Melanie Reid and Oliver Gillie
Times Online
Thu, 05 Feb 2009
Multiple sclerosis could be prevented through daily vitamin D supplements, scientists told The Times last night.
The first causal link has been established between the "sunshine vitamin" and a gene that increases the risk of MS, raising the possibility that the debilitating auto-immune disease could be eradicated.
George Ebers, Professor of Clinical Neurology at the University of Oxford, claimed that there was hard evidence directly relating both genes and the environment to the origins of MS.
His work suggests that vitamin D deficiency during pregnancy and childhood may increase the risk of a child developing the diease.
He has also established the possibility that genetic vulnerability to MS, apparently initiated by lack of vitamin D, may be passed through families.
These risks might plausibly be reduced by giving vitamin D supplements to pregnant woman and young children.
"I think it offers the potential for treatment which might prevent MS in the future," Professor Ebers said.
"Our research has married two key pieces of the puzzle. The interaction of vitamin D with the gene is very specific and it seems most unlikely to be a coincidence of any kind."
Warnings over sun exposure could now also be called into question - sunlight allows the body to produce the vitamin.
Professor Ebers said: "Serious questions now arise over the wisdom of current advice to limit sun exposure and avoid sunbathing. We also need to give better advice and help to the public on vitamin D supplements, particularly pregnant and nursing mothers."
The news has momentous implications for Scotland and other northern countries, where the incidence of multiple sclerosis is the highest in the world. It will give added urgency to recent moves by Scotland's Chief Medical Officer to consider recommending vitamin D supplements.
Deficiency in vitamin D, caused by lack of exposure to sunshine, has been increasingly linked to the cloudier climate in Scotland and other northern latitudes. The deficiency is twice as common among the Scots as it is amongst the English - and Orkney and Shetland have among the highest rates.
Studies have also shown that fewer people with MS are born in November and more in May, implicating a lack of sunshine during pregnancy.
The breakthrough comes after a groundswell of expert belief in the importance of vitamin D. Last November, at a conference organised by the Scottish Government, international experts urged vitamin D supplements for Scots to be tested "sooner rather than later" to find whether they could improve the nation's health.
Researchers for the World Health Organisation said there should be large, randomised trials as there was strong evidence that increased daily intake of vitamin D could significantly improve health.
The seminar followed evidence, revealed in The Times, that Scotland's poor health record has close links to vitamin D deficiency. Last September this newspaper reported evidence from scientists in Canada that children with early symptoms of multiple sclerosis have low levels of vitamin D.
Until now there has been no scientific proof of the links. However, Professor Ebers and his team have shown that vitamin D affects a particular genetic variant, identified as the one that increases the risk of developing MS threefold.
They suggest that a shortage of the vitamin alters this variant, thus preventing the immune system from functioning normally.
Professor Ebers said: "Whether it's at the core of MS is going to take some further work, but it does look like a reasonably good chance."
Last October Professor Ebers, in an article in The Times, backed the idea of distributing vitamin D supplements in Scotland to guard against conditions that may be linked to a deficiency, including MS.
"It is plausible that some 200 cases a year of MS might be prevented in Scotland alone by giving vitamin D to mothers and children," he wrote.
"Over a trial duration of 25 years, 5,000 cases of this disease might be otherwise prevented.
"The economic impact of each person with MS is at least an extra million pounds during a lifetime.
"Over 25 years £5 billion is at issue in this disease without factoring in the human cost, the increasing rate of MS or inflation. A large-scale programme providing vitamin D could provide scientific evidence."
Disease of the North: MS rates per 100,000 of the population
Canada 240
Scotland 150 - 200
Norway 110
England and Wales 90 - 110
Australia 78
Spain 59
Brazil 18
Sources: Atlas of Multiple Sclerosis
jeudi 5 février 2009
lundi 2 février 2009
Autologous non-myeloablative haemopoietic stem cell transplantation in relapsing-remitting multiple sclerosis: a phase I/II study
The Lancet Neurology, Early Online Publication, 30 January 2009
Background
Autologous non-myeloablative haemopoietic stem cell transplantation is a method to deliver intense immune suppression. We evaluated the safety and clinical outcome of autologous non-myeloablative haemopoietic stem cell transplantation in patients with relapsing-remitting multiple sclerosis (MS) who had not responded to treatment with interferon beta.
