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MS Damage May Be Reversed By Leukemia Drug
Some interesting news about an experimental drug for MS. Overall the results are very encouraging, though excitement is tempered by the risk of the serious side effects, in particular the deaths of participant in the study due to developing immune thrombocytopenic purpura. Read on:
"MS Damage May Be Reversed By Leukemia Drug
--------------------------------------------------------------------------------
Researchers in the UK found that alemtuzumab, a drug initially developed to treat leukemia, stopped the advance of multiple sclerosis (MS) in patients with early stage active relapsing-remitting multiple sclerosis (RRMS) and may even have reversed some of the damage caused by this debilitating neurological disease.
The study was the work of scientists at the University of Cambridge and was published online on 23rd October in the New England Journal of Medicine (NEJM).
The Cambridge group has a long connection with alemtuzumab, a monoclonal antibody that started out as Campath-1H and is now licensed for the treatment of chronic lymphocytic leukaemia. The drug has also been tested for use in other diseases like MS that are caused by an overactive immune system.
MS is a disease where the immune system attacks nerve fibres and the protective myelin sheath that surrounds them. The damage means that electrical signals can't travel so well in the nerve fibres and leak through the damaged sheath, leading to loss of physical skills, sensation, vision, bladder control, and intellectual ability.
Alemtuzumab is a humanized monoclonal antibody that targets the immune system cells that attack the nerve fibres and the myelin sheath.
The study was a phase 2, randomized, blinded trial involving 334 participants who had not been treated for early, relapsing-remitting multiple sclerosis (RRMS). They had all scored 3.0 or less on the Expanded Disability Status Scale and had had the disease for three years or less.
Relapsing-remitting multiple sclerosis (RRMS) is the most common form of the disease and is often followed by the more disabling form which is called secondary-progressive MS (SPMS).
The participants were randomized to one of two groups. One group received alemtuzumab intravenously (at a dose of either 12 or 24 mg a day) for five days and then again for three days one year later. The other group received 44 microgram injections of interferon beta-1a three times a week.
The participants were followed for 36 months to find out how effective the treatments were and how their disabilities changed.
The alemtuzumab therapy was stopped after one annual cycle because three patients died after developing immune thrombocytopenic purpura (low platelet count). The interferon beta-1a group continued with treatment for the rest of the study period.
The results showed that:
Compared with interferon beta-1a, alemtuzumab significantly reduced the rate of sustained accumulation of disability (26.2 versus 9.2 per cent respectively).
The annual rate of relapse in the interferon beta-1a group was significantly higher than the alemtuzumab group (0.36 versus 0.10).
On a 10-point scale of disability, the mean score significantly improved by 0.39 point in the alemtuzumab group and worsened by 0.38 point in the interferon beta-1a group.
The lesion burden (a way of assessing the neurological damage of the disease using a method called T2-weighted magnetic resonance imaging or MRI) in the alemtuzumab group was lower than that of the interferon beta-1a group.
From month 12 to month 36 of the study, brain volume (measured by viewing T1-MRI scans) increased in the alemtuzumab group but decreased in the interferon beta-1a group.
There were some serious increases in adverse events in the alemtuzumab group compared to the interferon beta-1a group. These were: two types of autoimmunity event (thyroid disorders [23 versus 3 per cent respectively] and immune thrombocytopenic purpura [3 versus 1 per cent]) and infections (66 versus 47 per cent respectively).
There were no signficant differences between the two doses of alemtuzumab (12 mg and 24 mg).
The researchers concluded that:
"In patients with early, relapsing-remitting multiple sclerosis, alemtuzumab was more effective than interferon beta-1a but was associated with autoimmunity, most seriously manifesting as immune thrombocytopenic purpura. The study was not powered to identify uncommon adverse events."
The next stage will be a phase 3 trial, which principal investigator Alastair Compston, Professor of Neurology and the Head of the Department of Clinical Neurosciences at the University of Cambridge hopes will confirm that alemtuzumab "can both stabilize and allow some recovery of what had previously been assumed to be irreversible disabilities".
Head of research at the MS Society in the UK, Lee Dunster, welcome the study. He said in a press statement that:
"The MS Society has been following this trial closely and we are delighted that it has reported such positive results."
"This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in, day out," said Dunster, and although more research is needed to prove the drug's long term effectiveness, the society is:
"Very much looking forward to the results of the next stage of this important research, which is already underway."
There are nearly 100,000 people living with MS in the UK, about 400,000 in the US and several million worldwide."
-----------------------------------------------------------------------------------------------
"Alemtuzumab vs. Interferon Beta-1a in Early Multiple Sclerosis."
The CAMMS223 Trial Investigators.
N Engl J Med , Volume 359, Number 17, pages 1786-1801, published online October 23, 2008 .
"MS Damage May Be Reversed By Leukemia Drug
--------------------------------------------------------------------------------
Researchers in the UK found that alemtuzumab, a drug initially developed to treat leukemia, stopped the advance of multiple sclerosis (MS) in patients with early stage active relapsing-remitting multiple sclerosis (RRMS) and may even have reversed some of the damage caused by this debilitating neurological disease.
