WebMD Medical News
Brenda Goodman, MA
Laura J. Martin, MD
Oct. 19, 2011 -- Researchers in Norway say they’ve been able to treat symptoms of chronic fatigue syndrome by giving patients a biologic drug that affects the immune system.
The drug, rituximab (Rituxan), works by depleting immune cells called B-cells. It is FDA approved to treat non-Hodgkin’s lymphoma, chronic lymphocytic leukemia, rheumatoid arthritis, and two kinds of vasculitis.
For the study, researchers recruited 30 people with chronic fatigue syndrome (CFS). Half got two infusions of rituximab given two weeks apart. The other half got infusions of saline solution as a placebo.
Ten patients in the rituximab group (67%) and two patients in the placebo group (13%) saw at least moderate reductions in fatigue.
In most of the patients, improvements were transient and faded within eight to 44 weeks.
But three patients, two in the rituximab group and one that got the placebo, continue to be symptom free 2 1/2 years after their treatments. Those three patients have all returned to full-time jobs, researchers say.
The study is published in the journal PLoS One.
“Our thought is that in fact CFS is an autoimmune disease in most patients,” says study researcher Olav Mella, MD, PhD, an oncologist at Haukeland University Hospital in Bergen, Norway.
Mella and his colleague, Oystein Fluge, MD, PhD, say they accidentally discovered that rituximab might help chronic fatigue syndrome after they used it to treat three patients who suffered from both CFS and non-Hodgkin’s lymphoma. All three patients reported significant improvements in fatigue after rituximab infusions. They eventually relapsed and were given more doses of rituximab. All three again had improvements in their CFS, though those eventually faded.
Their cases were reported in BioMedCentral Neurology in 2009.
Researchers say they aren’t sure why the drug is working.
“We cannot know for sure, but what we see is that there’s a delay from the rapid B-cell depletion after rituximab treatment to the clinical response. The delay can be from three to perhaps eight months before the response is thought to occur,” says Fluge, who is an oncologist and medical physicist at Haukeland Hospital.
B-cells are part of the immune system. They roam the body in relatively small numbers searching for foreign invaders. When a B-cell finds one, it springs into action, becoming an infection-fighting chemical factory.
In some diseases, like leukemia, B-cells may go haywire and cause cancer. In rheumatoid arthritis, B-cells may attack the body's own tissues.
In CFS, however, it’s unclear why killing off B-cells might help.
One theory, held by researchers who believe CFS may be caused by an infection, suggests that retroviruses may hide out in dormant B-cells, only becoming active when the cell is triggered and rapidly multiplies.
But Fluge thinks if that’s the case, patients would see quicker improvements after taking the rituximab.
“We think what we see could be best explained with an autoimmune mechanism and gradual elimination of auto-antibodies,” he says.
Other, more circumstantial evidence supports the idea that CFS may be an autoimmune disease.
Like other autoimmune conditions, it tends to be much more common in women than in men, for example. Many people report getting CFS after a bout with triggering illness. The risk of getting chronic fatigue appears be similar to the risk for getting other kinds of immune disorders.
Despite the positive results of the study, researchers stressed that it was far too early for people with chronic fatigue to seek treatment with rituximab.
“For the time being, this is a clinical trial. It is not for routine use. We need at least one more large study, partly here and partly somewhere else, to confirm the results,” Mella says.
Rituximab is expensive. A single course of treatment for cancer can cost more than $20,000. Rarely, fatal reactions have been reported after infusions of the drug, although no significant adverse events were reported in the current study.
“The most exciting news from the study is the possibility of disease-modifying treatment for at least some people with CFS,” Kim McCleary, president and chief executive officer of the CFIDS Association of America, says in an email. “This study also provides support for other possible approaches to repair immune abnormalities that have been identified in CFS patients.”
SOURCES:Fluge, O. PLoS One, October 2011.Olav Mella, MD, PhD, oncologist, Haukeland University Hospital, Bergen, Norway.Oystein Fluge, MD, PhD, oncologist and medical physicist, Haukeland University Hospital, Bergen, Norway.Kim McCleary, president and chief executive officer, CFIDS Association of America.
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