[Co-Cure ME/CFS & Fibromyalgia Information Exchange Forum Logo]

Co-Cure Weekly Digest of research and medical posts only - 7 May 2007 to 14 May 2007

Topics of the week:
[Return to digest index]

                       This is a special digest of
                  Co-Cure Research & Medical posts only
               Problems? Write to mailto:mods@co-cure.org
E-Mail mailto:Co-Cure-HMC-signoff-request@listserv.nodak.edu to unsubscribe


Date:    Tue, 8 May 2007 15:34:16 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Prevalence of temporomandibular disorders in fibromyalgia and failed back syndrome patients: A blinded prospective comparison study

Prevalence of temporomandibular disorders in fibromyalgia and failed back
syndrome patients: A blinded prospective comparison study.

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007 May 4; [Epub ahead
of print]

Balasubramaniam R, de Leeuw R, Zhu H, Nickerson RB, Okeson JP, Carlson CR.

Former Resident, Orofacial Pain, Orofacial Pain Center, University of Kentucky.

PMID: 17482850

OBJECTIVES: The objective of this study was to determine the prevalence of
temporomandibular disorders (TMD) and evaluate psychosocial domains in
patients with fibromyalgia (FM) compared with patients with failed back
syndrome (FBS).

STUDY DESIGN: The study included 51 (32 FM and 19 FBS) adult patients who
were administered orofacial pain and psychological questionnaires before a
clinical examination. Presence of TMD was diagnosed according to the
Research Diagnostic Criteria for TMD.

RESULTS: Fifty-three percent of the FM patients reported having face pain
compared with 11% of the FBS patients. Of those FM patients who reported
face pain, 71% fulfilled the criteria for a diagnosable TMD. FM patients
had significantly higher subscale scores for somatization,
obsessive-compulsive, medication used for sleep, and fatigue compared with
FBS patients. Eighty-seven percent of the FM patients reported a stressful
event and 42.3% had symptoms indicating posttraumatic stress disorder.

CONCLUSION: The high prevalence of TMD and psychosocial dysfunction among
FM patients suggests wide-reaching dysregulation of autonomic and
hypothalamic-pituitary-adrenal axis functions.

[Return to top]


Date:    Wed, 9 May 2007 10:30:36 -0700
From:    "Jodi Bassett <jodibassett bigpond.com>
Subject: ACT, NOT, MED: The myths about M.E. and the symptoms of M.E.

*permission to repost*

The myths about M.E. and the symptoms of M.E. written by Jodi Bassett, May

Because of the vast amount of inaccurate information being propagated about
M.E. by various vested interest groups (helped immeasurably by the creation
of a number of vague umbrella terms such as 'CFS' 'ME/CFS' 'CFS/ME' 'CFIDS'
and Myalgic 'Encephalopathy' etc.) it is important to explain briefly what
are the myths about M.E., and the symptoms of M.E.

M.E. has nothing to do with being tired all the time. If you are very
fatigued for an extended period of time this does not mean you are having a
'bout' of M.E. To suggest such a thing is no less absurd than to say that
prolonged fatigue means you are having a 'bout' of multiple sclerosis,
Parkinson's disease or Lupus. If you are constantly fatigued you do not have
M.E. no matter how severe or prolonged your fatigue is. Fatigue is a symptom
of many different illnesses as well as a feature of normal everyday life -
but it is not a defining symptom of M.E., nor even an essential symptom of

There are a number of post-viral fatigue states or fatigue syndromes which
may follow common infections such as mononucleosis/glandular fever,
hepatitis, Q fever, Ross river virus and so on. M.E. is an entirely
different condition to these self-limiting fatigue syndromes however, the
science is very clear on this point. People suffering with any of these
post-viral fatigue states or fatigue syndromes do not have M.E. M.E. is also
not the same condition as Lyme disease, athletes over-training syndrome,
burnout, depression, somatisation disorder, candida, multiple chemical
sensitivity syndrome or Fibromyalgia, or indeed any other illness. M.E. is a
distinct neurological illness with a distinct; onset, symptoms, aetiology,
pathology, response to treatment, long and short term prognosis - and World
Health Organization classification (G.93.3).

