Having problems with message search?
http://www.webmd.
Public release date: 8-Jan-2007
Contact: Louis Bergeron
louisb3@stanford.
650-723-0272
Stanford University Medical Center
New therapy for chronic fatigue syndrome to be tested at Stanford
STANFORD, Calif. -- A preliminary study suggests
there may be hope in the offing for some
sufferers of chronic fatigue syndrome with a new
therapy being tested by researchers at the
Stanford University School of Medicine.
José Montoya, MD, associate professor of medicine
(infectious diseases), and postdoctoral scholar
Andreas Kogelnik, MD, PhD, have used the drug
valganciclovir - an antiviral often used in
treating diseases caused by human herpes viruses
- to treat a small number of CFS patients.
The researchers said they treated 25 patients
during the last three years, 21 of whom responded
with significant improvement that was sustained
even after going off the medication at the end of
the treatment regimen, which usually lasts six
months. The first patient has now been off the
drug for almost three years and has had no
relapses. A paper describing the first dozen
patients Montoya and Kogelnik treated with the
drug was published in the December issue of Journal of Clinical Virology.
"This study is small and preliminary, but
potentially very important," said Anthony
Komaroff, MD, professor of medicine at Harvard
Medical School, who was not involved in the
study. "If a randomized trial confirmed the value
of this therapy for patients like the ones
studied here, it would be an important landmark
in the treatment of this illness."
Montoya has received a $1.3 million grant from
Roche Pharmaceutical, which manufactures the drug
under the brand name Valcyte, to conduct a
randomized, placebo-controlled, double-blind
study set to begin this quarter at Stanford. The
study will assess the effectiveness of the drug
in treating a subset of CFS patients.
Montoya is speaking about his efforts at the
biannual meeting of the International Association
for Chronic Fatigue Syndrome in Fort Lauderdale on Jan. 11 and 12.
Chronic fatigue syndrome has baffled doctors and
researchers for decades, because aside from
debilitating fatigue, it lacks consistent
symptoms. Although many genetic, infectious,
psychiatric and environmental factors have been
proposed as possible causes, none has been nailed
down. It was often derided as "yuppie flu," since
it seemed to occur frequently in young
professionals, though the Centers for Disease
Control and Prevention says it's most common in
the middle-aged. But to those suffering from it,
CFS is all too real and its effects are
devastating, reducing once-vigorous individuals
to the ranks of the bedridden, with an
all-encompassing, painful and sleep-depriving fatigue.
More than 1 million Americans suffer from the
disorder, according to the CDC. The disease often
begins with what appears to be routine flulike
symptoms, but then fails to subside completely -
resulting in chronic, waxing and waning debilitation for years.
Valganciclovir is normally used against diseases
caused by viruses in the herpes family, including
cytomegalovirus, Epstein-Barr virus and human
herpes virus-6. These diseases usually affect
patients whose immune systems are severely
weakened, such as transplant and cancer patients.
Montoya, who had used the drug in treating such
patients for years, decided to try using it on a
CFS patient who came to him in early 2004 with
extremely high levels of antibodies for three of
the herpes family viruses in her blood. At the
time, she had been suffering from CFS for five years.
When a virus infects someone, the levels of
antibodies cranked out by the immune system in
response typically increase until the virus is
overcome, then slowly diminish over time. But
Montoya's patient had persistently high
antibodies for the three viruses. In addition,
the lymph nodes in her neck were significantly
enlarged, some up to eight times their normal
size, suggesting her immune system was fighting
some kind of infection, even though a
comprehensive evaluation had failed to point to any infectious cause.
Concerned about the unusual elevations in
antibody levels as well as the swelling of her
lymph nodes, Montoya decided to prescribe
valganciclovir. "I thought by giving an antiviral
that was effective against herpes viruses for a
relatively long period of time, perhaps we could
impact somehow the inflammation that she had in her lymph nodes," said Montoya.
Within four weeks, the patient's lymph nodes
began shrinking. Six weeks later she phoned
Montoya from her home in South America,
describing how she was now exercising, bicycling
and going back to work at the company she ran
before her illness. "We were really shocked by this," recalled Montoya.
Of the two dozen patients Montoya and Kogelnik
have since treated, the 20 that responded all had
developed CFS after an initial flulike illness,
while the non-responders had suffered no initial flu.
Some of the patients take the drug for more than
six months, such as Michael Manson, whose battle
with CFS has lasted more than 18 years. The
former triathlete was stricken with a viral
infection a year after his marriage. After trying
unsuccessfully to overcome what he thought were
lingering effects of the flu, he had no choice
but to drastically curtail all his activities and eventually stop working.
