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    You are here : Home » MS Research News » Drugs » Statins


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    Statin may slow progressive MS

    StatinsHigh-dose simvastatin (Zocor) significantly reduced brain atrophy and slowed advancement of disability for 2 years in patients with secondary progressive multiple sclerosis, researchers said here.

    In a 140-patient randomized trial, patients receiving 80 mg/day of simvastatin had an annualized rate of brain volume loss of just 0.298% compared with 0.589% among those given placebo (P=0.003), reported Jeremy Chataway, MA, PhD, of University College London in England.

    Significant reductions in disability progression, as measured by EDSS and MS Impact Score (MSIS), were also seen with simvastatin in the trial, he told attendees at the annual meeting of the European Committee for Treatment and Research in Multiple Sclerosis.

    On the other hand, differences between the treatment groups in specific functional outcomes, such as walking ability and hand dexterity, did not reach statistical significance.

    But, Chataway noted, despite the high dose of simvastatin, adverse effects were similar between groups and there were no cases of serious muscle toxicity. "Treatment was generally very well tolerated," he said.

    With the advent of several effective drugs to prevent MS relapses, the major unmet clinical need in the disease is treatment for progressive forms. Most patients with relapsing-remitting MS eventually develop the secondary progressive form, in which disability continues to increase even though acute attacks have stopped.

    Because statin drugs have a range of anti-inflammatory effects, apart from their cholesterol-lowering activity, they have attracted attention as a possible therapy for MS.

    A 2004 trial in patients with relapsing-remitting MS showed reductions in brain lesions as seen in MRI scans, suggesting an effect on the underlying disease process. Other trials were conducted in this form of the disease, which ultimately pointed to a lack of clinical benefit.

    But researchers now believe that the disease changes its basic nature when converting from relapsing-remitting to progressive, such that statins might have more benefit at the later stage.

    That prompted the current trial, in which patients with established secondary progressive MS were randomized to high-dose simvastatin or placebo for 2 years.

    The investigators chose brain atrophy as the trial's primary endpoint because, Chataway told MedPage Today, they wanted to mainly evaluate effects on the underlying disease process at this stage of development. He said that a phase III trial would ideally use clinical outcomes as primary endpoints.

    Brain MRI scans were performed 2 weeks before starting treatment, after 1 year, and after 2 years, with the final scan taken 30 days after the last drug dose. Ten patients had missing or inadequate MRIs, leaving 130 in the efficacy analysis.

    Mean participant age was about 51, with an average duration of progressive MS of 7 years. About two-thirds of the sample were women. Some 14% had experienced a relapse within the past year and 18% had had one within the previous 2 years, with a higher rate of such relapses in patients randomized to placebo.

    Median EDSS score at baseline was 6, with a mean of 5.8. Mean MSIS score was 70.

    Patients assigned to simvastatin received 40 mg/day for the first month, with the dosage then increased to 80 mg/day for the remainder of the study. Compliance was good, with 70% to 90% of patients taking the full protocol dose at any given point.

    For the primary outcome of annualized reduction in total brain volume, the difference between the simvastatin and placebo groups came to 0.254 percentage points favoring the statin group (95% CI 0.085 to 0.423).

    The following secondary outcomes, expressed as the difference in change from baseline with simvastatin versus placebo, also showed a significant advantage for active treatment:

    EDSS score: -0.254 (95% CI -0.464 to -0.069)
    MSIS total score: -4.78 (95% CI -9.39 to -0.02)
    MSIS physical subscore: -3.73 (95% CI -7.18 to -0.28)

    Chataway noted that about 10% of patients in the simvastatin group showed an actual improvement of at least 0.5 points relative to baseline in EDSS scores, compared with no one in the placebo group.

    All other secondary clinical outcome measures also favored simvastatin but failed to reach statistical significance. These included the MSIS psychological subscore and functional abilities evaluated with the MS Functional Composite index, both overall and for individual types of activity.

    No differences between treatment groups were seen in the number or rate of new and enlarging T2 lesions or in relapses, but Chataway told MedPage Today that such results would be expected in the secondary progressive population.

    About 20% of patients in both groups had adverse events judged by the blinded investigators as treatment-related. Chataway said the group was on alert for muscle-related complaints because of the high statin dose used, but the concerns were not borne out.

    He told MedPage Today that not only was a phase III trial warranted in secondary progressive MS, but also a phase II study in primary progressive MS.

    At a press conference held after Chataway's report, leaders of ECTRIMS said the findings were encouraging but that it was too soon to say that simvastatin is effective against secondary progressive MS.

    Michel Clanet, MD, the group's president, pointed out that brain atrophy was a surrogate outcome. Before clinicians should consider prescribing statins in this population, there will need to be conclusive proof of disability prevention, he suggested.

    ECTRIMS Secretary Xavier Montalban, MD, echoed the comment. "We need that bridge" between surrogate and clinically relevant outcomes, he said.

    The chair of the 2012 meeting, Christian Confavreux, MD, added that the data on brain atrophy were incomplete. Although the study demonstrated a reduction in loss of total brain volume, he noted that it remained unclear, for example, whether that reflected preservation of actual brain tissue or merely the prevention of water loss.

    The study was supported by the Moulton Charitable Foundation, Berkeley Group, the Multiple Sclerosis Trials Collaboration, and the U.K. National Institute of Health Research.

    All study authors declared they had no relevant financial interests.

    Clanet reported consulting/speaking fees from Genzyme, Biogen Idec, and Bayer Schering and research grants from Bayer Schering, Biogen Idec, Merck Serono, Novartis, sanofi aventis and Teva Pharma.

    Confavreux reported consulting fees from Biogen Idec, Genzyme, Novartis, Merck Serono, sanofi aventis, Teva Pharma, and UCB Pharma; lecture fees from Bayer-Schering, Biogen Idec, Genzyme, LFB, Merck Serono, sanofi aventis and Teva Pharma; and research support from Bayer-Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, sanofi aventis and Teva Pharma.

    Montalban reported relationships with Bayer Schering Pharma, Biogen Idec, EMD Merck Serono, Genentech, Genzyme, Novartis, sanofi-aventis, Teva Pharmaceuticals, Almirall and BTG.

    Primary source: European Committee for Treatment and Research in Multiple Sclerosis
    Source reference:
    Chataway J, et al "The MS-STAT trial: High dose simvastatin demonstrates neuroprotection without immune-modulation in secondary progressive multiple sclerosis (SPMS) – a phase II trial" ECTRIMS 2012; Abstract 38a.

    Source: MedPage Today © 2012 MedPage Today, LLC (10/10/12)

    Another blow for Simvastatin add-on in Multiple Sclerosis

    StatinsResults from the SIMCOMBIN trial, the largest to date, found no benefit of simvastatin added to interferon in relapsing-remitting multiple sclerosis (MS).