M.E. is also not defined by 'fatigue following exertion which can last up to
24 hours' as the bogus definitions of 'CFS' describe. Fatigue following
activity (or post-exertional fatigue or malaise) is a common symptom of a
large number of different illnesses - but what is happening in M.E. is quite
different. Overexertion does not cause fatigue in M.E. but instead a
worsening of the severity of the illness generally and of various
neurological, cognitive, cardiac, cardiovascular, immunological, muscular
and gastrointestinal (and other) symptoms. The severity of these symptoms
can range from mild to severe to life-threatening. The effects of
overexertion can last for hours, days, weeks or even many months in M.E., or
can even be permanent. The onset of these post-exertional effects can be
significantly delayed so that very often the worsening of the illness caused
by overexertion has not even begun within 24 hours in M.E., let alone been
completely resolved in that time. The reaction people with M.E. have to
physical and mental activity, sensory input and orthostatic stress not only
has nothing to do with mere fatigue (or 'malaise') but is in fact unique to
M.E. in a number of ways.

This reaction is so abnormal in fact that exercise testing is one of the
series of tests which can be used to help confirm a M.E. diagnosis, as are
various tests which measure the abnormal responses to orthostatic stress
seen in M.E. This is simply not the case in post-viral fatigue syndromes,
Lyme disease, Fibromyalgia and so on. These patient groups do not exhibit
the same measurable pathological abnormalities as M.E. patients in these
(and other) tests. Recent research has also shown that postural stress
exacerbates cardiac insufficiency in M.E. and that this cardiac
insufficiency is the cause of many of the symptoms and much of the
disability of M.E. This pathology is also not seen in any of those illnesses
causing fatigue after exertion which are commonly misdiagnosed as 'CFS.' The
way people with M.E. respond to physical activity and orthostatic stress
(etc.) is profoundly different than in these other illnesses; it is an
entirely different problem, of a much greater magnitude.

What defines M.E. is not 'chronic fatigue' but a specific type of acquired
damage to the brain. M.E. is an acutely acquired illness with multi system
involvement which is characterised by post encephalitic damage to the brain
stem; a nerve centre through which many spinal nerve tracts connect with
higher centres in the brain in order to control all vital bodily functions -
this is always damaged in M.E. (Hence the name Myalgic Encephalomyelitis.)

This diffuse brain injury is initiated by a virus infection which targets
the brain; M.E. represents a major attack on the central nervous system
(CNS) by the chronic effects of a viral infection. M.E. is an infectious and
primarily neurological disease process which occurs in epidemic and sporadic
forms, over 60 outbreaks of M.E. have been recorded worldwide since 1934.
M.E. is primarily neurological, but because the brain controls all vital
bodily functions every bodily system is affected and so symptoms can also be
manifested by virtually all bodily systems including: cognitive, cardiac,
cardiovascular, immunological, endocrinological, respiratory, hormonal,
gastrointestinal and musculo-skeletal dysfunctions and damage. Symptoms are
also caused by a loss of normal internal homeostasis in M.E.; the body/brain
no longer responds appropriately to (to varying extents): physical activity,
cognitive exertion, sensory input and orthostatic stress.

At first glance a list of M.E. symptoms it may seem that every symptom
possible is mentioned, but the seemingly random list of symptoms in fact
form unique and distinct patterns - they are anything but 'random' for those
with knowledge of the illness and/or of how the illness effects the body's
various systems. Different people have a lot of different symptoms but the
general pattern and evolution of major symptoms are remarkably coherent from
patient to patient in M.E.; they fit a precise pattern that is nearly
identical from one patient to the next.

There is just no other illness that is even remotely like M.E.

