen Idec, Novartis Pharmaceuticals, and Bayer Healthcare.
Dr. Filippi has received research support from Bayer-Schering Pharma, Biogen-
Dompé AG, Genmab A/S, Merck Serono, Teva Pharmaceutical Industries Ltd.,
Fondazione Italiana Sclerosi Multipla (FISM), and Fondazione Mariani; consultancy and speaking
honoraria from Bayer Schering Pharma, Biogen-Dompé AG, Genmab A/S, Merck Serono, Teva
Pharmaceutical Industries Ltd.
Dr. Freedman has received research support from the Canadian MS Society, EMD Merck-
Serono, Genzyme, and Bayer Schering Pharma; consultancy and speaking honoraria from Teva
Neuroscience, Bayer Healthcare, and EMD Merck-Serono.
Dr Barkhof has received research support from the Dutch MS Research Foundation and Merck-
Serono; consultancy and speaking honoraria from EMD Merck-Serono, Bayer-Schering Pharma,
Biogen-Idec, UBC, Sanofi-Aventis, Novo-Nordisk.
Dr Dore-Duffy has received research support from the NMSS and the NIH.
Dr Trapp has received research support from the NIH, NMSS, Canadian MS Society, Ohio Third
Frontier, Vertex, and EMD Merck-Serono; consultancy and speaking honoraria from Teva
Neuroscience, Biogen Idec and Pfizer.
Dr. Bar-Or has received research support from the MS Society of Canada (MSSC) and the MSSC
Research Foundation, The Canadian Institutes of Health Research, the FRSQ, Bayhill
Therapeutics, Biogen Idec, Bio MS, Genentech, and Teva Neuroscience; consultancy and
speaking honoraria from Biogen Idec, Eli Lilly, Genentech, MerckSerono, Novartis, Roche and
Teva Neuroscience.
Dr Lisak has received research support from the NMSS, NIH, Teva Neuroscience, and Questcor;
consultancyand speaking honoraria from Teva Neuroscience and Bayer Healthcare.
Drs Siegel, Lassmann, and Zak have nothing to disclose.
Kto jest online
Użytkownicy przeglądający to forum: Obecnie na forum nie ma żadnego zarejestrowanego użytkownika i 46 gości