    The phase 4 results, published in the August issue of the Lancet Neurology, are the latest in a series of unsuccessful attempts to pair simvastatin with interferon, and some say it's the end of the road for this statin in MS.

    Investigators are not excluding the possibility, however, that another combination of statins with disease-modifying drugs could still be beneficial.

    Simvastatin has been criticized recently for increasing the risk for muscle damage. In June, the US Food and Drug Administration warned that physicians should limit using the 80-mg dose of the drug — the same dose used in this study — to patients who have been taking the drug for a year, if there is no evidence of myopathy.

    "Simvastatin 80 mg should not be started in new patients, including patients already taking lower doses of the drug," the agency said.


    In the current trial, investigators led by Per Soelberg Sorensen, MD, from Copenhagen University Hospital in Denmark reported no unexpected adverse events with simvastatin. "Generally, adverse events were mild and there were no group differences in infections or musculoskeletal disorders, including myalgia. Rhabdomyolysis and myoglobinuria were not reported and there were no differences in serum creatine phosphokinase."

    Investigators studied 307 treatment-naive patients with relapsing-remitting MS. After starting interferon beta-1a at 30 μg weekly, patients were randomly assigned to simvastatin, 80 mg, or placebo.

    The absolute difference in annual relapse rate was 0.059 (95% confidence interval [CI], -0.21 to 0.09; P = .35).

    In the simvastatin group, 6% of patients had no disease activity. In the placebo group, the rate was 13% (odds ratio, 0.42; 95% CI, 0.17 - 1.00; P = .05).

    "We conclude that the combination of interferon beta and simvastatin should not be used as treatment for relapsing-remitting multiple sclerosis, although combination of other statins with other disease-modifying drugs such as glatiramer acetate could still be beneficial for treatment of this disease," the researchers note.

    In an accompanying editorial, Scott Zamvil, MD, from the University of California at San Francisco and Lawrence Steinman, MD, from Stanford University, California, said, "One ought to be careful when combining treatments in multiple sclerosis. In view of the lack of benefit and the potential for antagonism, one might want to think twice before adding a statin to interferon beta in multiple sclerosis treatment."

    The authors and editorialists say SIMCOMBIN is the only study to date to yield class 1 evidence.

    Asked by Medscape Medical News to comment, Emmanuelle Waubant, MD, from the University of California at San Francisco, agreed this is the best study looking at this combination published to date; however, she disagrees it meets the threshold for class 1 evidence.

    "In my opinion, the trial was underpowered to answer the question it was trying to address," she said.

    Dr. Waubant is also critical of the researcher's anticipated relapse rate. "I think a 39% relative reduction was overestimating the effect and there was no reference from where that number came from."

    STAYCIS Trial

    Dr. Waubant is the lead investigator of STAYCIS, another highly anticipated statin trial to be published in the coming months.

    Efforts to evaluate atorvastatin in patients with clinically isolated syndrome were crippled by slow enrollment and recruitment problems, and the trial ended without an answer to the study question.

    The 18-month study proved to be a tough sell for patients who were scheduled to receive atorvastatin or placebo for 12 months and then no treatment for the remaining 6 months of the study.

    "There was a major change in clinical practice in the middle of recruitment," Dr. Waubant said. "This was a major challenge, there was some competition with other trials, and we couldn't increase the number of sites due to funding restraints."

    Dr. Waubant admits the trial was a tough, uphill climb, and there are many things she is doing differently now. "For one, I focus on per patient funding, not a lump sum budget," she said. "I think it helps when centers have incentive."

    This study was funded by Biogen Idec. Some of the researchers and the editorialists have worked as consultants for the company.

    Sources: Lancet Neurol. 2011;10:691-701 & Medscape News Today © 1994-2011 by WebMD LLC. (02/09/11)

    No benefit from adding Statin in early MS

    StatinsAdjunctive simvastatin provided no benefit in multiple sclerosis patients taking intramuscular interferon beta-1a (Avonex), results of a new study showed.

    "The study gave a clear result that simvastatin cannot be recommended as an add-on therapy for intramuscular interferon beta-1A," according to Per Soelberg Sorensen, MD, of Copenhagen University Hospital in Denmark.

    But while simvastatin offered no additional disease control compared with placebo, it was safe, Soelberg Sorensen said at the European Committee for Treatment and Research in Multiple Sclerosis meeting.

    "We know that statins have immunomodulatory properties" he said, and in a small open trial, simvastatin reduced gadolinium-enhancing lesions in MS. However, a small trial of atorvastatin as combination therapy in MS indicated it might reduce the effect of subcutaneous interferon beta-1a.

    Soelberg Sorensen and colleagues decided to test the effect of simvastatin with intramuscular interferon beta-1a, randomizing 307 early MS patients already talking IM interferon to receive placebo or simvastatin for up to three years. The dose of simvastatin was titrated to 80 mg a day, double the most common dose for control of hypertension.

    The trial was initiated by the investigators -- from 34 different countries -- and sponsored by Biogen Idec.

    By the end of the trial, 90% of patients had completed at least 12 months of treatment, equally divided between the two treatment arms.

    Annualized relapse -- the primary endpoint -- was 0.19 for patients on placebo, and 0.14 for patients on simvastatin. The difference between the two was not significant.

    Similarly, there were no significant differences in total relapses, time to documented first relapse, rate of disability progression, or multiple imaging measures.

    The only secondary endpoint in which the two groups differed was percent of disease-free patients, which was greater in the placebo group, "but this was of borderline significance," Soelberg Sorensen said.

    "There was no beneficial effect for simvastatin as an add-on therapy to interferon beta-1a" intramuscular, he concluded.

    Neither, however, was there any safety difference between the two arms, he noted.

    Although the trial was designed to test efficacy in MS, the safety result indicates that MS patients receiving simvastatin for hypertension are not at greater risk.

    Carlo Pozzilli, of La Sapienza University in Rome, said that the negative result was valuable.

    Although there was no benefit for MS, he said, "there has been some thought that this combination could be potentially harmful." Especially since the tested dose of simvastatin was higher than the usually prescribed dose, "from this point of view, it is important to say the combination is not dangerous."

    He noted, though, that because of the relative youth of the MS population, "there are not a lot of MS patients on statins."

    Source: MedPage Today © 2004-2010 MedPage Today, LLC (17/10/10)

    Statins have detrimental effects on remyelination in MS

    StatinsSimvastatin interferes with process outgrowth and branching of oligodendrocytes.


    Statins have attracted interest as a treatment option for multiple sclerosis (MS) because of their pleiotropic antiinflammatory and immunomodulatory effects.