Methods
Eligible patients had relapsing-remitting MS, attended Northwestern Memorial Hospital, and despite treatment with interferon beta had had two corticosteroid-treated relapses within the previous 12 months, or one relapse and gadolinium-enhancing lesions seen on MRI and separate from the relapse. Peripheral blood haemopoietic stem cells were mobilised with 2 g per m2 cyclophosphamide and 10 μg per kg per day filgrastim. The conditioning regimen for the haemopoietic stem cells was 200 mg per kg cyclophosphamide and either 20 mg alemtuzumab or 6 mg per kg rabbit antithymocyte globulin. Primary outcomes were progression-free survival and reversal of neurological disability at 3 years post-transplantation. We also sought to investigate the safety and tolerability of autologous non-myeloablative haemopoietic stem cell transplantation.
Findings
Between January, 2003, and February, 2005, 21 patients were treated. Engraftment of white blood cells and platelets was on median day 9 (range day 8—11) and patients were discharged from hospital on mean day 11 (range day 8—13). One patient had diarrhoea due to Clostridium difficile and two patients had dermatomal zoster. Two of the 17 patients receiving alemtuzumab developed late immune thrombocytopenic purpura that remitted with standard therapy. 17 of 21 patients (81%) improved by at least 1 point on the Kurtzke expanded disability status scale (EDSS), and five patients (24%) relapsed but achieved remission after further immunosuppression. After a mean of 37 months (range 24—48 months), all patients were free from progression (no deterioration in EDSS score), and 16 were free of relapses. Significant improvements were noted in neurological disability, as determined by EDSS score (p<0·0001), neurological rating scale score (p=0·0001), paced auditory serial addition test (p=0·014), 25-foot walk (p<0·0001), and quality of life, as measured with the short form-36 (SF-36) questionnaire (p<0·0001).
Interpretation
Non-myeloablative autologous haemopoietic stem cell transplantation in patients with relapsing-remitting MS reverses neurological deficits, but these results need to be confirmed in a randomised trial.
Funding
Division of Immunotherapy, Northwestern University.
Background
Autologous non-myeloablative haemopoietic stem cell transplantation is a method to deliver intense immune suppression. We evaluated the safety and clinical outcome of autologous non-myeloablative haemopoietic stem cell transplantation in patients with relapsing-remitting multiple sclerosis (MS) who had not responded to treatment with interferon beta.
Methods
Eligible patients had relapsing-remitting MS, attended Northwestern Memorial Hospital, and despite treatment with interferon beta had had two corticosteroid-treated relapses within the previous 12 months, or one relapse and gadolinium-enhancing lesions seen on MRI and separate from the relapse. Peripheral blood haemopoietic stem cells were mobilised with 2 g per m2 cyclophosphamide and 10 μg per kg per day filgrastim. The conditioning regimen for the haemopoietic stem cells was 200 mg per kg cyclophosphamide and either 20 mg alemtuzumab or 6 mg per kg rabbit antithymocyte globulin. Primary outcomes were progression-free survival and reversal of neurological disability at 3 years post-transplantation. We also sought to investigate the safety and tolerability of autologous non-myeloablative haemopoietic stem cell transplantation.
Findings
Between January, 2003, and February, 2005, 21 patients were treated. Engraftment of white blood cells and platelets was on median day 9 (range day 8—11) and patients were discharged from hospital on mean day 11 (range day 8—13). One patient had diarrhoea due to Clostridium difficile and two patients had dermatomal zoster. Two of the 17 patients receiving alemtuzumab developed late immune thrombocytopenic purpura that remitted with standard therapy. 17 of 21 patients (81%) improved by at least 1 point on the Kurtzke expanded disability status scale (EDSS), and five patients (24%) relapsed but achieved remission after further immunosuppression. After a mean of 37 months (range 24—48 months), all patients were free from progression (no deterioration in EDSS score), and 16 were free of relapses. Significant improvements were noted in neurological disability, as determined by EDSS score (p<0·0001), neurological rating scale score (p=0·0001), paced auditory serial addition test (p=0·014), 25-foot walk (p<0·0001), and quality of life, as measured with the short form-36 (SF-36) questionnaire (p<0·0001).
Interpretation
Non-myeloablative autologous haemopoietic stem cell transplantation in patients with relapsing-remitting MS reverses neurological deficits, but these results need to be confirmed in a randomised trial.
Funding
Division of Immunotherapy, Northwestern University.