During his longest period of extreme fatigue, 13
1/2 weeks, Manson said, "My wife literally
thought I was passing away. I could hear the
emotion in her voice as she tried to wake me, but
I couldn't wake up to console her. That was just maddening."
Now in his seventh month of treatment, Manson is
able to go backpacking with his children with no
ill after-effects. Prior to starting the
treatment, Manson's three children, ages 9 to 14, had never seen him healthy.
Montoya and Kogelnik emphasized that even if
their new clinical trial validates the use of
valganciclovir in treating some CFS patients, the
drug may not be effective in all cases. In fact,
the trial will assess the effectiveness of the
medication among a specific subset of CFS
patients; namely, those who have viral-induced
dysfunction of the central nervous system.
"This could be a solution for a subset of
patients, but that subset could be quite large,"
said Kristin Loomis, executive director of the
HHV-6 Foundation, which has helped fund a
significant portion of the preparatory work for
the clinical trial. "These viruses have been
suspected in CFS for decades, but researchers
couldn't prove it because they are so difficult
to detect in the blood. If Montoya's results are
confirmed, he will have made a real breakthrough.
"What is desperately needed is the completion of
the randomized, double-blind, placebo-controlled
clinical trial that we are about to embark on," Montoya said.
###
BROADCAST MEDIA CONTACT: M.A. Malone at (650) 723-6912 (mamalone@stanford.
People interested in participating in the
clinical trial must live in the San Francisco Bay
Area. More information about the clinical trial
is available online at http://www.vicd.
Stanford University Medical Center integrates
research, medical education and patient care at
its three institutions - Stanford University
School of Medicine, Stanford Hospital & Clinics
and Lucile Packard Children's Hospital at
Stanford. For more information, please visit the
Web site of the medical center's Office of
Communication & Public Affairs at http://mednews.
What is HHV-6?
Human herpesvirus HHV-6 is one of the eight known members of the human herpesvirus family.
A photograph of HHV-6 virus particles taken with an electron microscope is at right.
The virus,was discovered in 1986 in the United States at the National Cancer Institute infects cells of the immune and central nervous systems. Researchers have identified HHV-6 as the cause of childhood roseola (exanthem subitum). An HHV-6 infected and dying human white blood cell is shown in the photograph below. Note the fragmentaion of the cell nucleus and the cluster of newly formed virus particles at the bottom of the photograph.
Serologic testing reveals that more than 95% of the world's population is positive for antibodies to HHV-6, indicating an
immune response to an infection by the virus. Transmission
of this virus is believed to occur as a result of exposure to
saliva. After this initial infection, HHV-6 viral DNA remains
latent, or dormant, within the nuclei of cells.
Two variants of HHV-6 are recognized: HHV-6A and HHV-6B. Primary infection of
HHV-6B is the cause of roseola in children and greater than 95% of the population has
antibodies to this variant. Primary infection with HHV-6A is believed to occur later in
childhood or during adulthood and may occur without symptoms. The prevalence of HHV-6A infection is not known.
HHV-6 reactivation in adulthood can result in illness. Reactivation means that the virus is no longer dormant and begins to replicate. In most individuals, reactivations are extinguished by the immune system and the virus is forced back into latency. However, in some individuals the reactivated virus causes illness.
The factors that lead to reactivation in people with intact and functioning immune systems are unclear and probably include genetic and environmental causes (such as hormones, other infections, and exposure to chemicals). Most instances of reactivation will not result in chronic, active infection as the normal immune system will suppress the reactivated virus and return it to a latent state. However, reactivation of HHV-6 in normal adults has been associated with a mononucleosis syndrome, autoimmune disorders, and nervous system diseases.
Recent studies have revealed active HHV-6 infections in single, random blood samples taken from Multiple Sclerosis (MS) patients (56% positive) and Chronic Fatigue Syndrome (CFS) patients (39% positive). Normal, healthy controls were negative for active HHV-6 virus (0% positive). This demonstrates that active HHV-6 infections are abnormal and are not seen in healthy people without these disease associations.
In individuals whose immune systems have been compromised by disease (AIDS) or medical treatment (e.g. chemotherapy for cancer or immunosuppressive drugs after transplantation), a reactivation of HHV-6 can result in suppression of the bone marrow or inflammation of the tissues of the brain, liver or lungs.
Offline 
Send Email