    However, contradictory results have been described when they are applied to oligodendrocytes (OLGs), the cell type predominantly affected in MS. In this study we focus on the in vitro effect of statins on process outgrowth in OLN-93 cells, a well-characterized OLG-derived cell line, and primary cultures of neonatal rat OLGs.

    Application of the lipophilic simvastatin, as low as 0.1-1 μM, disturbs process formation of both cell types, leading to less ramified cells.

    We show that both protein isoprenylation and cholesterol synthesis are required for the normal differentiation of OLGs.

    It is further demonstrated that the expression of 2',3'-cyclic-nucleotide-3' phosphodiesterase (CNP) and tubulin is lowered, concomitant with a reduction of membrane-bound CNP as well as tubulin. Therefore, we propose that lack of isoprenylation of CNP could help to explain the altered morphological and biochemical differentiation state of treated OLGs.

    Moreover, expression of specific myelin markers, such as myelin basic protein, myelin-associated glycoprotein, and myelin oligodendrocyte glycoprotein, was compromised after treatment.

    We conclude that simvastatin treatment has detrimental effects on OLG process outgrowth, the prior step in (re)myelination, thereby mortgaging long-term healing of MS lesions.

    Smolders I, Smets I, Maier O, Vandeven M, Steels P, Ameloot M.

    Biomedical Research Institute, School of Life Sciences, Hasselt University and Transnational University Limburg, Diepenbeek, Belgium.

    Source: J Neurosci Res. 2010 Sep 20 © 2010 Wiley-Liss, Inc. & Pubmed PMID: 20857509 (24/09/10)

    Simvastatin & interferon beta 1a trial in Relapsing/Remitting MS


    Objectives: This study was conducted to evaluate the effect of simvastatin (40 mg/day) as an adjuvant therapy to interferon beta (IFNb 1a, 30 mug once weekly) in relapsing-remitting multiple sclerosis patients, compared with placebo.

    Methods: We enrolled 85 patients with relapsing-remitting multiple sclerosis (71% female) who were already receiving IFNb 1a (Avonex), with Expanded Disability Status Scale score of less than 5.0. The patients were assigned (in random and double-blinded fashion) into the two groups of simvastatin and placebo. All patients continued to receive their current IFNb treatment. The outcome measures were total relapse rate, Expanded Disability Status Scale score, and the number of gadolinium-enhanced (Gd+) and new T2 lesions in magnetic resonance imaging after a 1-year follow-up. We used Mann-Whitney and one-way multivariate analysis of variances to analyze the data.

    Results: Four patients in the placebo and two in the simvastatin group prematurely withdrew from the study due to experiencing two attacks. The total attack number in the simvastatin group was significantly lower than placebo group (moderate effect size r = 0.29) (p = 0.01). The final Expanded Disability Status Scale scores were lower in the simvastatin group (1.01 +/- 1.40, mean +/- SD) than in the placebo group (1.73 +/- 1.49, mean +/- SD), but this difference was not significant after controlling the baseline Expanded Disability Status Scale score (p = 0.07). In the simvastatin group, the mean +/- SD of gadolinium-enhanced and new T2 lesions were 0.66 +/- 1.18 and 3.39 +/- 3.55, respectively, (compared with 0.74 +/- 1.21 and 3.39 +/- 3.55 in the placebo group). Although there was a decreasing trend in lesions on magnetic resonance imaging, this difference was not statistically significant (p = 0.62). The combination therapy was safe and well tolerated, and no serious adverse effect was noted.

    Conclusion: Our study supports the safety and efficacy of simvastatin as an add-on therapy to INFb 1a in patients with relapsing-remitting multiple sclerosis.

    TRIAL REGISTRATION: NCT00668343.This interventional study provides Class I evidence stating that adding simvastatin 40 mg/day to IFNb 1a 30 mug a week in patients with relapsing-remitting multiple sclerosis may reduce the relapse rate (moderate effect size r = 0.29) (p = 0.01) compared with treatment with IFNb 1a alone.

    Togha M, Ahmadi Karvigh S, Nabavi M, Beladi Moghadam N, Harirchian MH, Sahraian MA, Enzevaei A, Nourian A, Ghanaati H, Firouznia K, Jannati A, Shekiba M.

    Sina Hospital, Iran/Tehran University of Medical Sciences, Iran.

    Source: Pubmed PMID: 20488825 (28/05/10) 

    Neurologists debating statins in Multiple Sclerosis

    StatinsEvidence is slim, but many neurologists remain hopeful there will one day be a role for statins in treating multiple sclerosis. Here at the American Academy of Neurology 62nd Annual Meeting, investigators weighed the possible benefits and risks.

    The hypothesis is that popular cholesterol-lowering agents such as Pfizer's atorvastatin (Lipitor) may also play a role in immunomodulation, but demonstrating this link has proven tricky.

    No one perhaps knows this better than investigators from the STAYCIS study — the group whose highly anticipated statin trial failed. Attempts to evaluate atorvastatin in patients with clinically isolated syndrome were crippled by slow enrollment and recruitment problems and ended without an answer to the study question.

    First results from the study were presented in September in Germany at the 25th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. The latest numbers were released at the American Academy of Neurology meeting here in Toronto.

    The trial has been criticized for its lack of power. When the bad news about the failure first broke, Henry McFarland, MD, acting chief of the Cellular Immunology Section of the National Institutes of Health, expressed his disappointment to Medscape Neurology. "If you start a study," he said, "you have an ethical obligation to see it through and do everything possible to ensure there is a sufficient cohort."

    Gavin Giovannoni, MBBCh, PhD, from the Institute of Cell and Molecular Science at Barts and the London School of Medicine and Dentistry, in the United Kingdom, called the situation tragic. "This is an ethical issue and really highlights how important it is to consider logistics and think things through."

    Failed STAYCIS Trial

    However, session moderator Benjamin Greenberg, MD, from the University of Texas Southwestern in Dallas, said he hopes history will judge the STAYCIS investigators more kindly.

    "This was a situation where there was a paradigm change right in the middle of the trial. Treatments shifted and recruiting became untenable," he said.

    When the trial was first launched in 2005, it was still common not to treat patients right away with disease-modifying therapy. That quickly changed, and the success of agents such as interferon left clinicians questioning whether they should encourage patients to enter a statin trial — especially one with a placebo group.

    The 18-month trial proved to be a tough sell for patients who were scheduled to receive atorvastatin or placebo for 12 months and then no treatment for the remaining 6 months of the study.

    "The ethics debate could go either way," Dr. Greenberg said. "The resources are spent, do you continue investing in the trial or do you just stop early?" Dr. Greenberg suggests the investigators had a point.

    Presenting at the meeting, Emmanuelle Waubant, MD, from the University of California–San Francisco, outlined the problems with the trial but also described a potential benefit with atorvastatin in clinically isolated syndrome.

