Ironjustice 2009-09-21 15:10:40
IFN-beta-1a may represent a promising novel treatment approach in ulcerative
Gut. 2003 Sep;52(9):1286-90. Related Articles, Links
Interferon beta-1a in ulcerative colitis: a placebo controlled, randomised,
dose escalating study.
Nikolaus S, Rutgeerts P, Fedorak R, Steinhart AH, Wild GE, Theuer D, Mohrle J,
Christian-Albrechts University, Kiel, Germany.
BACKGROUND: and aims: Administration of interferon (IFN)-beta may represent a
rational approach to the treatment of ulcerative colitis through its
immunomodulatory and anti-inflammatory effects. The present study was performed
to evaluate the efficacy and tolerability of IFN-beta-1a. METHODS: Patients
(n=18) with moderately active ulcerative colitis were randomised to receive
IFN-beta-1a or placebo. IFN-beta-1a was started at a dose of 22 micro g three
times a week subcutaneously, and the dose was increased at two week intervals
to 44 micro g and then to 88 micro g if no response was observed. The maximum
duration of treatment was eight weeks. End points were clinical treatment
response, defined as a decrease of at least 3 points from baseline in the
ulcerative colitis scoring system (UCSS) symptoms score and induction of
endoscopically confirmed remission. RESULTS: Baseline characteristics and
disease severity were similar in both groups. Data from 17 patients are
included in this report (10 patients in the IFN-beta-1a group and seven
patients in the placebo group). Clinical response was achieved in five patients
(50%) in the IFN-beta-1a group and in one (14%) in the placebo group (P=0.14).
Remission was achieved in three patients in the IFN-beta-1a group and in none
in the placebo group (p=0.02). Most adverse reactions associated with
IFN-beta-1a were influenza-like symptoms or injection site reactions, and were
mild or moderate in severity. CONCLUSIONS: IFN-beta-1a may represent a
promising novel treatment approach in ulcerative colitis.
PMID: 12912859 [PubMed – in process]
Would / could the ‘action’ / mode of operation / efficacy OF interferon beta-1a
be ALSO the SAME as in multiple sclerosis .. ?
Interferon Beta-1A May Lessen Brain Atrophy in MS Patients
Specialists in neuroimaging at the University at Buffalo have proposed a
mechanism by which interferon beta-1a may limit brain atrophy in multiple
sclerosis (MS) patients. The positive effect of interferon beta-1a, a standard
treatment for MS, on brain atrophy is well known, but the process through which
that occurs remains a mystery. UB scientists have shown that the treatment
appears to limit atrophy by minimizing the toxic effect of pathologic iron
deposits found in gray-matter structures of MS patients.
From the University of Buffalo:
Study Proposes Interferon Beta-1A May Lessen Brain Atrophy in MS Patients by
Minimizing Effects of Toxic Iron Deposits
Release date: Thursday, April 10, 2003
Contact: Lois Baker, email@example.com
Phone: 716-645-5000 ext 1417
BUFFALO, N.Y. — Specialists in neuroimaging at the University at Buffalo have
proposed a mechanism by which interferon beta-1a may limit brain atrophy in
multiple sclerosis (MS) patients.
The positive effect of interferon beta-1a, a standard treatment for MS, on
brain atrophy is well known, but the process through which that occurs remains
a mystery. UB scientists have shown that the treatment appears to limit atrophy
by minimizing the toxic effect of pathologic iron deposits found in gray-matter
structures of MS patients.
While the treatment did not diminish iron concentrations that had already
accumulated, it appeared to interfere with the accumulation of iron-induced
damage, said Robert A. Bermel, a fourth-year medical student in UB’s School of
Medicine and Biomedical Sciences and lead author on the study.
Bermel presented the research findings on April 3 at the annual meeting of the
American Academy of Neurology in Hawaii. He also presented the study in March
at the annual meeting of the American Society of Neuroimaging, which selected
the work to receive the society’s 2003 Oldendorf Award for the best research
project first-authored by a trainee.
The MRI imaging work was conducted at the Buffalo Neuroimaging Analysis Center
(BNAC) of the Jacobs Neurological Institute, affiliated with UB’s School of
Medicine and Biological Sciences and Kaleida Health. This group reported
previously for the first time that in addition to the characteristic
white-matter lesions that are a traditional marker of the disease, MS patients
show shrinkage, or atrophy, of certain structures in the brain’s deep gray
Their imaging studies have shown also that in MS patients these deep
gray-matter structures appear hypointense, or darker than normal, signaling the
presence of iron concentrations. The researchers hypothesize that brain atrophy
is linked to these iron deposits.
“We know that MS patients have defective blood-brain barriers, the filter that
keeps chemicals, like iron, from leaking into the brain,” said Bermel. “Our
hypothesis is that this defect allows iron to accumulate in certain parts of
the brain, which then can be directly neurotoxic to cells, causing atrophy.”
Knowing that interferon beta-1a treatment has a positive effect on brain
atrophy, Bermel and colleagues set out to determine if the pathway of action
was associated with iron concentration. They followed 159 patients who were
enrolled in a randomized, double-blind treatment trial for the relapsing form
of the disease for two years. Eighty-one patients received treatment; 78 who
received placebo served as controls.
Researchers took MRI scans of all patients to determine hypointensity and brain
atrophy at baseline and at two years. Results showed that hypointensity at
baseline was linked to brain atrophy over that time period in controls, but not
in the treatment group. Hypointensity remained unchanged in the treatment
group, but brain atrophy was significantly less.
“These findings suggest that interferon may disrupt the relationship between
baseline T2H (hypointensity) and atrophy over time,” Bermel said, noting that
there may be several explanations for the finding.
“Interferon beta-1a is known to lower the levels of inflammatory cytokines in
the blood of patients with MS. When the body is in a state without
inflammation, as it is normally, its cells, including neurons, can better
regulate their contents and byproducts, including iron. In untreated MS, which
is characterized by brain inflammation, iron may be allowed to build up to
toxic levels in certain brain structures, causing toxic chemical reactions and
death of nerve cells, leading to what we see as brain atrophy on MRI scans.
“Also, interferon is known to help restore the body’s natural blood-brain
barrier, which would keep toxic iron from seeping into the cells,” Bermel said.
“This study shows for the first time that interferon treatment may result in
less brain atrophy in MS through a cascade of events that interferes with the
pathologic iron deposition.”
Additional authors on the study from Buffalo were: Srinivas R. Puli, M.D.,
former research associate in the BNAC; Andrew J. Fabiano, third-year medical
student doing research in the BNAC; Bianca Weinstock-Guttman, M.D., assistant
professor of neurology; Frederick E. Munschauer, M.D., professor and chair of
the Department of Neurology, and Rohit Bakshi, M.D., associate professor of
neurology and director of the BNAC.
Elizabeth Fisher, Ph.D., and Richard A. Rudick, M.D., from the Cleveland
Clinic, performed measurements of whole brain atrophy. Jack H. Simon, M.D.,
Ph.D., from the University of Colorado, performed additional analysis.
The research was funded by a grant from Alpha Omega Alpha and a scholarship
from the American Academy of Neurology to Bermel and by a grant to Bakshi from
the National Institutes of Health.
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Tpasco8136 2009-09-21 15:10:48
If you think prednisone has severe
side effects, wait til you try
Pred is like a cake-walk in
Viviane beulle 2009-09-21 15:11:28
Please, could let me know the name of
the chinese herbs you worked with?
I’d like to study them.
Thanks in advance,