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Multiple Sclerosis Treatments What drug treatments are available for MS and its symptoms? Below is a table of drugs used to treat multiple sclerosis and its symptoms. It only lists drug therapies and does not deal with other forms of therapy - These shall be posted to this section in a short period of time. It is vital that you are prescribed and take any of these medications in consultation with a fully qualified medical practitioner who is familiar with your case history. Many of these drugs have potentially serious side-effects especially in combination with other medications.
The list is by no means complete and new treatments are being
researched and coming into use all the time. It should be emphasized
that none of these drugs are a "cure" for either MS nor for any of
its symptoms. The only medications available at the moment either
slow down the course of the disease at best or are palliative on its
symptoms.
"Is there a cure for MS?" Sadly not - currently there is no cure for MS but there are treatments both to slow down the course of the disease and mitigate against its effects. There are a number of new treatments that are in the research stage or are in clinical trials. Some of these are very promising indeed and the current mood in MS research is very optimistic - we can look forward to more effective treatments in the near future. ABC Treatments Perhaps the most effective treatments currently available today deal with the autoimmune component of multiple sclerosis and work by regulating aspects of the immune system. They are known as the "ABC" treatments, where "A" stands for Avonex, "B" stands for Betaseron/Betaferon and "C" stands for Copaxone. Avonex and Betaseron are both varieties of beta interferon. A third drug, Rebif, is also beta interferon. ABCR would be a more accurate acronym though clearly less appealing to those of us with a crossword-solving mentality. Copaxone is a completely different drug altogether - the active ingredient being glatiramer acetate, Co-polymer-1 or COP-1. A fifth drug, Novantrone, has recently become available. This is a chemotherapeutic agent which I shall deal with in a later section. Beta interferon Beta Interferon comes in two varieties, beta interferon-1a (Avonex and Rebif) and beta interferon-1b (Betaseron in the US and Betaferon in Europe). Beta interferon (IFN-b) is a naturally occurring biochemical in the human body and belongs to a group of biochemicals known as interferons (IFNs) which regulate the functioning of the immune system. The mechanism by which IFN-b functions is complex and not fully understood. I shall explore this more fully in a later section but for now we can summarize it as:
How effective is IFN-beta? A lot of studies have now been done on the efficacy of beta interferons in both relapsing-remitting and secondary progressive MS. The methods of evaluation that have been used are measurements of MRI lesion activity, relapse rate and EDSS (degree of disability). The bottom line of this research is that the drug is effective at reducing relapses and burden of disease under MRI in both types of MS. Most studies imply that the drugs also affect long-term progression though the evidence for this is less clear. Most studies also imply that IFN-b is dose dependent - that is, the higher the dose used, the greater the efficacy [Durelli et al, 2001; Coyle, 2002; Ref 1998]. However, one study contradicts these findings [Ref, 2001]. Before going into the statistics thrown up by these studies I'd like to address what seems to me to be a very important misconception that's been floating around the MS community. People who are using beta interferon (or Copaxone, for that matter) sometimes believe that the drug is not working for them because their disease continues to progress. Others say that the drug only works for one third of users. The first of these statements is probably incorrect and the second is almost definitely wrong. In the first place, we know that MS is a very unpredictable disease and none of us know where, nor on what time scale it is heading. If it continues to progress while you are using IFN-b, that doesn't mean that the drug isn't working - it could have progressed faster if you hadn't been using it. In fact, this is the implication of the studies. Secondly, when research shows an x% reduction in the burden of new lesions between the people being treated with IFN-b as compared to a placebo group (those not receiving the drug) over a one year period, it is very hard to tell whether it has worked fully for some people, partially for some others and not at all for the rest. This is because no one has any idea of what would have happened to any particular person. Unless the studies are extremely large, all that can be said is that the drug reduces lesion load by an average of x% over a certain period of time. It may be that the ABCR drugs don't work for everybody and, indeed, some other people seem to do very well with them whereas others do not. However, at this point in time, it's very difficult to say whether this is due to the drugs, the individuals or the interaction between the two. Probably, the best advice is to switch medication from one to another or to Novantrone if your disease seems to be running out of control. What IFN-b is not, is a cure for some people and no good at all for others. The bottom line is that, even if it doesn't appear to be working for you, it may very well be. But how effective is beta interferon? Gimme some numbers! In relapsing-remitting MS the number of relapses and their severity is reduced by 25% and upwards, depending on the dose. The reduction in lesion load measured on MRI scans is much greater than this at upwards of 70%. It is believed that the minority of lesions detectable on MRI scans produce clinically measurable symptoms, but the benefits of these massive reductions may pay dividends years later after onset of a secondary progressive phase. One recent hotly-disputed study [Coyle, 2002] has showed that interferon beta 1a administered according to the Rebif regime is more effective than the same compound administered according to the Avonex regime. Another study [Durelli et al, 2001] has shown that