Cellules souches - Résultats encourageants contre la sclérose en plaque
Cécile Dumas
Sciences-et-Avenir.com
30/01/09
Un petit essai clinique, mené sur 21 personnes atteintes de sclérose en plaques, montre qu’une ‘auto-greffe’ de cellules souches issues de la moelle osseuse permet d'améliorer l’état des patients. Ces résultats encourageants devront être vérifiés sur une plus large cohorte et comparés à d’autres traitements pour être consolidés.
Environ 80.000 personnes en France souffrent de cette maladie dont les formes et l’évolution varient grandement d’un patient à l’autre. La sclérose en plaque est caractérisée par une destruction de la myéline, la couche protectrice qui entoure les fibres nerveuses et qui transporte l’influx nerveux. Troubles de la coordination, problèmes de vue, vertiges, problèmes moteurs sont quelques-uns des symptômes de la maladie.
Il s’agit d’une affection auto-immune, autrement dit d’une attaque du système immunitaire, via des lymphocytes devenus agressifs, qui s’en prennent à l’organisme lui-même (en l’occurrence à la myéline). C’est pourquoi des chercheurs essaient de ‘’reprogrammer’’ le système immunitaire en greffant des cellules souches hématopoïétiques, issues de la moelle osseuse, précurseurs des globules rouges et des globules blancs (dont font partie les lymphocytes).
L’équipe de Richard Burt, de Chicago (USA), a prélevé des cellules souches hématopoïétiques chez les patients. Ceux-ci ont ensuite subi un traitement destiné à détruire les lymphocytes qui attaquent leur myéline avant de recevoir une greffe autologue de cellules souches. Trois ans après, 17 patients sur 21 ont connu une amélioration de leur état (définie comme un point gagné sur l’échelle de Kurtzke utilisée pour décrire l’évolution de la maladie)*.
Ce n’est pas la première fois que cette technique est testée sur des personnes mais les précédents essais n’avaient pas obtenus de résultats concluants. La différence tient à l’âge des patients et au stade de la maladie : il s’agit de trentenaires dont la sclérose évolue par poussées, suivies de périodes de rémissions. C’est généralement la première phase de la maladie (dite forme rémittente), suivie d’une phase progressive où les symptômes semblent irréversibles.
* Travaux publiés en ligne (édition anticipée) par The Lancet Neurology (en mars dans la revue papier).
Sciences-et-Avenir.com
30/01/09
Un petit essai clinique, mené sur 21 personnes atteintes de sclérose en plaques, montre qu’une ‘auto-greffe’ de cellules souches issues de la moelle osseuse permet d'améliorer l’état des patients. Ces résultats encourageants devront être vérifiés sur une plus large cohorte et comparés à d’autres traitements pour être consolidés.
Environ 80.000 personnes en France souffrent de cette maladie dont les formes et l’évolution varient grandement d’un patient à l’autre. La sclérose en plaque est caractérisée par une destruction de la myéline, la couche protectrice qui entoure les fibres nerveuses et qui transporte l’influx nerveux. Troubles de la coordination, problèmes de vue, vertiges, problèmes moteurs sont quelques-uns des symptômes de la maladie.
Il s’agit d’une affection auto-immune, autrement dit d’une attaque du système immunitaire, via des lymphocytes devenus agressifs, qui s’en prennent à l’organisme lui-même (en l’occurrence à la myéline). C’est pourquoi des chercheurs essaient de ‘’reprogrammer’’ le système immunitaire en greffant des cellules souches hématopoïétiques, issues de la moelle osseuse, précurseurs des globules rouges et des globules blancs (dont font partie les lymphocytes).
L’équipe de Richard Burt, de Chicago (USA), a prélevé des cellules souches hématopoïétiques chez les patients. Ceux-ci ont ensuite subi un traitement destiné à détruire les lymphocytes qui attaquent leur myéline avant de recevoir une greffe autologue de cellules souches. Trois ans après, 17 patients sur 21 ont connu une amélioration de leur état (définie comme un point gagné sur l’échelle de Kurtzke utilisée pour décrire l’évolution de la maladie)*.
Ce n’est pas la première fois que cette technique est testée sur des personnes mais les précédents essais n’avaient pas obtenus de résultats concluants. La différence tient à l’âge des patients et au stade de la maladie : il s’agit de trentenaires dont la sclérose évolue par poussées, suivies de périodes de rémissions. C’est généralement la première phase de la maladie (dite forme rémittente), suivie d’une phase progressive où les symptômes semblent irréversibles.