M.E. is a distinct, recognisable disease entity which contrary to popular
belief is not difficult to diagnose and can in fact be diagnosed relatively
early in the course of the disease (within just a few weeks) - providing
that the physician has some experience with the illness. (The usual case of
M.E. is so distinct that people with M.E. can recognise fellow sufferers
almost in an instant.) Although there is (as yet) no single test which can
be used to diagnose M.E. there are a series of tests which can confirm a
suspected M.E. diagnosis. If all tests are normal, if specific abnormalities
are not seen on certain of these tests (eg. brain scans), then a diagnosis
of M.E. cannot be correct. (See Testing for Myalgic Encephalomyelitis for
more information.)

All of this is not simply theory, but is based upon an enormous body of
clinical information which has been published in prestigious peer-reviewed
journals all over the world and spans over 60 years. Confirmation of this
hypothesis is supported by electrical tests of muscle and of brain function
(including the subsequent development of PET and SPECT scans) and by
biochemical and hormonal assays. Newer scientific evidence is increasingly
strengthening this hypothesis. M.E. is neither 'mysterious' nor 'medically
unexplained. Many aspects of the pathophysiology of the disease have,
indeed, been medically explained in volumes of research articles. These are
well-documented, scientifically sound explanations for why patients are
bedridden, profoundly intellectually impaired, unable to maintain an upright
posture and so on.

M.E. affects all races and socio-economic groups and has been diagnosed all
over the world with a similar strike rate to multiple sclerosis. Children as
young as five can get M.E., as well as adults of all ages. M.E. can be
extremely disabling. 25% of M.E. sufferers are severely affected and
housebound and bedbound. In some cases Myalgic Encephalomyelitis can also be
progressive, or fatal. Governments around the world are currently spending
$0 a year on M.E. research.


Note 1:

For more information about the medical and political facts of M.E. (and for
references) see: Testing for Myalgic Encephalomyelitis, Putting Research and
Articles into Context, The Ultra-comprehensive Myalgic Encephalomyelitis
Symptom List and What is Myalgic Encephalomyelitis?


Note 2:

Note that many different illnesses may share a percentage of the individual
neurological, gastrointestinal or cognitive features of M.E., (and so on)
but there is no other illness which encompasses each of the specific
neurological, cognitive, immunological, gastrointestinal, cardiac and
cardiovascular, endocrinological, respiratory, hormonal and other features
and symptoms which make up M.E. This specific combination of symptoms is not
seen in any other illness. There are also a number of characteristics of
M.E. which are unique to the illness; most notably the way in which people
with M.E. react to physical and mental activity, and orthostatic stress etc.
and the way in which even low levels of these activities (beyond a person's
individual limits) can negatively affect long-term prognosis. The acute
onset of M.E. also sets it apart from many other illnesses commonly
associated with a gradual onset, as do many other characteristics. See: M.E.
and other illnesses and The misdiagnosis of CFS for more information.


Note 3:

What is CFS? CFS was created in a response to an outbreak of what was
unmistakably M.E., but this new name and definition did not describe the
known signs, symptoms, history and pathology of M.E. It described a disease
process that did not, and could not exist. All each of these flawed CFS
definitions 'define' is a heterogeneous (mixed) population of people with
various misdiagnosed psychiatric and miscellaneous non-psychiatric states
which have little in common but the symptom of fatigue (a symptom seen in
many illnesses but not a defining feature of M.E. nor even an essential
symptom of M.E.). The disease category 'CFS' has undoubtedly been used to
impose a false psychiatric paradigm of M.E. by allying it with various
unrelated psychiatric fatigue states and post-viral fatigue syndromes (etc)
for the benefit of various (proven) financial and political interests. CFS
and M.E. are NOT the same. For more information on this topic, including how
the CFS scam also negatively affects the media, doctors and the public etc.,
see: The misdiagnosis of CFS, Smoke and mirrors and Why the disease category
of 'CFS' must be abandoned. The truth about the organic and distinct
neurological illness M.E. must not be allowed to be buried under cover of
'fatigue' and 'CFS' for another 20 years!