The study was the work of scientists at the University of Cambridge and was published online on 23rd October in the New England Journal of Medicine (NEJM).
The Cambridge group has a long connection with alemtuzumab, a monoclonal antibody that started out as Campath-1H and is now licensed for the treatment of chronic lymphocytic leukaemia. The drug has also been tested for use in other diseases like MS that are caused by an overactive immune system.
MS is a disease where the immune system attacks nerve fibres and the protective myelin sheath that surrounds them. The damage means that electrical signals can't travel so well in the nerve fibres and leak through the damaged sheath, leading to loss of physical skills, sensation, vision, bladder control, and intellectual ability.
Alemtuzumab is a humanized monoclonal antibody that targets the immune system cells that attack the nerve fibres and the myelin sheath.
The study was a phase 2, randomized, blinded trial involving 334 participants who had not been treated for early, relapsing-remitting multiple sclerosis (RRMS). They had all scored 3.0 or less on the Expanded Disability Status Scale and had had the disease for three years or less.
Relapsing-remitting multiple sclerosis (RRMS) is the most common form of the disease and is often followed by the more disabling form which is called secondary-progressive MS (SPMS).
The participants were randomized to one of two groups. One group received alemtuzumab intravenously (at a dose of either 12 or 24 mg a day) for five days and then again for three days one year later. The other group received 44 microgram injections of interferon beta-1a three times a week.
The participants were followed for 36 months to find out how effective the treatments were and how their disabilities changed.
The alemtuzumab therapy was stopped after one annual cycle because three patients died after developing immune thrombocytopenic purpura (low platelet count). The interferon beta-1a group continued with treatment for the rest of the study period.
The results showed that:
Compared with interferon beta-1a, alemtuzumab significantly reduced the rate of sustained accumulation of disability (26.2 versus 9.2 per cent respectively).
The annual rate of relapse in the interferon beta-1a group was significantly higher than the alemtuzumab group (0.36 versus 0.10).
On a 10-point scale of disability, the mean score significantly improved by 0.39 point in the alemtuzumab group and worsened by 0.38 point in the interferon beta-1a group.
The lesion burden (a way of assessing the neurological damage of the disease using a method called T2-weighted magnetic resonance imaging or MRI) in the alemtuzumab group was lower than that of the interferon beta-1a group.
From month 12 to month 36 of the study, brain volume (measured by viewing T1-MRI scans) increased in the alemtuzumab group but decreased in the interferon beta-1a group.
There were some serious increases in adverse events in the alemtuzumab group compared to the interferon beta-1a group. These were: two types of autoimmunity event (thyroid disorders [23 versus 3 per cent respectively] and immune thrombocytopenic purpura [3 versus 1 per cent]) and infections (66 versus 47 per cent respectively).
There were no signficant differences between the two doses of alemtuzumab (12 mg and 24 mg).
The researchers concluded that:
"In patients with early, relapsing-remitting multiple sclerosis, alemtuzumab was more effective than interferon beta-1a but was associated with autoimmunity, most seriously manifesting as immune thrombocytopenic purpura. The study was not powered to identify uncommon adverse events."
The next stage will be a phase 3 trial, which principal investigator Alastair Compston, Professor of Neurology and the Head of the Department of Clinical Neurosciences at the University of Cambridge hopes will confirm that alemtuzumab "can both stabilize and allow some recovery of what had previously been assumed to be irreversible disabilities".
Head of research at the MS Society in the UK, Lee Dunster, welcome the study. He said in a press statement that:
"The MS Society has been following this trial closely and we are delighted that it has reported such positive results."
"This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in, day out," said Dunster, and although more research is needed to prove the drug's long term effectiveness, the society is:
"Very much looking forward to the results of the next stage of this important research, which is already underway."
There are nearly 100,000 people living with MS in the UK, about 400,000 in the US and several million worldwide."
-----------------------------------------------------------------------------------------------
"Alemtuzumab vs. Interferon Beta-1a in Early Multiple Sclerosis."
The CAMMS223 Trial Investigators.
N Engl J Med , Volume 359, Number 17, pages 1786-1801, published online October 23, 2008 .
No, this is not about Rituxan [trade name for Rituximab].
This article is about alemtuzumab, trade name is Campath.
Both drugs are classed as monoclonal antibodies, and both treat cancer, but different kinds as I understand it.
I hope that the Rituxan is of benefit to you, both for your MS and arthritis. Do you know if the dosage/protocol is the same for treating both diseases?
This article is about alemtuzumab, trade name is Campath.
Both drugs are classed as monoclonal antibodies, and both treat cancer, but different kinds as I understand it.
I hope that the Rituxan is of benefit to you, both for your MS and arthritis. Do you know if the dosage/protocol is the same for treating both diseases?