* Travaux publiés en ligne (édition anticipée) par The Lancet Neurology (en mars dans la revue papier).
Turning down gene expression promotes nerve cell maintenance
February 2nd, 2009
Anyone with a sweet tooth knows that too much of a good thing can lead to negative consequences. The same can be said about the signals that help maintain nerve cells, as demonstrated in a new study of myelin, a protein key to efficient neuronal transmission.
Normal nerve cells have a myelin sheath, which, much like the insulation on a cable, allows for rapid and efficient signal conduction. However, in several diseases - the most well-known being multiple sclerosis - demyelination processes cause the breakdown of this "insulation", and lead to deficits in perception, movement, cognition, etc. Thus, in order to help patients of demyelinating disease, researchers are studying the pathways that control myelin formation and maintenance.
A new study by University of California scientists examines the role of a structural protein, called lamin, in maintaining myelin. They found that, while lamin is necessary in the initial stages of myelin formation, too much lamin promotes myelin breakdown. Further investigation led the researchers to the discovery of a signal that fine-tunes lamin expression. This signal, a microRNA called miR-23, can turn down lamin gene expression, and thereby prevent demyelination due to lamin overexpression.
This new work reported in Disease Models & Mechanisms (DMM), adds another piece to the puzzle that is understanding myelin formation and maintenance. Additionally, the identification of miR-23 as a myelin regulator introduces a new potential drug target in developing treatments for demyelinating illness.
The report was written Shu-Ting Lin and Ying-Hui Fu at the Department of Neurology, University of California San Francisco. The report is published in the March/April issue of Disease Models & Mechanisms (DMM), a research journal published by The Company of Biologists, a non-profit based in Cambridge, UK.
Anyone with a sweet tooth knows that too much of a good thing can lead to negative consequences. The same can be said about the signals that help maintain nerve cells, as demonstrated in a new study of myelin, a protein key to efficient neuronal transmission.
Normal nerve cells have a myelin sheath, which, much like the insulation on a cable, allows for rapid and efficient signal conduction. However, in several diseases - the most well-known being multiple sclerosis - demyelination processes cause the breakdown of this "insulation", and lead to deficits in perception, movement, cognition, etc. Thus, in order to help patients of demyelinating disease, researchers are studying the pathways that control myelin formation and maintenance.
A new study by University of California scientists examines the role of a structural protein, called lamin, in maintaining myelin. They found that, while lamin is necessary in the initial stages of myelin formation, too much lamin promotes myelin breakdown. Further investigation led the researchers to the discovery of a signal that fine-tunes lamin expression. This signal, a microRNA called miR-23, can turn down lamin gene expression, and thereby prevent demyelination due to lamin overexpression.
This new work reported in Disease Models & Mechanisms (DMM), adds another piece to the puzzle that is understanding myelin formation and maintenance. Additionally, the identification of miR-23 as a myelin regulator introduces a new potential drug target in developing treatments for demyelinating illness.
The report was written Shu-Ting Lin and Ying-Hui Fu at the Department of Neurology, University of California San Francisco. The report is published in the March/April issue of Disease Models & Mechanisms (DMM), a research journal published by The Company of Biologists, a non-profit based in Cambridge, UK.
dimanche 18 janvier 2009
Eyes reveal health secrets of the brain
Duncan Graham-Rowe
New Scientist
Sun, 18 Jan 2009
The eyes may be the windows to the soul, but they also make pretty good peepholes into the brain. Thanks to an optical version of ultrasound, it is becoming possible to locate and monitor the growth of brain tumours, and to track neurodegenerative conditions like multiple sclerosis, Alzheimer's and Parkinson's disease - all by peering into the eye.The brain is connected to each eye by an optic nerve, so any degeneration of the brain caused by such diseases can also damage cells along the nerve and in the retina, says Helen Danesh-Meyer, an eye surgeon and neuro-ophthalmologist at the University of Auckland Medical School in New Zealand. Indeed, a loss of visual function is one of the first symptoms in many people with a neurodegenerative condition.
Although evidence of a link between degeneration of the optic nerve and diseases such as Alzheimer's has been around since the late 1980s, without instruments capable of measuring the retinal changes accurately it is only recently that this knowledge could be put to use, says Danesh-Meyer.