Best wishes everyone,
Jodi Bassett
A Hummingbirds Guide to Myalgic Encephalomyelitis:
Taking fatigue as the flagship symptom of a disease not only bestows the
disease with a certain Rip Van Winkle humour, but it removes the urgency of
the fact that the majority of [M.E.] symptoms are in effect CNS symptoms. To
most physical [M.E.] scientists and clinicians, [M.E.] represents a major
attack on the CNS by the chronic effects of a viral infection. Byron Hyde MD
in 'The Clinical and Scientific basis of M.E. edited by Byron Hyde MD. p

[Return to top]


Date:    Thu, 10 May 2007 13:06:55 -0400
From:    "Bernice A. Melsky" <bernicemelsky VERIZON.NET>
Subject: RES: Association between thyroid autoimmunity and fibromyalgic disease severity

Association between thyroid autoimmunity and fibromyalgic disease severity.

Clin Rheumatol. 2007 May 9; [Epub ahead of print]

Bazzichi L, Rossi A, Giuliano T, De Feo F, Giacomelli C, Consensi A,
Ciapparelli A, Consoli G, Dell'osso L, Bombardieri S.

Division of Rheumatology, Department of Internal Medicine, University of
Pisa, Via Roma, 67, 56100, Pisa, Italy, l.bazzichi int.med.unipi.it

PMID: 17487449

Our objectives were to investigate thyroid abnormalities and autoimmunity
in 120 patients affected by fibromyalgia (FM) and to study their
relationships with clinical data and symptoms.

Thyroid assessment by means of antithyroglobulin antibodies, antithyroid
peroxidase antibodies, free triiodo-thyronine, free thyroxine, and thyroid
stimulating hormone analyses was carried out. The clinical parameters
"Fibromyalgia Impact Questionnaire", pain, tender points, fatigue, and
other symptoms, and the presence of depression or anxiety disorders were

The basal thyroid hormone levels of FM patients were in the normal range,
while 41% of the patients had at least one thyroid antibody. Patients with
thyroid autoimmunity showed a higher percentage of dry eyes, burning, or
pain with urination, allodynia, blurred vision, and sore throat.
Correlations found between thyroid autoimmunity and age or with the
presence of depression or anxiety disorders were not significant. However,
in the cohort of post-menopausal patients, the frequency of thyroid
autoimmunity was higher with respect to pre-menopausal patients.

In conclusion, autoimmune thyroiditis is present in an elevated percentage
of FM patients, and it has been associated with the presence of typical
symptoms of the disease.

[Return to top]


Date:    Fri, 11 May 2007 17:33:00 +0200
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: act,med:ME/CFS -the Whittemore Peterson Institute


Send an Email for free membership
       >>>> Help ME Circle  <<<<
 >>>>       11 May 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV




Chronic Fatigue Awareness Week Kicks Off May 12th

May 10, 2007

In order to recognize the debilitating effects of Chronic Fatigue
Syndrome (CFS) and call attention to the millions of families
affected by the disease, May 12th - May 19th has been
designated National Chronic Fatigue Syndrome Awareness

"This week presents a unique opportunity for us to create
awareness about Chronic Fatigue Syndrome and rally support
for a disease that is oftentimes forgotten and unrecognized in
research and treatment circles," said Annette Whittemore,
Founding Director of the Whittemore Peterson Institute for
Neuro-Immune Disease. "We are thrilled that the Nevada
legislature is giving us the opportunity to testify and rally support
during this special month."

The National Institute of Health reports CFS affects millions of
individuals around the world with the largest single population of
unmet medical need in the U.S. One out of every 300 Americans
suffer from CFS, but currently there are no medications
approved by the Food and Drug Administration for treating CFS.

Full recovery is estimated at only 5-percent to 10-percent of all
patients and CFS can be as disabling as multiple sclerosis,
lupus, rheumatoid arthritis, congestive heart failure and similar
chronic conditions. The estimated economic impact is
$17-billion in lost income and an additional $7-billion in
healthcare costs.