Do you happen to know if this drug is named Rituxan? I am on that now (just started) for arthritis and the doctors claim it will serve as my MS drug also. It hasn't been approved for MS - it's still in trials so they can't use it as a treatment for our MS legally yet. It was originally a cancer med and was approved for certain types of arthritis. Some doctors are able to give it to their MS patients is they have another disease to claim that's why it was given.
Everything I have been given has failed and I thought it sounded good but if it's the same as the one you were talking about I'm having second thoughts.
Thanks,
Erin0313
Everything I have been given has failed and I thought it sounded good but if it's the same as the one you were talking about I'm having second thoughts.
Thanks,
Erin0313
DV,
I first encountered immunothromocytopenia purpura (did I spell it right after all these years?) when our daughter was 3 years old. She had been on repeated rounds of antibiotics for ear infections and eventually her spleen stopped working. By the time it was recognized that she had all these hemmorages going on all over her body her platelet( is that the right thing?) count had dropped to 15,000. She had so many bruises all over her body if my pediatrician hadn't known me so well I think they would have called children's protective services and looked at it as an abuse case. They had me take her immediately to the hospital, did a bone marrow looking for cancers - fortunately there were none. Then started her on steroids. When her count got to 50,000 we were allowed to go home but she continued on steroids for some time to head off the possibility of hemmoraging. That was 25 years ago and the memory is almost like it happened yesterday. At least there's something left in my brain! :-)
My best,
Lulu
I first encountered immunothromocytopenia purpura (did I spell it right after all these years?) when our daughter was 3 years old. She had been on repeated rounds of antibiotics for ear infections and eventually her spleen stopped working. By the time it was recognized that she had all these hemmorages going on all over her body her platelet( is that the right thing?) count had dropped to 15,000. She had so many bruises all over her body if my pediatrician hadn't known me so well I think they would have called children's protective services and looked at it as an abuse case. They had me take her immediately to the hospital, did a bone marrow looking for cancers - fortunately there were none. Then started her on steroids. When her count got to 50,000 we were allowed to go home but she continued on steroids for some time to head off the possibility of hemmoraging. That was 25 years ago and the memory is almost like it happened yesterday. At least there's something left in my brain! :-)
My best,
Lulu
Will do!
The only reason I know anything about ITP is because my mother was dx'ed with this a few years ago. She was getting more and more tired, this went on for months, finally daignosed with ITP and started on oral prednisone. She had all of its nasty side effects but has been off the meds for more than a year. They keep a close eye on her platelet count, and fortunately it has remained stable even since going off the prednisone. No idea how she developed it, so it's just called idiopathic. Before this happened I had never heard of it. At the time, I don't think I fully appreciated how serious this was. Now that she has a small abdominal aortic aneurysm, I have more than enough to worry about. :(
BTW, since then I have a friend who gets ITP whenever she's pregnant, so she has to be watched carefully. Her doc was not happy when she got pregnant for the third time. Fortunately for her, the ITP goes away after the baby's born.
Our bodies do some very strange things, don't they?
The only reason I know anything about ITP is because my mother was dx'ed with this a few years ago. She was getting more and more tired, this went on for months, finally daignosed with ITP and started on oral prednisone. She had all of its nasty side effects but has been off the meds for more than a year. They keep a close eye on her platelet count, and fortunately it has remained stable even since going off the prednisone. No idea how she developed it, so it's just called idiopathic. Before this happened I had never heard of it. At the time, I don't think I fully appreciated how serious this was. Now that she has a small abdominal aortic aneurysm, I have more than enough to worry about. :(
BTW, since then I have a friend who gets ITP whenever she's pregnant, so she has to be watched carefully. Her doc was not happy when she got pregnant for the third time. Fortunately for her, the ITP goes away after the baby's born.
Our bodies do some very strange things, don't they?
I caught three interesting points out of this.
1) They studied the drug on very new cases of MS and those with very little accumulated disability. Several prior studies have indicated that this group is the most likely to benefit from all treatments
2) The alemtuzumab group actually saw an INCREASE in brain volume, implying the regrowth of previously "lost" brain cells. This blew me away!
3) 3 deaths in a group of about 68 people - not good. It is a small group, but the 3% death rate in the 2 years is very worrisome. Compare that with the 1 in 1000 deaths (0.1%) of Tysabri that gets people worried about using it.
4) Clearly they are onto something.!
DeeBee - Would you add this to the Health Pages under RESEARCH?
Quix
1) They studied the drug on very new cases of MS and those with very little accumulated disability. Several prior studies have indicated that this group is the most likely to benefit from all treatments
2) The alemtuzumab group actually saw an INCREASE in brain volume, implying the regrowth of previously "lost" brain cells. This blew me away!
3) 3 deaths in a group of about 68 people - not good. It is a small group, but the 3% death rate in the 2 years is very worrisome. Compare that with the 1 in 1000 deaths (0.1%) of Tysabri that gets people worried about using it.
4) Clearly they are onto something.!
DeeBee - Would you add this to the Health Pages under RESEARCH?
Quix
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