interferon beta 1b administered according to the Betaseron regime is more effective than interferon beta 1a administered according to the Avonex regime. In one study, IFN-b, was shown to reduce the relapse rate in secondary progressive multiple sclerosis by a statistically significant amount. However, two other similar studies failed to show statistically significant effects. It is known that relapse rate falls off during the course of the disease and that inflammatory activity is correlated with relapses. It is also believed that the mechanism of disease activity changes from an inflammatory one to a neuro-degenerative one during the secondary progressive phase of the disease. Based on these and other results, it seems likely that IFN-b is only effective at preventing inflammation and thus relapses and not effective at preventing neuro-degeneration. Long term studies show that, for most people, beta interferons continue to be effective with continued use during the relapsing-remitting phase of the disease. However, a sizeable minority of patients develop neutralising antibodies to the drugs which may reduce their efficacy. Are there any side-effects of beta interferon? Five year studies of beta interferon use have turned up no serious side-effects. This has always struck me as strange. T-cell mediated immunity is vital for survival - look at AIDS to see what happens if you don't have any T-cells. However, some people genetically lack the ability to produce any gamma interferon at all and this apparently has no effect on their life-expectancy (presumably none of them get MS or at least not very badly). Avonex appears to give fewer side effects than Betaseron or Rebif, perhaps due to its lower dose - injections are once a week as opposed to every other day or three times per week. The principle side-effect of beta interferon use are 'flu-like symptoms - fever, night sweats and muscle aches. These can be very unpleasant but often subside after a few months and respond well to ibuprofen. Liver toxicity has been noted in some patients particularly at higher doses though this symptom is usually mild. Be sure to notify your doctor if you are experiencing new symptoms whether or not they appear to be attributable to multiple sclerosis. Depression is another potential side-effect. Injection site reactions can also be a problem and it is advisable to rotate the injection site to mitigate against these. Numbing the skin at the injection site with ice, getting the drug up to room temperature before injecting and taking antihistamines before injecting all help. One of the difficulties many people have is the problem of having to inject themselves. Autoinjectors are available or you can get someone else to help you with this. Most people get over this barrier eventually. Copaxone, glatiramer acetate, COP-1 Glatiramer acetate is a collection of synthetic peptide strings derivatives that is believed to work by modifying the body's T-cell mediated immune response to myelin. As with beta interferon, its method of action is complex and is not fully understood. One theory goes that, by flooding the body with the antigens similar to those in proteins found in the myelin sheath, the drug acts as a decoy and draws some of the attack away from the CNS. Glatiramer acetate arose from studies done on mice. They were first infected with EAE, an experimentally induced disease that resembles multiple sclerosis. The mice were then injected with the drug and responded well to the treatment. Glatiramer acetate is manufactured under the brand name Copaxone by Teva Marion Partners. It was known as copolymer during its development phase which became copolymer-1 (COP-1) when copolymer-2 started to be developed. How effective is Copaxone? Copaxone is about as effective as beta interferons. There have been two double blind studies both over two years and both done on relapsing/remitting patients. The first was at a single site and reported a 75% reduction in relapse rate, the second multi-site study reported a 29% reduction in relapse rate. The wide discrepancy between the two studies is probably explained by the widely fluctuating results deriveable from the relatively small population bases that make up such trials. The first single-centre trial was done with 25 patients receiving glatiramer acetate and 25 receiving a placebo. The second multi-centre one had 125 receiving the drug and 126 the placebo. The initial trials also indicated a reduction in EDSS progession in multiple sclerosis. More recent evidence has shown Copaxone to significantly reduce the rate of brain atrophy. The results of a contraversial and disputed comparative trial between Avonex, Betaseron and Copaxone were released in 1999. These indicated that Copaxone was as effective as Betaseron and more so than Avonex. What are the side-effects of Copaxone? Copaxone is generally better tolerated than beta interferon, though as a synthetic drug that doesn't occur naturally in the human body and with a track record of only a few years, it is hard to evaluate its long-term effects. However no serious side-effects have been reported thus far. Copaxone is injected sub-cutaneously on a daily basis. The most common problem that users have are injection site reactions which include itching and inflammation. These reactions can be mitigated against by revolving the injection site, preparing it with ice and ensuring that the drug is at room temperature before injecting. Some users experience flushing, chest and joint pains, weakness, nausea, anxiety and muscle stiffness. These tend to resolve after about a quarter of an hour without special treatment. Availablity of ABC treatments ABC treatments are very expensive, but they are available to ALL those with MS. Talk to your neurologist. Each manufacturer has a funding program if you are uninsured, or if your insurance won’t pay for it. There isn't much that works for MS, but these drugs do and we need to preserve our myelin until newer and better treatments become available. The huge reduction in "silent" lesions (those which are not associated with clinical symptoms) observed with the use of ABCRs seems to me to bode well for the longer term prognosis of MS.
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