Headquartered in the University of Nevada School of Medicine's
Center for Molecular Medicine, which broke ground in early
March 2007, the Whittemore Peterson Institute is the nation's
first facility dedicated to the research and treatment of
neuro-immune disease.  The center is the first new medical
research facility to be built at UNR in 20 years.

"It is the mission of this institute to facilitate and advance patient
care, research the patho-physiology and develop therapeutics,
diagnostics and prevention strategies for a spectrum of
neuro-immune diseases," Whittemore said.  "This is a
first-of-its-kind organization that fills a national healthcare void,
treating patients that suffer from Chronic Fatigue Syndrome and
other neuro-immune diseases."

Annette Whittemore and others from the Whittemore Peterson
Institute will testify at the Nevada Legislature in Carson City on
Monday, May 14th at 9:00 am to gain further support for the
institute and its mission.

The general public is welcome to attend the hearing and show
their support for this important cause at the Legislative Building,
room 3137, in Carson City or log onto www.wpinstitute.org for
more information.

[Return to top]


Date:    Fri, 11 May 2007 21:41:25 +0200
From:    Jan van Roijen <j.van.roijen CHELLO.NL>
Subject: not,res: Journal of Chronic Fatigue Syndrome - Current Contents


Send an Email for free membership
       >>>> Help ME Circle  <<<<
 >>>>       11 May 2007       <<<<
Editorship : j.van.roijen chello.nl
Outgoing mail scanned by Norton AV

Current Contents with Abstracts for
Journal of Chronic Fatigue Syndrome

Volume 13, Issue 4
Kenny De Meirleir , MD, PhD
Neil R. McGregor , BDS, MDSc, PhD
Elke Van Hoof , ClinPsy, PhD

This issue is now available online and will soon be mailed to
subscribers in approximately 4-6 weeks.

NOTE: If the URLs in this email are not active hyperlinks, copy
and paste the URL into the address/location box in your



Elke Van Hoof, Kenny De Meirleir, Neil McGregor

Conservation of Resources and Quality of Life in
Individuals with Chronic Fatigue Syndrome
René R. Taylor, Supriya Kulkarni, Yukiko Shiraishi

Antiviral Pathway Deregulation of Chronic Fatigue
Syndrome Induces Nitric Oxide Production in Immune
Cells That Precludes a Resolution of the Inflammatory
Marc Frémont, Freya Vaeyens, C. Vincent Herst, Kenny De
Meirleir, Patrick Englebienne

Long-Term Treatment with a Staphylococcus Toxoid
Vaccine in Patients with Fibromyalgia and Chronic Fatigue
Carl-Gerhard Gottfries, Ove Häger, Björn Regland, Olof

Reliability of a Chronic Fatigue Syndrome Questionnaire
Caroline Hawk Hines, Leonard A. Jason, Susan R.

Lyme Disease Presenting as Chronic Fatigue Syndrome
Samuel Shor

Depression, Chronic Fatigue Syndrome, and
Fibromyalgia: An Update
Kenneth R. Kaufman, Paul J. Goodnick

Journal of Chronic Fatigue Syndrome is published both in print
and electronically. Library subscribers may be entitled to
electronic site wide access with paid subscriptions. For more
information go to
http://www.haworthpress.com/journals/libraryonlinejour.asp or
contact online_help@haworthpress.com

For more information about the journal:

[Return to top]


Date:    Fri, 11 May 2007 18:41:49 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Conservation of Resources and Quality of Life in Individuals with Chronic Fatigue Syndrome

Conservation of Resources and Quality of Life in Individuals with Chronic
Fatigue Syndrome

Journal: Journal of Chronic Fatigue Syndrome, Vol. 13, Issue 4 (2006), Pub
Date: 4/5/2007, Page Range: 5 - 18

Contributors and affiliations:
René R. Taylor PhD, Associate Professor, Licensed Clinical Psychologist,
Department of Occupational Therapy , University of Illinois at Chicago,
Chicago, IL, 60612
Supriya Kulkarni MS, OTR/L, Graduate Student, Department of Occupational
Therapy, University of Illinois at Chicago
Yukiko Shiraishi PhD, Project Coordinator, Department of Occupational
Therapy, University of Illnois at Chicago


Objective: To examine the relationship between resources and quality of
life in individuals with chronic fatigue syndrome (CFS).