    Fewer Lesions

    Dr. Waubant pointed to imaging data suggesting the drug may reduce the risk for new brain lesions. The percentage of patients who did not develop new T2 lesions up to month 12 or when starting interferon was 55.3% in the atorvastatin group and 27.6% in the placebo group (P = .032).

    Investigators report that the odds of remaining free of new T2 lesions were higher in the atorvastatin group (odds ratio, 3.93; P = .012 on 2-stage regression). The odds of remaining gadolinium-positive free also tended to be higher in the atorvastatin group (odds ratio, 2.70; P = .078 on 2-stage regression).

    The primary endpoint for the trial included a clinical endpoint, as well as an imaging one. Investigators say in hindsight, it was unlikely they were going to make the endpoint with this design.

    Dr. McFarland says he agrees the trial should have had a clinical endpoint or an imaging one.

    Dr. Greenberg says he hopes the investigators will continue crunching the numbers and reporting more magnetic resonance imaging data. "I think there is still more to learn here," he said. "And this will provide closure."

    This study was supported by the National Institute of Allergy and Infectious Diseases. It was managed by the Immune Tolerance Network with support by Pfizer, Biogen-Idec, and the Nancy Davis Foundation.

    American Academy of Neurology 62nd Annual Meeting: Scientific Session S21.005. Presented April 14, 2010.

    Source: Medscape Today © 1994-2010 by WebMD LLC (22/04/10)

    Statins may slow progression of multiple sclerosis, new study finds

    StatinsA UCSF-led study examining the impact of statins on the progression of multiple sclerosis found a lower incidence of new brain lesions in patients taking the cholesterol-lowering drug in the early stages of the disease as compared to a placebo.

    Study participants received an 80 milligram daily dose of atorvastatin, marketed by Pfizer Inc. as Lipitor.

    Although the study was small with only 81 participants and its primary endpoint, designed to evaluate MS progression in patients following their first attack, was not met, the researchers found over the 12-month course that 55.3 percent of participants did not develop new brain lesions when administered statins compared with 27.6 percent of the placebo group.

    Study findings were presented by University of California, San Francisco researchers during the annual American Academy of Neurology scientific meeting in Toronto.

    The trial was a phase II, multi-center, randomized, placebo-controlled follow up to a landmark study published by principal investigator Scott S. Zamvil, MD, PhD, associate professor of neurology at UCSF (Youssef, et al., Nature 2002), after his laboratory first observed that statins cause T cell immune modulation that could be beneficial in multiple sclerosis and other autoimmune diseases.

    Co-led by Zamvil and Emmanuelle Waubant, MD, PhD, associate professor of neurology at the UCSF MS Center, the study tested whether the drug could be used to prevent conversion to definite multiple sclerosis in individuals who have had a first attack.

    “Our data is preliminary, and we need a larger study to confirm the effects of the drug and its magnitude.  It is important that we understand how statins impact the progression of multiple sclerosis in order to better inform physicians and patients of their effect since these drugs are so broadly used throughout the United States and the world, and to learn whether a relatively inexpensive oral therapy can slow the course of disease,” said Waubant.

    MS is considered possibly as an autoimmune disease where immune cells attack the central nervous system.  Nerves are made up of axons (nerve fibers) surrounded by a myelin sheath.  MS occurs when the immune system attacks myelin, leaving scars or lesions in the demyelinated areas of the brain and spinal cord.  Damage to myelin disrupts the ability of nerves to transmit information to nerve cells, resulting in neurological disability.

    The team employed MRI to look at the activity of the medication on the disease course.  More than 150 patients were originally intended, but enrollment was stopped due to slow recruitment after 81 patients were randomized.  Each subject was asked to come in every three months (five scans over 12 months) for serial brain MRI evaluation.  The subject pool was 76.5 percent female, 92.6 percent white, and ranged in age from 24 – 48 years.

    Central MRI reading and coordinating was provided by Daniel Pelletier, MD, associate professor of neurology and a member of the Multiple Sclerosis Research Group at UCSF.

    “The exciting finding in this study is that reducing new brain MRI lesions should be meaningful for patients since new lesions are reliable correlates of future clinical attacks in MS,” said Pelletier.

    In addition to UCSF, the multi-center trial involved Oregon Health & Science University, The Cleveland Clinic, Virginia Mason MS Center, Washington University School of Medicine John L. Trotter MS Center, Montreal Neurological Institute, Barrow Neurological Institute, University of Texas Southwestern Medical Center, University of Rochester, The Multiple Sclerosis Comprehensive Care Center at USC Keck School of Medicine, Yale MS Research Center, Jacobs Neurological Institute, Johns Hopkins University, and Mount Sinai School of Medicine.

    The research was performed as a project of the Immune Tolerance Network, a clinical research consortium headquartered at UCSF and sponsored by the National Institute of Allergy & Infectious Diseases.  Atorvastatin, placebo and additional support were provided by Pfizer.  Biogen-Idec provided Avonex, an immune system regulator drug (interferon beta-1a) for study participants who displayed disease activity while on placebo or atorvastatin.  Additional funding was provided by the Nancy Davis Foundation and the Maisin Foundation.

    Source: The University of California © 2010, The Regents of the University of California (15/04/10)

    Atorvastatin Combined To Interferon to Verify the Efficacy (ACTIVE) in relapsing-remitting active multiple sclerosis patients: a longitudinal controlled trial of combination therapy


    Interferon beta (IFNb) is a first-line treatment for people with MS, but its efficacy may vary amongst different people. Statins are known to have anti-inflammatory properties. In this unicentre controlled clinical trial carried out with 45 participants, the authors aimed to assess safety, tolerability and efficacy of low-dose atorvastatin, which belongs to the group of statins, plus subcutaneous IFNb-1a (Rebif44®), given for 24 months, in people with MS responding poorly to interferon beta-1a.

    The people that received the combined therapy (atorvastatin plus IFNb-1a) had better outcome than those that received IFNb-1a alone, in terms of active inflammatory lesions in the MRI, relapses, and risk of increasing disability. The authors have concluded that low-dose atorvastatin may be beneficial, as add-on therapy, in poor responders to high-dose interferon beta-1a alone.

    A large body of evidence suggests that, besides their cholesterol-lowering effect, statins exert anti-inflammatory action. Consequently, statins may have therapeutic potential in immune-mediated disorders such as multiple sclerosis.

    The objectives were to determine safety, tolerability and efficacy of low-dose atorvastatin plus high-dose interferon beta-1a in multiple sclerosis patients responding poorly to interferon beta-1a alone.