The accuracy of ophthalmological tools has greatly improved in the last few years. Developments include a type of laser-camera technique called Heidelberg retina tomography (HRT), and a laser device called GDx, both of which can be used to scan the shape and thickness of optical nerve fibres at the back of the eye.
Both tools are now widely used to manage glaucoma, but in 2006 Danesh-Meyer became one of the first researchers to use them to study neurodegenerative diseases by looking at the region of the retina where ganglion cells meet to form the optic nerve - a region known as the optic nerve disc (OND). In a trial involving 40 Alzheimer's patients and 50 healthy volunteers, she was able to show that people with Alzheimer's had a distinctive enlargement to a cup-shaped part of their OND and a progressive thinning of the retinal nerve fibres within the disc.
Following this discovery, researchers have been using even more accurate instruments to track degenerative changes in the OND to monitor the progression of diseases like Alzheimer's, Parkinson's and MS. But it has been the emergence of optical coherence tomography (OCT) that appears most promising: it became commercially available in 2006 and is fast becoming a standard tool for the management of glaucoma and diabetic retinopathy. When applied to the OND, it produces highly detailed two and three-dimensional images of the subsurface retinal tissue, says Denise Valenti at Boston University, who has been using OCT to study Parkinson's and Alzheimer's.
The technique works very much like ultrasound, but bounces light off the tissue instead of sound waves. One beam of light is fired at the tissue and another at a reference mirror. When the reflected beams have travelled an identical distance, interference will make their combined beam brighter than if the distances are different. So by reflecting one beam off of different layers of tissue, and moving the reference mirror until the combined reflected beam is brightest, the technique can measure the depths of each section of tissue and build up a detailed image of its structure.
It has proved particularly useful in ophthalmology because the semi-transparent nature of retinal tissue makes it possible for OCT to penetrate to greater depths - up to several millimetres. When applied to the OND it can give information about both the shape and thickness of retinal nerve fibres, allowing even subtle changes to be tracked.
Such changes can be used to monitor the progression of diseases non-invasively and relatively cheaply. Unlike MRI, which is expensive and can require patients to remain still for an hour or more, OCT is increasingly available in clinics and can be carried out in a few minutes. "It's extremely inexpensive compared to other tests," says Valenti.
MRI : IRM
One possibility is to use OCT to monitor the effectiveness of treatments for neurodegenerative diseases, says Danesh-Meyer: "These drugs can have a lot of side effects, so if they are not having a benefit then you won't want to continue with them."
Laura Balcer, a neurologist at the University of Pennsylvania School of Medicine in Philadelphia, has been using OCT on patients taking part in MS drug trials to try to establish if the system can accurately gauge drug efficacy. Such an objective tool would allow symptoms to be picked up that might otherwise go unreported, she says. For example, OCT has already shown that even in people with MS whose eye function is normal, there are marked differences in OND shape and fibre thickness compared with healthy people. "MS researchers are very excited about OCT," she says.
The technology is also proving its value as a tool for monitoring brain tumours, which can affect vision by pressing on the optic nerve. Such pressure will cause damage to different parts of the OND, depending on where in the brain the tumour is located, says Danesh-Meyer. What's more, the extent of the thinning of the nerve-disc fibre can also reveal whether vision will be restored upon removal of the tumour.
In the case of one patient who was 24 weeks pregnant following several IVF attempts, OCT monitoring allowed surgeons to hold off on removing her brain tumour until well into the third trimester, when the fetus had a better chance of survival. The usual treatment would have been to operate immediately to prevent permanent vision loss, but this would have risked inducing premature labour. By monitoring the compression on the optic nerve to ensure it did not reach the point at which permanent damage was inevitable, Danesh-Meyer was able to keep tabs on the tumour's growth and delay the surgery. As a result, the baby was born safely and the patient kept her vision.
The ultimate aim for many using OCT is to diagnose diseases before symptoms arise. The difficulty with this is that the thickness of retinal nerve fibres can vary from person to person, says Danesh-Meyer, so there is not always a clear baseline from which to compare patient scans.
Eventually though, the low cost and simplicity of the technology may make it feasible for people to be given an OCT scan of each eye at a young age, to give doctors a record of their healthy retinal nerve, says Danesh-Meyer. With regular screening, some neurological conditions could be spotted incredibly early. "We're really just at the cusp of knowing where this is all going."
mercredi 7 janvier 2009
Extreme Mercury Toxicity Sidelines Actor Jeremy Piven
Chicago actor Jeremy Piven has unexpectedly left the cast of the Broadway revival of "Speed-the-Plow" because of a mercury count that his doctor said was the highest level he'd ever seen.