Participants and Study Design: A cross-sectional design was used to
describe associations between resource loss and gain and quality of life
for 47 individuals diagnosed with CFS.

Main Outcome Measures: The Conservation of Resources Evaluation was used to
measure resources in terms of perceived loss and gain. Health-related
quality of life was assessed with the Quality of Life Index.

Results: Total resource loss and total resource gain were significant
correlates of overall quality of life. Gains in self-esteem, energy, and
work resources were associated with higher-perceived quality of life.
Material loss and energy loss were associated with lower-perceived quality
of life.

Conclusions: Findings for the relationships between perceived resources of
self-esteem, work, material items, and energy and perceived quality of life
can be used inform future rehabilitation efforts. These relationships
appear to occur independently of illness severity among individuals CFS.

[Return to top]


Date:    Sat, 12 May 2007 04:16:22 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Antiviral Pathway Deregulation of Chronic Fatigue  Syndrome Induces Nitric Oxide Production in Immune Cells That  Precludes a Resolution of the Inflammatory Response

Antiviral Pathway Deregulation of Chronic Fatigue Syndrome Induces Nitric
Oxide Production in Immune Cells That Precludes a Resolution of the
Inflammatory Response

Journal: Journal of Chronic Fatigue Syndrome, Volume: 13 Issue: 4 (2006),
Page Range: 17 - 28, Pub Date: 4/5/2007

Contributors and affiliations:
Marc Frémont PhD, RED Laboratories, Brussels, B-1731, Belgium
Freya Vaeyens MS, RED Laboratories N.V., Brussels, B-1731, Belgium
C. Vincent Herst PhD, RED Laboratories N.V., Brussels, B-1731, Belgium
Kenny De Meirleir MD, PhD, Department of Human Physiology and Medicine,
Vrije Universiteit Brussel, Brussels, B-1051, Belgium
Patrick Englebienne PhD, Department of Nuclear Medicine, Free University of
Brussels, Brugmann Hospital, Brussels, B-1020, Belgium, penglebi@ulb.ac.be

Chronic fatigue syndrome (CFS) is a poorly defined medical condition
diagnosed by exclusion, which, besides severe chronic fatigue as the
hallmark symptom, involves inflammatory and immune activation stigma.
Although viral infections are not systematically found in CFS patients, the
type I interferon antiviral pathway has been repeatedly shown to be
activated in peripheral blood mononuclear cells (PBMC) of the most
afflicted patients.

An abnormal truncated form of ribonuclease L (37-kDa RNase L) is also found
in the PBMC of CFS patients and this protein has been proposed as a
biological marker for CFS. Recently, the levels of this abnormal protein
have been significantly correlated to the extent of inflammatory symptoms
displayed by CFS patients.

We report here that active double-stranded RNA-dependent kinase (PKR) is
expressed and activated in parallel to the presence of the 37-kDa RNase L
and to an increase in nitric oxide production by immune cells. However, PKR
upregulation results also in a significant increase followed by a decrease
in caspase 3 activity for the samples containing the highest levels of
37-kDa RNase L. This caspase 3 downregulation does not result from
increased expression of the anti-apoptotic proteins Bcl-2 and Bcl-XL.

These results therefore suggest that chronic inflammation due to excess
nitric oxide production plays a role in CFS and that the normal resolution
of the inflammatory process by NF-kB activation and apoptotic induction is
impaired. These observations draw new directions for the therapeutic
approach of CFS.

