Monday, October 18, 2010

Glatirimer Acetate Beats Interferon for MS Fatigue

Note: As the study authors note, the impact of immunomodulatory drugs
on fatigue has not been extensively tested and biomarkers for fatigue
reduction instead of self-report do not really exist - this particular
drug is thought to work both because of it's anti-inflammatory
components as well as neuroprotective components.

Glatiramer Acetate Beats Interferon for MS Fatigue

By Richard Robinson, Contributing Writer, MedPage Today
Published: October 17, 2010
Reviewed by Michael J. Olek, DO; Director, Newport Doctors Multiple
Sclerosis Clinic and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner 

Action Points

    * Note that this study was published as an abstract and presented
at a conference. These data and conclusions should be considered to be
preliminary until published in a peer-reviewed journal.

    * Note that patients receiving glatiramer acetate for one year had
more improvement in their fatigue symptoms than those receiving
interferon beta-1b or placebo.

GOTHENBURG, Sweden -- Glatiramer acetate (GA) reduces fatigue in
multiple sclerosis patients more than interferon beta-1b (IFN-1b)
after 1 year of treatment, according to a new study.

IFN-1b had no impact on two clinical measures of fatigue, while GA
(Copaxone) reduced the score on the Fatigue Severity Scale (FSS) by
20%, and the score on the Fatigue Descriptive Scale (FDS) by 34%,
according to a study presented here at the European Committee for
Treatment and Research in Multiple Sclerosis meeting.

Based on the results, the authors, Tatiana Shmidt and a colleague at
the Kozhevnikov Clinic for Neurological Diseases in Moscow, Russia,
concluded in their poster, "Copaxone is recommended as a first-line
imunomodulating drug for patients with severe fatigue." The authors
were unavailable for comment at press time.

While fatigue may be a significant symptom in multiple sclerosis (MS),
"the impact of immunomodulatory drugs on fatigue has not been
extensively investigated," they wrote. So the authors compared GA,
IFN-1b, and no treatment in patients with severe fatigue in a clinical
study, supplemented by a laboratory study to find biomarkers for
fatigue reduction.

They enrolled 63 patients with relapsing-remitting MS who had FSS
scores of at least 4. The FSS is a 9-item scale assessing the impact
of fatigue on daily living, with a minimum score of 1 and a maximum of
9. An FSS score greater than 4 indicates severe fatigue.

Patients received either GA (n=27), IFN-1b (n=19), or no
immunomodulatory treatment (n=17), and were followed for 1 year.

At the end of the year, FSS score in GA-treated patients had fallen
(improved) from 4.5 to 3.61 (P<0.01), while there was no significant
change in patients receiving IFN-1b. Scores in untreated patients rose
from 4.48 to 4.82 (P<0.05).

Scores on the FDS, an alternative measure of fatigue severity, fell
(improved) from 7.26 to 4.78 for GA-treated patients (P<0.01),
remained unchanged in IFN-1b-treated patients, and rose from 6.92 to 8
in untreated patients (P<0.05).

A similar pattern was seen for measures of cognitive fatigue and the
Fatigue Impact Scale.

Patients in the GA-treated group had a "trend to reduced IL-6 and to
increased vanillylmandelic acid and homovanillic acid," which, the
authors concluded, "may be suggested as presumable markers of fatigue
in relapsing-remitting MS." Data for these biochemical changes were
not presented in the poster session.

"The positive impact of this drug on fatigue in relapsing-remitting MS
is possibly associated with its double mechanism of action," they
said, involving both anti-inflammatory and neuroprotective components.

The authors reported no disclosures.

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