Piven, 43, wanted to continue but he was advised to stop. Dr. Carlon Colker, who had been treating Piven, said Piven was suffering from "extreme mercury toxicity" and that "a test revealed that Jeremy had ... six times a healthy amount of mercury in his system." Piven has long been a sushi eater, often twice a day, which may be the ultimate cause of the problem.
A major symptom of mercury poisoning is extreme fatigue. Piven was also experiencing neuro-muscular dysfunction, which resulted in his having trouble lifting his arms and legs.
Piven has won Emmy Awards for his role as foul-mouthed Hollywood agent Ari Gold in the HBO series Entourage. He had been performing to critical praise in "Speed-the-Plow" since October.
http://articles.mercola.com/sites/articles/archive/2009/01/06/extreme-mercury-toxicity-sidelines-actor-jeremy-piven.aspx
Piven, 43, wanted to continue but he was advised to stop. Dr. Carlon Colker, who had been treating Piven, said Piven was suffering from "extreme mercury toxicity" and that "a test revealed that Jeremy had ... six times a healthy amount of mercury in his system." Piven has long been a sushi eater, often twice a day, which may be the ultimate cause of the problem.
A major symptom of mercury poisoning is extreme fatigue. Piven was also experiencing neuro-muscular dysfunction, which resulted in his having trouble lifting his arms and legs.
Piven has won Emmy Awards for his role as foul-mouthed Hollywood agent Ari Gold in the HBO series Entourage. He had been performing to critical praise in "Speed-the-Plow" since October.
http://articles.mercola.com/sites/articles/archive/2009/01/06/extreme-mercury-toxicity-sidelines-actor-jeremy-piven.aspx
lundi 10 novembre 2008
Another Tysabri patient has PML
boston.com
Todd Wallack
Globe Staff / October 30, 2008
Biogen Idec Inc. reported late yesterday that another patient contracted a potentially fatal brain disease after taking the multiple sclerosis drug Tysabri, the third case since the biotechnology giant reintroduced the treatment two years ago. The news sent shares tumbling 12.1 percent in after-hours trading.
The Cambridge company originally launched Tysabri in 2004, but pulled it from the market just three months later after a few patients were diagnosed with progressive multifocal leukoencephalopathy, or PML. Two died. The company reintroduced Tysabri with its Irish partner, Elan Corp., in July 2006 with stricter prescribing guidelines - designed to minimize the risk of contracting the disease - and a warning that one in 1,000 patients could contract PML.
Three months ago, Biogen Idec said two additional patients had contracted PML, sparking fears that some doctors and patients will decide Tysabri isn't worth the risk.
But despite the chance of contracting the disease, many patients have been willing to use Tysabri to treat serious forms of MS and Crohn's disease when other treatments fail. As of the end of September, more than 35,500 patients were taking Tysabri, and Biogen Idec predicts 100,000 will use the drug by 2010.
Biogen Idec provided few details about the latest PML case, saying only the patient is receiving medical care.
Todd Wallack
Globe Staff / October 30, 2008
Biogen Idec Inc. reported late yesterday that another patient contracted a potentially fatal brain disease after taking the multiple sclerosis drug Tysabri, the third case since the biotechnology giant reintroduced the treatment two years ago. The news sent shares tumbling 12.1 percent in after-hours trading.
The Cambridge company originally launched Tysabri in 2004, but pulled it from the market just three months later after a few patients were diagnosed with progressive multifocal leukoencephalopathy, or PML. Two died. The company reintroduced Tysabri with its Irish partner, Elan Corp., in July 2006 with stricter prescribing guidelines - designed to minimize the risk of contracting the disease - and a warning that one in 1,000 patients could contract PML.
Three months ago, Biogen Idec said two additional patients had contracted PML, sparking fears that some doctors and patients will decide Tysabri isn't worth the risk.
But despite the chance of contracting the disease, many patients have been willing to use Tysabri to treat serious forms of MS and Crohn's disease when other treatments fail. As of the end of September, more than 35,500 patients were taking Tysabri, and Biogen Idec predicts 100,000 will use the drug by 2010.
Biogen Idec provided few details about the latest PML case, saying only the patient is receiving medical care.
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