    Relapsing-Remitting multiple sclerosis patients, aged 18-50 years, with contrast-enhanced lesions or relapses while on therapy with interferon beta-1a 44 microg (three times weekly) for 12 months, were randomized to combination therapy (interferon + atorvastatin 20 mg per day; group A) or interferon alone (group B) for 24 months. Patients underwent blood analysis and clinical assessment with the Expanded Disability Status Scale every 3 months, and brain gadolinium-enhanced magnetic resonance imaging at screening, and 12 and 24 months thereafter.

    Primary outcome measure was contrast-enhanced lesion number. Secondary outcome measures were number of relapses, EDSS variation and safety laboratory data. Forty-five patients were randomized to group A (n = 21) or B (n = 24).

    At 24 months, group A had significantly fewer contrast-enhanced lesions versus baseline (p = 0.007) and significantly fewer relapses versus the two pre-randomization years (p < 0.001). At survival analysis, the risk for a 1-point EDSS increase was slightly higher in group B than in group A (p = 0.053). Low-dose atorvastatin may be beneficial, as add-on therapy, in poor responders to high-dose interferon beta-1a alone.

    Source: MS Society Of Canada (02/03/10)

    Statins may have a negative impact in Multiple Sclerosis (MS) patients


    Statins, a commonly prescribed class of drugs used by millions worldwide to effectively lower blood cholesterol levels, may actually have a negative impact in Multiple Sclerosis (MS) patients treated with high daily dosages.

    A new study by researchers at the Montreal Neurological Institute (MNI), McGill University, demonstrates that statin therapy in mice inhibits myelin repair or remyelination in the central nervous system. The findings, published in The American Journal of Pathology, highlight the crucial need to monitor the effects of central nervous system-accessible immune therapies on the myelin repair processes in patients with MS and other progressive demyelinating diseases.

    Canadians have one of the highest rates of MS in the world. An estimated 50, 000 Canadians have MS, with approximately 1,000 new cases diagnosed each year. MS is an autoimmune disease of the central nervous system (CNS), in which immune cells attack the myelin sheath (the protective insulation of nerve fibres), and the myelin-producing cells of the CNS (oligodendrocytes), causing demyelination. This causes damage which disrupts the nerve cell's ability to transmit signals throughout the nervous system.

    In the early stages of MS, following an immune system attack on myelin, oligodendrocyte progenitor cells or stem cells in the CNS are recruited to the lesion. These cells mature and produce new myelin to repair the damage.

    "Statins, which are known to modify the immune system response and have a wide array of effects on other cellular processes, were propelled into clinical trials based on studies in an animal model of MS indicating a reduction in clinical disease severity," says Dr. Veronique Miron, post-doctoral fellow in Dr. Jack Antel's lab at the MNI, and lead investigator in the study. "The mechanism of statin action in these studies was not determined. That is, does statin directly effect myelin and/or the oligodendrocytes or is disease severity reduced indirectly due to the dampening of the immune response. This issue required further investigation, particularly due to the ability of statins to cross the blood-brain barrier and access the CNS, and the enrichment of cholesterol in the myelin sheath."

    The objective of the MNI study was to determine the direct impact of simvastatin, a statin in clinical trials, on the integrity of myelin in the brain and on the remyelination process. The study uses a model of myelin damage that has relatively little inflammation and mimics the demyelinating aspect of MS, allowing MNI researchers to determine the direct effect of long-term statin therapy on remyelination, independent of its indirect effects mediated via immune modulation.

    "The results of our study indicate that simvastatin has in fact, a slightly deleterious effect on myelin under non-pathological conditions," adds Dr. Miron. "During remyelination, there is a decrease not only in myelin production but also in oligodendrocyte number as a result of simvastatin treatment. The findings also suggest that simvastatin inhibits CNS remyelination by blocking oligodendrocyte progenitor cell differentiation or maturation into myelinating oligodendrocytes."

    This study underscores the necessity of monitoring the long-terms effects of CNS accessible immune therapies, particularly those that can impact cell types that are postulated to be targeted in neurological disease processes and that are implicated in any brain tissue repair processes. Understanding the underlying mechanisms of these therapies will lead to improved and enhanced treatment strategies and ultimately improved quality of life for people who suffer from a variety of neurological diseases.

    This work was supported by grants from the Foundation of the Multiple Sclerosis Society of Canada, The National Multiple Sclerosis Society and the Canadian Institutes of Health Research.

    Source: Medical News Today © 2009 MediLexicon International Ltd (30/05/09)

    Lovastatin induces the formation of abnormal myelin-like membrane sheets in primary oligodendrocytes


    Statins, well-known inhibitors of cholesterol synthesis and protein isoprenylation, have been proposed as therapeutic drugs for multiple sclerosis (MS).

    As lovastatin and simvastatin, which are currently tested for their use in MS, can cross the blood-brain barrier, they may affect cellular processes in the central nervous system. This is especially relevant with respect to remyelination as a proposed additional treatment for MS, because cholesterol is a major component of myelin.

    Here, we show that primary oligodendrocytes, treated with lovastatin, form extensive membrane sheets, which contain galactosphingolipids. However, these membrane sheets are devoid of the major myelin proteins, myelin basic protein (MBP) and proteolipid protein (PLP).

    Reduced MBP protein expression was confirmed by SDS-PAGE and Western blotting, and in situ hybridization experiments revealed that lovastatin blocks MBP mRNA transport into oligodendrocyte processes.

    In contrast, PLP expression was only mildly affected by lovastatin. However, lovastatin treatment resulted in intracellular accumulation of PLP and prevented its translocation to the cell surface.

    Interestingly, another inhibitor of cholesterol synthesis (ro48-8071), which does not interfere with isoprenylation, had a similar effect on the localization of PLP, but it did not affect MBP expression and localization.

    These results suggest that lovastatin affects PLP transport predominantly by the inhibition of cholesterol synthesis, whereas reduced MBP expression is caused by impaired isoprenylation.

    Based on these results we recommend to carefully monitor the effect of statins on myelination prior to their use in demyelinating diseases.

    Maier O, De Jonge J, Nomden A, Hoekstra D, Baron W.
    Section of Membrane Cell Biology, Department of Cell Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.

    Source: Pubmed PMID: 18814266 (29/01/09)

    Beta interferon and atorvastatin combination may increase disease activity in multiple sclerosis.

    A combination treatment with interferon beta 1a and atorvastatin in people with MS was investigated. Surprisinglyit was found that people who took both medications had more relapses and more activity on MRI......

    OBJECTIVE: To explore whether high dose atorvastatin can be administered safely to persons with relapsing remitting multiple sclerosis (MS) taking thrice weekly, 44 mcg dose subcutaneous interferon beta-1a.