Keywords: RNase L pathway, nitric oxide, PKR, chronic inflammation

[Return to top]


Date:    Sun, 13 May 2007 19:47:53 +0200
From:    ME/CFS <me_cfs GLOCALNET.NET>
Subject: RES: Epigenetic hypothesis about ME


I believe that ME might be caused by epigenetic changes. Many patients
report that they are converted into the ME state over one night. Maybe that
is achieved by cells being reprogrammed by changes in the phenotype
(epigenetic layer). That means that for example a methyl group has attached
(or left) the DNA at specific places, resulting into the gene sequence to be
switched off (or on).

Stress or infection may be the trigger of such a change of phenotype.

Maybe hypothalamus (and/or other parts of the body pertaining to the neuro
endocrine immune system) is put into a different mode (reprogrammed) by such
a change of phenotype.

If epigenetic is a part of ME, than ME research needs to involve specialists
in epigenetics. It is not sufficient to look at messenger molecules as for
example cytokines, neuropeptides and hormones. It is necessary to also study
the signal system that triggers epigenetic changes.

If the people undergo epigenetic changes, then their bodies might no longer
obey biomedical laws valid for healthy people. This means that scientific
knowledge about bodily processes for healthy persons, may be invalid for a
person with an epigenetic change. Thus, one can not assume that a
biochemical process in a healthy person would be the same in a person with
an epigenetic change.

/Kasper Ezelius, M.Sc., Sweden (http://goto.glocalnet.net/me_cfs)

Some links about epigenetics:

[Return to top]


Date:    Mon, 14 May 2007 19:49:06 -0400
From:    Fred Springfield <fredspringfield VERIZON.NET>
Subject: RES: Long-Term Treatment with a Staphylococcus Toxoid Vaccine in Patients with Fibromyalgia and Chronic Fatigue Syndrome

Long-Term Treatment with a Staphylococcus Toxoid Vaccine in Patients with
Fibromyalgia and Chronic Fatigue Syndrome

Journal: Journal of Chronic Fatigue Syndrome, Volume: 13 Issue: 4,  Page
Range: 29 - 40 (2006) Pub Date: 4/5/2007

Authors and affiliations:
Carl-Gerhard Gottfries MD, PhD, Professor Emeritus, Institute of Clinical
Neuroscience, University of Gothenburg, Sahlgren University Hospital,
Mölndal, Sweden, <carl-gerhard.gottfries@vgregion.se>
Ove Häger, Research Nurse, Institute of Clinical Neuroscience, University
of Gothenburg, Sweden, <ove.hager@vgregion.se>
Björn Regland MD, PhD, Assistant Professor, Institute of Clinical
Neuroscience, University of Gothenburg, Sweden, <bjorn.regland@vgregion.se>
Olof Zachrisson MD, PhD, Institute of Clinical Neuroscience, University of
Gothenburg, Sweden, <olof.zachrisson@vgregion.se>

One hundred and sixty patients with fibromyalgia and chronic fatigue
syndrome, who were on a continuous treatment with a Staphylococcus vaccine,
were followed during one year with repeated consultation visits. The
patients had participated in controlled studies and been on continuous
treatment with the vaccine for 22 ±10 months before inclusion into this
follow-up study.

They were treated with 1 mL of the vaccine subcutaneously every third to
fourth week. Adverse events were few. The adherence to the treatment was
very good. Over a period of one year, 8% withdrew, and in only 5%, the
withdrawal was due to insufficient clinical effect. Only in two cases where
the patients were allergic to the preservative of the vaccine, the side
effects caused the withdrawal of the treatment. Ratings with scales
(CPRS-15 and FibroFatigue) showed improvement from start of treatment and
also further improvement during the follow-up year.

In view of the natural history for these disorders the result is of interest.

Keywords: Fibromyalgia, chronic fatigue syndrome, Staphylococcus vaccine,
long-term treatment

[Return to top]


End of Co-Cure Weekly Digest of research and medical posts only - 7 May 2007 to 14 May 2007

[Return to digest index] 

Copyright © 2007 Co-Cure
Last Revision: May 15, 2007
Please report any problems with this page to the Webmaster.