Asthma Drug May Help MS patients

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Asthma Drug May Help MS patients

Postby North52 » Tue Sep 14, 2010 8:53 am

Please see the following study.

http://www.medpagetoday.com/Neurology/M ... osis/22153

Interestingly, it showed that albuterol (AKA Ventolin) may improve outcomes in MS. Albuterol is a beta adrenergic agonist that is principally used in asthma to open up the airways by relaxing the smooth muscle around them. As smooth muslce is present around veins, it should relax and dilate them as well. Could this be the reason for the improved outcomes?

Here is the article pasted below as well:

Asthma Drug May Help MS Patients

By Crystal Phend, Senior Staff Writer, MedPage Today
September 13, 2010


MedPage Today Action Points
This is a small pilot add-on study of albuterol to Copaxone which did not
meet its primary endpoint, although there was some benefit in time to first
relapse and some composite measures.


Albuterol is relatively safe and inexpensive and may be effective add-on
therapy if verified in larger trials.

Review
The bronchodilator albuterol may boost the efficacy of treatment for
multiple sclerosis and improve early outcomes, based on results of a small
pilot study.

Adding albuterol to glatiramer acetate (Copaxone) improved composite
functional scores at six and 12 months compared with addition of a placebo
(P=0.005 and P=0.04, respectively) in the randomized trial led by Samia J.
Khoury, MD, of Brigham and Women's Hospital and Harvard in Boston.

Albuterol was also associated with delay in the time to first relapse
(P=0.03), the researchers reported in the September issue of the Archives of
Neurology.
However, the trial missed its primary efficacy endpoint, showing no extra
benefit from albuterol at the end of the 24-month trial for change in
Multiple Sclerosis Functional Composite score, they noted.

Albuterol eases bronchospasm in asthma and other respiratory conditions
through its action as a beta-2 adrenergic agonist but has also been shown to
decrease interleukin-12 levels.

This cytokine is typically elevated in multiple sclerosis patients and
promotes generation of a type of helper T cell implicated in the nerve
demyelination that is a hallmark of the disease.

Rather than just improving multiple sclerosis outcomes through better lung
function, albuterol may accelerate clinical response at the initiation of
standard therapy for the disease, Khoury's group speculated.

Because glatiramer acetate's benefits often take nine months or more to kick
in clinically, enhancing or speeding up the efficacy may be meaningful,
Khoury told MedPage Today.

"It's a small study, but given the safety of the drug I think it's feasible
for people to try it," Khoury said in an interview.

A larger trial is needed to validate the results, but funding may be a
problem because of the generic availability of albuterol, she noted.

The single-center trial included 44 patients with relapsing-remitting MS
randomized to double-blind treatment with a subcutaneous injection of
glatiramer acetate (20 mg) plus an oral dose of either placebo or albuterol
daily for two years.

Patients had no prior immunomodulatory or immunosuppressive treatment.

Albuterol yielded a mean 0.26-point higher score on the Multiple Sclerosis
Functional Composite at six months than was seen in the placebo group (95%
confidence interval for difference 0.08 to 0.43).

At 12 months, the difference was a significant 0.210 points favoring
albuterol.

But at 24 months, the difference declined to only 0.09 points and lost
statistical significance (95% CI -0.17 to 0.35).

The early advantage of albuterol largely derived from differences in the
timed 25-foot walk, which improved in patients who took albuterol but
worsened in those who didn't.

But the ambulation index and disability scores didn't show a benefit from
adding albuterol to glatiramer acetate.

Relapses occurred in two albuterol-group patients and eight control-group
patients for a rate of 0.09 versus 0.37 relapses per year. Time to first
relapse was faster among those in the control group (P=0.03).

For the primary immunologic endpoints, expression of interleukin-13 and
interferon gamma fell in both groups -- a response expected from glatiramer
acetate treatment, according to the researchers.

But this immune response was significantly greater for IL-13 with albuterol
at the 12-month time point (P<0.05).

If the asthma drug is boosting the disease-modifying nature of glatiramer
acetate treatment, deceleration of brain atrophy by reducing inflammation
and possibly promotion of remyelination and repair might be seen, the
researchers noted.

In the study, brain atrophy didn't slow significantly with albuterol versus
glatiramer acetate plus placebo (P=0.10), but the study was underpowered to
show a difference, and the time frame might have been too short to find an
effect, Khoury and colleagues noted.

Adverse events were generally mild. The only moderate or severe events
considered related to the treatment were reaction at the glatiramer acetate
injection site, leg weakness, and chest tightness.

Mild tremor was more common with albuterol (11 reports versus two in the
control group, P=0.008). Anxiety and nervousness were also reported more
frequently with the addition of albuterol, though not significantly so.

"Albuterol is generally a safe medication but may not be appropriate for
patients taking beta-blockers or monoamine oxidase inhibitors or for
patients with anxiety disorders," Khoury's group cautioned in the paper.

The study was supported in part by an Autoimmunity Center of Excellence
Study grant from the National Institute of Allergy and Infectious Diseases.

Khoury reported receiving consulting or lecture fees from EpiVax, LifeCycle
Pharmaceutical, PDL, BioPharma, Repligen, and Wyeth Pharmaceuticals.

Primary source: Archives of Neurology
Source reference:
Khoury SJ, et al "A randomized controlled double-masked trial of albuterol
add-on therapy in patients with multiple sclerosis" Arch Neurol 2010; 67:
1055-1061.
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North
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Postby debp » Tue Sep 14, 2010 1:03 pm

Asthma is also an autoimmune disease with no cure and no real explanation. Some people with childhood asthma "grow out of it".

I wonder if people with Asthma have bad veins...
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Postby scorpion » Tue Sep 14, 2010 1:11 pm

debp wrote:Asthma is also an autoimmune disease with no cure and no real explanation. Some people with childhood asthma "grow out of it".

I wonder if people with Asthma have bad veins...


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Postby cheerleader » Tue Sep 14, 2010 1:40 pm

debp wrote:Asthma is also an autoimmune disease with no cure and no real explanation. Some people with childhood asthma "grow out of it".

I wonder if people with Asthma have bad veins...


Although asthma has mast cells and other things in common with autoimmune diseases, it's considered a chronic inflammatory disease, not autoimmune...and it's not about veins. BUT it does appear to be about endothelial dysfunction---
http://ajrccm.atsjournals.org/cgi/conte ... 1-0038PPv1

It was actually Dr. Elliot Frohman (head of neurology at Southwestern) that posited that perhaps all autoimmune diseases were related to venous congestion. I have his quote from the Bologna conference--

Dr. Frohman makes the introduction. CCSVI is removed from how we think about MS or any other immune mediated diseases. Could other diseases we currently classify as autoimmune be related to venous disease? AI diseases share in common molecular adhesion molecules. Perhaps Crohn’s could be venous? Validating CCSVI in MS may affect the classification of other autoimmune disorders. This venous model has been overlooked.

Micrographs, histopathology, periventricular cuffs, red cells we see in post- capillary venules. This is not new. In 1863 -before Charcot- G.E. Rindfleisch writes of venous congestion in MS.

Could the immune system go anywhere blood goes? Is this why there is an inappropriate immune response? He notes the large crowd in the room (it’s packed) and says he hopes people will speak out. (they will!)


Dr. Frohman's quote points to endothelial dysfunction. That the immune system will follow where there is a breakdown of blood vessels, plasmic cells escaping the vessels and inflammation. Could be the mechanism of connection ....more research ahead.
cheer
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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