    METHODS: Persons with clinically stable, relapsing remitting MS, on standard high dose subcutaneous interferon beta-1a, were randomized in a double blinded fashion to receive either placebo or atorvastatin at dosages of 40 mg or 80 mg per day for 6 months. Blinded neurologic examinations and brain MRI readings were obtained at months 0, 3, 6, and 9. Laboratory blood testing was performed monthly. Main outcome measures were the determination of drug toxicity using blood tests and ECG and determination of MS-related disease activity, either clinical relapses, or new or contrast enhancing lesions on MRI.

    RESULTS: Twenty-six subjects received at least one dose of study drug. Ten of 17 subjects on either 80 mg or 40 mg of atorvastatin per day had either new or enhancing T2 lesions on MRI or clinical relapses. One of the nine subjects on placebo had a relapse with active lesions on MRI. The subjects receiving atorvastatin were at greater risk for either clinical or MRI disease activity compared to placebo (p = 0.019). Significant changes in blood tests were noted only for lower cholesterol levels in subjects receiving atorvastatin.

    CONCLUSION: The combination of 40 or 80 mg atorvastatin with thrice weekly, 44 mcg interferon beta-1a in persons with multiple sclerosis resulted in increased MRI and clinical disease activity. Caution is suggested in administering this combination.

    Source: PubMed PMID: 18525027 (18/06/08)

    Scientists discover why statins help MS
    Scientists say statin drugs, well-known for lowering cholesterol, seem to reduce inflammation that causes nerve cell damage in people with multiple sclerosis.

    Previous research, still considered preliminary, has suggested that MS patients who also take statins have less nerve damage over time.

    Scientists at the University of North Carolina, at Chapel Hill, tested blood samples from people with relapsing-remitting MS to find out why.

    They found that statins inhibited the formation of lymphocytes and monocytes. Those immune-system cells cause inflammation by attacking nerve cells in people with MS.

    The researchers say statins may be used to enhance current treatments for MS, which slow the progressive disease but don't stop it.

    The study was published July 25 in the online Journal of Neuroimmunology.

    Source: South Bend Tribune Copyright © 1994-2006 South Bend Tribune New Media Director's Blog: http://newmediadirections

    A Statin Improves Performance of Multiple Sclerosis Drug
    The same researchers who showed that a cholesterol-lowering statin drug might prevent development of full-blown multiple sclerosis are now reporting that statin therapy might improve the performance of existing MS drugs.

    The first discovery led to a nationwide study in which people who have the initial symptoms of the autoimmune nerve-damaging disease are taking a statin in hopes of avoiding MS.

    "What we have shown now is that we have data in an animal model, that when this statin is used in combination with Copaxone, it may augment the activity of Copaxone," said study co-author Dr. Scott Zamvil, associate professor of neurology at the University of California, San Francisco. "That is provocative data supporting human testing of this combination."

    While the research has so far been limited to lab mice, the scientists hope the findings might one day lead to improved treatments for people with the disease. The findings appear in the March 16 online edition of the Journal of Clinical Investigation.

    Combination therapy is desirable because Copaxone, like other MS drugs, is effective in only 30 percent to 35 percent of cases of the most common form of the disease, Zamvil said. In one animal study, adding high doses of atorvastatin (Lipitor) dramatically reduced central nervous system inflammation and seemed to eliminate the paralysis caused by a model disease that closely resembles MS. In contrast, there was no reversal of the disease in animals that received low doses of Lipitor or Copaxone.

    In multiple sclerosis, immune cells attack a layer of insulation known as myelin that surrounds nerve fibers in the brain and spinal cord. Copaxone is one of a family of drugs that suppresses the activity of the chemicals that destroy myelin.

    Lipitor also appears to act against the destructive immune system activity, but through a different mechanism, Zamvil said. "They can have an additive effect," he said, referring to the combination of Lipitor and Copaxone. "We were able to see a clinical and immunological benefit."

    The reults do not necessarily apply to all statin drugs, he said. "They all act on the same enzyme to reduce cholesterol but they differ in their ability to cause immune modulation," Zamvil said. Data from unpublished studies indicate that Lipitor has more immune system activity, he said.

    Zamvil said he's aware that some people with MS are already taking a statin, but he advised against it at this point to combat the disease. "We don't know if it is effective or not at this stage," he said. "Even though they [statins] are relatively safe, we are speaking of higher doses."

    That caution was echoed by Dr. Jeffrey Cohen, a neurologist at the Cleveland Clinic, one of 14 U.S. centers involved in a trial of statin therapy to prevent MS in people who have had a first neurological event that often leads to the disease. The trial has been going on for a year, and five people have been enrolled at the Cleveland Clinic, he said, adding that results of the trial might start to emerge in a year or two.

    "There is a lot of interest in statins and they are generally well tolerated, but we are cautioning people not to rely on statins for multiple sclerosis treatment," Cohen said. "The doses are on the high side, so there is some potential for side effects and toxicity."

    Inevitably, some people treated for MS at the Cleveland Clinic are taking a statin because they have high cholesterol, Cohen said. "It doesn't appear to have an adverse effect on MS, and at this point it is hard to determine whether it is helpful for MS," he said.

    The full scientific article : TITLE: Immunomodulatory synergy by combination of atorvastatin and glatiramer acetate in treatment of CNS autoimmunity  can be viewed here: 

    Source: Yahoo News Copyright © 2006 Yahoo! Inc.  and Eureka! All rights reserved.

    Cholesterol Drug may be a lot more
    Cancer. Alzheimer's. Diabetes. Osteoporosis. These are just some of the diseases that researchers hope can be treated or prevented with statins.
    By Ronald Kotulak

    Not since aspirin has a class of drugs come along that does so much more than originally intended that it could end up being used as a preventive against many major diseases.

    Statins, which lower cholesterol, have been proved in clinical trials to reduce heart attacks and strokes by 30 to 50 percent. They are the most widely prescribed drugs in the U.S.; 1 in 10 adults take them.

    But their full value in improving the nation's health rests with research attempting to establish the ability of statins to prevent cancer, Alzheimer's disease, diabetes, osteoporosis, high blood pressure, multiple sclerosis and macular degeneration.

    Already, observational studies suggest that people who take statins are at lower risk of developing those illnesses. Researchers are exploring why the drugs might have such a broad protective effect and are finding the drugs may affect critical systems of the body in ways that head off disease.

    "Statins are one of the real miracle drugs from the last generation of research," said Dr. Thomas H. Lee, a cardiologist at Harvard Medical School and Brigham and Women's Hospital. "No one realized when they came out just how broad their impact would be. There are reasonable people who believe that if statins were completely free, everyone should take them."

    Lee and others caution, however, that the drugs still must undergo rigorous clinical trials to prove that they can safely and effectively do all the things they have been billed to do.

    "If we determine down the road that statins help reduce things like Alzheimer's disease, osteoporosis and cancer, they still should be given to people who are at higher risk of developing those things, [rather] than just to everybody across the board," said Dr. Mathew Sorrentino, director of preventive cardiology at the University of Chicago.

    Statins are taken to lower levels of cholesterol, especially low-density lipoprotein or LDL, the so-called "bad cholesterol" linked to heart disease. They do that work very well.

    "The average cholesterol level in the country has been going down and the number of heart attacks and strokes have clearly been reduced," Sorrentino said. "Statins are changing the health of the whole United States. It's pretty remarkable to have an agent that's doing that."

    Cholesterol, which is made naturally in the liver, is a vital component used to build all cells in the body and to maintain their function. It becomes dangerous when blood levels are too high--usually due to diet--and excess cholesterol builds up in artery walls, causing heart disease.

    Statins work against cholesterol in two ways: They reduce the liver's ability to manufacture it, and they speed the elimination of LDL from the body.

    But researchers are discovering that statins have other surprising effects. In the process of reducing cholesterol, the drugs set in motion a chain of events that appears to improve many functions in the body, from blood pressure to inflammation.

    In the body, a long series of chemical steps leads up to the manufacture of cholesterol, and each of those steps plays a role in cellular function. Trouble appears to occur when cholesterol levels get too high and the chemical steps begin to behave abnormally, helping to set the stage, scientists believe, for such disorders as cancer, heart disease and Alzheimer's.

    By slowing the first step of the chemical pathway to cholesterol production, statins help prevent that from happening.

    Evidence suggests that statins thereby help the body in many ways, such as getting rid of cancer cells, improving the flow of blood through arteries, eliminating brain plaques in Alzheimer's disease, beefing up immunity, reducing inflammation, thwarting blood clots, reducing fractures, preventing arterial blockages from breaking off and causing heart attacks or strokes, and snuffing out free-radical damage.

    "Three of every 100 proteins need something from this cholesterol pathway to function," said Jim Dimitroulakos of the Ottawa Regional Cancer Center, who is trying to determine how statins may block cancer. "There could be thousands of proteins affected by these drugs, and they seem to be beneficial for disease prevention. I don't think there's been another drug that affects so many different things."

    Dr. Gregory R. Mundy of the University of Texas Health Science Center, San Antonio, found, for instance, that one product of the cholesterol pathway stimulates bone growth, a finding that suggests why statins may be useful against osteoporosis.

    This broad range of metabolic activity even surpasses that of aspirin. Initially marketed in 1899 as a pain reliever, aspirin over time was found to have a role in reducing the risk of heart attacks, strokes, arthritis, inflammation and colon cancer.

    The first statin, Mevacor, was marketed in 1987, but doctors were nervous about prescribing it, fearing side effects. Those fears evaporated by the mid-'90s after several studies showed statins effectively reduced the risk of heart attacks and were relatively safe. The floodgates opened, and physicians now write about 150 million statin prescriptions annually.

    Studies indicate statins pose no cancer risk and side effects are minimal. Doctors check patients for elevated liver enzymes, but so far not one case of liver damage has been tied to statins. Serious side effects causing muscle damage and kidney failure occur in about one in a million users. Muscle aches are the most common complaint, affecting about 1 in 100 people. Liver and muscle side effects are reversible when the drugs are discontinued or the dose lowered.

    "The most serious side effect from statins is on par or even less than a serious bleeding side effect of aspirin," Sorrentino said.

    The United Kingdom recently approved over-the-counter sales of a low dose of one statin, Zocor, to reduce the risk of heart attacks, and experts believe that the U.S. Food and Drug Administration also may eventually allow the purchase of statins without prescriptions. The American College of Physicians last year recommended that everyone with adult onset or type 2 diabetes should be on statins.

    "At this point the evidence is pretty overwhelming that statins reduce everyone's risk of heart attack by about a third," Lee said. "It doesn't matter whether your risk is elevated because of high cholesterol, or whether your risk is elevated because of diabetes, high blood pressure or cigarette smoking."

    Although a number of population studies suggest statins may protect against a large number of diseases, these studies cannot prove a cause-and-effect relationship. For that, researchers must turn to controlled clinical trials where the medication is compared to an inactive placebo. Such trials are under way for cancer, Alzheimer's disease and multiple sclerosis.

    The most impressive population research involves a series of retrospective studies on half a million veterans conducted by Dr. Vikas Khurana of the Overton Brooks VA Medical Center in Shreveport, La. Men who took statins for up to four years had about 50 percent fewer cancers of the lung, prostate, pancreas and esophagus. For those taking statins longer, the reduction was much greater, he said.

    Looking at nearly 40,000 female veterans, Khurana found that those taking statins had approximately 50 percent fewer breast cancers. The studies attempted to rule out other factors such as cigarette smoking, alcohol consumption, diet, income and physical activity.

    Statins may have at least two mechanisms for destroying cancer cells. Dimitroulakos' research suggests that when statins reduce the body's production of cholesterol they also reduce some chemicals that cancer cells need to grow, causing them to self-destruct.

    Biochemist Khandan Keyomarasi of the University of Texas M.D. Anderson Cancer Center found preliminary evidence that statins can also act directly on cancer cells in laboratory tests to shut down their division, also leading to cell death.

    "Statins are very promising but they are still not ready for prime time. We need randomized clinical studies and more convincing results," said Khurana, also an assistant professor of medicine at Louisiana State University. "Before people with low or normal cholesterol start using these drugs in the hope of preventing cancer, we need to make sure that the side effects are going to be minimal as compared to the potential cancer benefits they're going to get."

    Depending on the outcome of clinical trials, Alzheimer's disease may become the latest disorder that statins are used both to treat and to prevent.

    Cholesterol's link to Alzheimer's disease became the primary focus of Dr. Larry Sparks of the Sun Health Research Institute in Sun City, Ariz., when he discovered from autopsy studies in 1986 that people with heart disease and high cholesterol levels had plaques in their brains. The plaques were exactly like those of Alzheimer's patients, though they had not been diagnosed with the disease. Subsequent studies of rabbits fed high-cholesterol diets showed they too developed the brain-clogging hallmarks of Alzheimer's.

    As a result of population studies suggesting that people taking statins seemed to have a lower risk of Alzheimer's, Sparks undertook a small phase one clinical trial of Alzheimer's patients in which 32 people took Lipitor and 31 a placebo.

    After three months both groups continued to deteriorate at the same rate, Sparks reported recently. After six months, however, placebo patients continued their steady decline, but the memory of those taking Lipitor began to improve until it was superior to when the study started. After that, the memory enhancement began to wane.

    "Lipitor gave them a boost," Sparks said. "It slowed things down. We were able to demonstrate that the progression of the disease had probably been slowed. At the end of a year of treatment the Lipitor population were almost exactly the same as they were when they started the trial."

    Based on Sparks' findings Pfizer Inc., maker of Lipitor, launched a large clinical trial of 600 patients to determine if the drug can effectively treat Alzheimer's disease. The National Institutes of Health started another study with 450 patients to determine if Zocor slows the disease's progression.

    The mechanism by which cholesterol influences Alzheimer's disease is not known. Studies indicate that cholesterol may trigger a malfunction in the brain's garbage-removal detail, allowing a buildup of neuron-killing debris.

    What's needed next, Sparks said, are clinical trials to determine if statins can prevent the disease in healthy people. "The predominant weight of the data is that there is an influence of prior statin use on your later risk of Alzheimer's disease," Sparks said.

    As research into statins continues, many physicians are excited about the drugs' potential for healing--but also taking a wait-and-see approach.

    "Are they a wonder drug? That's hard to say," said Dr. Gerald McGwin Jr. of the University of Alabama, Birmingham, who is studying statins and macular degeneration. "They've been associated with a lot of things, but we haven't translated that research into clinical trials. Once we've done that and they are shown to be as good as we think, then maybe I'd call them a wonder drug."

    Source: Chicago Tribune Copyright © 2005

    Clinical Trial Tests Cholesterol Drug to Minimize Multiple Sclerosis

    New Haven, Conn.— Yale University School of Medicine is participating in the first clinical trial testing atorvastatin to delay or decrease disease in patients who have experienced a first attack of multiple sclerosis (MS).

    Statins, of which atorvastatin is one, are a relatively new group of drugs used to lower cholesterol levels. Researchers believe statins may affect the immune system, reducing brain inflammation associated with MS.

    Persons eligible to enroll in the trial, which is being conducted at 15 sites nationwide, have experienced a first attack, or clinically isolated syndrome (CIS), lasting at least 48 hours and involving either the optic nerve, spinal cord, brain stem, or cerebellum.

    “Because permanent neurologic damage can occur during the CIS stage, researchers are seeking new treatments,” said Jana Preiningerova, M.D., assistant professor in the Department of Neurology. “Currently, interferon is the only approved therapy for CIS patients, but it has reported side effects and is administered through weekly intra-muscular injections. Atorvastatin, if proven to be effective, can be taken orally and has an established tolerance profile, making it an attractive candidate for patients who need long-term treatment.”

    The primary objective of the trial is to evaluate the ability of atorvastatin to decrease or delay clinical and MRI-detected disease activity in patients with CIS and MRI findings suggestive of early MS, compared with placebo.

    This trial will also examine whether early intervention in patients with CIS may result in a state of immunological tolerance and whether statins have any residual effect after discontinuation.

    The trial is being conducted by the Immune Tolerance Network, which is sponsored by the National Institute for Allergy and Infectious Diseases. Sarah Harma is the study coordinator at Yale School of Medicine. Persons interested in participating in the trial can contact her at 203-764-8160 or [email protected]

    Copyright © 2005, Yale University

    Statins may treat MS

    Another study has shown that people with MS may benefit from treatment with cholesterol-lowering statin drugs according to a small study presented in April at the American Academy of Neurology meeting in Honolulu, Hawaii.

    "Our findings show that statins have potential in the treatment of multiple sclerosis," said Dr Timoth Vollmer, a neurologist from St Josi Hospital and Medical Center in Arizona.

    In the study, 28 patients received one daily dose of the drug simvastatin (Zocor) for six months. The patients ranged in age from 18 to 55 and had at least one multiple sclerosis-related lesion according to brain scans.

    During treatment, patients had fewer relapses than during the three month observation period before starting statins. They also had fewer multiple sclerosis lesions; before treatment patients had an average of 2.35 lesions and after treatment they had an average of 1.31.

    The volume of the lesions also decreased, Vollmer said. Although the investigators are still analysing results, they have documented no serious side effects in patients.

    Statin drugs appear to have anti-inflammatory properties in addition to their ability to cut cholesterol and are being studied for the treatment of autoimmune diseases such as multiple sclerosis and rheumatoid arthritis.

    Vollmer and his colleagues said that if statin drugs are shown to work in multiple sclerosis, they would offer certain advantages because they are taken as a pill and are safer and less expensive than current treatments for MS which are all taken by injection.

    However, a larger study is needed to confirm the preliminary findings.

    The study was funded by Merck, Inc. the manufacturer of Zocor.

    Ref: American Academy of Neurology, Reuters Health

    Anti-Cholesterol Drugs Lower Co-Q 10

    Anti-Cholesterol Drugs Lower Co-Q 10 and Could Increase Risk of Heart Attacks

    Statins, the drugs which reduce cholesterol, may deplete the body’s ability to produce a vitamin-like substance called CoQ10, which is essential for heart health. The claim was made by American doctor Dr Peter Langsjoen. Anyone taking statins should take CoQ10 supplements to offset this risk. A review of fifteen studies on humans and a further fifteen on animals show an acute depletion of Q-10 in the body when statins are prescribed.

    New research being conducted in Texas and Illinois by a leading cardiologist, notes that there is currently an epidemic of heart failure in the USA.

    In a small pilot study two thirds of patients treated with statins developed early weakening of the heart muscle after 6 months of treatment. This weakening of the heart returned to normal after 3 months of supplemental Q-10

    Ref: The Lancet Friday November 22, 2002

    Cholesterol Drugs Might Work For MS

    Drugs known as statins widely used to lower cholesterol may also be useful in the treatment of MS.

    In newly published research from the University of California, San Francisco, and Stanford University, the cholesterol-lowering drug Lipitor prevented disease progression and reversed paralysis in mice with an MS-like disease.

    Also, an Austrian study found that the statin Zocor slowed the growth of immune cells associated with MS. In mice experiencing their first attack of MS, the drug prevented progression to fully established disease. In animals that had already had a first attack, and were developing symptoms of a first relapse, treatment was found to reverse emerging paralysis.

    While the laboratory findings offer the promise of better treatments for MS and other immune system diseases, they have yet to be confirmed in human trials.

    A small study involving 32 MS patients is now underway in South Carolina, and the California researchers hope to enrol around 125 patients for a trial set to begin next year. A major objective of human trials will be to determine the optimal dosage in MS patients. In the mouse studies, the best responses were seen with the highest doses given. The California researchers plan to start human trials using 80 mg of Lipitor - the highest dose approved by the FDA for lowering cholesterol.

    The researchers plan to study patients in the earliest clinical stage of MS for one year to determine whether the statin can reduce the risk for a second recurrence. If effective, it would be the first drug for the disease that can be taken orally. This is not the first time that statins have proved useful in the treatment of MS. Similar findings were reported recently in the journal Neurology.

    Source:  Nature, (07/11/02)

    © Multiple Sclerosis Resource Centre

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