I am curious what the consensus among scientific minded lyme patients and LLMD's is about beta interferon or betaseron therapy for those with Lyme who exhibit MS like symptoms.
I looked it up and it said it blocks certain immune system cells--called T cells--from attacking myelin, the insulating material that protects nerve fibers (axons.) When T cells attack myelin, the nerves become damaged and cannot function properly. It inhibits cytokines (a type of protein), some of which are known to activate the immune system.
We know that lyme can attack the myelin and that lyme causes the immune system to attack the myelin because of molecular mimicry. So wouldn't it make sense we would want to decrease the attack on the myelin and that b interferon could do this?
Are there some Lyme docs trying this? I have some spots in the brain and am concerned about them getting worse. When I experience a major herx or relapse, what if this is a MS type relaspe that is doing more nerve damage?
It was suggested to me by a neurologist, not LLMD.
Posted by pineapple (Member # 11904) on :
I was thinking... if people with MS can take drugs that prevent relapse but do not necessarily eliminate all symptoms, why can't we take LT antibiotics to PREVENT relapse or development of ALS or death from Lyme?
I mean, the IDSA keeps saying there is no evidence that LT antibiotics "improves" symptoms, but do they have proof that LT antibiotics do NOT prevent relapse or further destruction? Do they have proof that after a short course of treatment there is NO evidence of further infection or that any remaining spirochetes are NOT doing any harm?
How can they say that LT antibiotics aren't helping when they cannot prove eradication of the bacteria or prove that the antibiotics are NOT needed to prevent death or neurological damage?
Huh?
Where is their "evidence"?
Posted by Marnie (Member # 773) on :
Prolactin is JUST NOW in trials...
It apparently SPONTANEOUSLY restores the myelin sheath.
That temporarily will be a good thing, but they have forgotten...need to rid the pathogen that is causing the destruction.
Posted by Jellybelly (Member # 7142) on :
My mom who was given the MS diagnosis is on an interferon drug, I think. It is Avonex. It makes her feel much better, BUT it does shut down her immune system.
That in my opinion is REALLY a BAD idea for most of us. With the immune system running at a lower level that just leaves the door wide open for the lyme to spread everywhere and multiply without hinderance.
The immune system is destoying the mylein for a reason, not that it is good, but it knows something is there. Inadvertantly it is harming us due to the nature of the beast.
Is it possible though to take these kind of drugs and STILL kill the lyme.......if that was the case then it may be a lessor of 2 evils. But you would have to kill without the help of the immune system which could mean even more abx.
I still feel that the immune sytem is the best killing machine our bodies have, but we just need to be able to drive these creatures out into the open where the immune system can see and identify them.
Posted by Marnie (Member # 773) on :
"Lactam antibiotics can reduce glutamate toxicity in models of CNS disease by increasing the expression of the glutamate transporter, GLT-1."
The myelin sheath is made up of amino acids...the body is trying to find another source for essential amino acids to make other protein fighters.
Posted by Vermont_Lymie (Member # 9780) on :
quote:Originally posted by pineapple: I was thinking... if people with MS can take drugs that prevent relapse but do not necessarily eliminate all symptoms, why can't we take LT antibiotics to PREVENT relapse or development of ALS or death from Lyme?
I mean, the IDSA keeps saying there is no evidence that LT antibiotics "improves" symptoms, but do they have proof that LT antibiotics do NOT prevent relapse or further destruction? Do they have proof that after a short course of treatment there is NO evidence of further infection or that any remaining spirochetes are NOT doing any harm?
How can they say that LT antibiotics aren't helping when they cannot prove eradication of the bacteria or prove that the antibiotics are NOT needed to prevent death or neurological damage?
These are good questions.
Many folks on lymenet, we here, are the living proof that long-term antibiotics improves symptoms.
Perhaps we should start a petition to go around to folks willing to sign, "My symptoms/my life has been improved by over X months of antibiotics..."
Posted by caat (Member # 2321) on :
Things that nourish and help build the nerve sheaths might help. I'd personally be afraid of anything that would comprimise the immune system.
I'm editing this post and so can't see the original post. Are you on antibiotics that cross the blood brain barrier effectivey? That would be important.
Posted by CaliforniaLyme (Member # 7136) on :
Just some related abstracts- *******************************
1: J Natl Med Assoc. 1995 Aug;87(8):561-8. Related Articles, Links
Immunomodulation in the treatment of multiple sclerosis and amyotrophic lateral sclerosis: a model for autoimmune disorders.
Alonso K, Medenica R.
Institute for Advanced Studies in Medicine, Atlanta, Georgia, USA.
Seventeen multiple sclerosis (MS) patients progressing under conventional therapy (average treatment duration: 3 years) with performance status 3-4 (mean Disability Status Scale [DSS]: 82) who demonstrated circulating lymphokine inhibitor factors were selected for a monthly immunomodulatory protocol using plasmapheresis, followed by 3 days of human intravenous immunoglobulin, and low-dose methylprednisolone, cyclophosphamide, interferon-a, and interferon-g, as well as octreide.
Twelve of the 17 patients presented with visual problems, 12 had lower extremity weakness or paraperesis/paralysis, and 6 had bladder/bowel dysfunction. Following 4 months of therapy, 4 recovered completely, 7 showed loss of paralysis/paraparesis, and 5 had improvement in lower extremity weakness. One patient progressed (mean DSS: 51). Lymphokine inhibitor factors declined in 14 patients with concomitant normalization of circulating immune complexes. Eight patients experienced rises in CD4 levels with stabilization of CD8 levels. Hypotension and hypocalcemia were observed during plasmapheresis.
Twelve patients with amyotrophic lateral sclerosis with poor performance status also were studied. Four of the 12 improved with the regimen, whereas six stabilized disease. Similar alterations in laboratory parameters were described. The rationale for this approach is discussed.
PMID: 7674346
1: Vopr Virusol. 2001 Jan-Feb;46(1):25-8. Related Articles, Links
[Comparative in vitro study of the effectiveness of various immunomodulating substances in tick-borne encephalitis]
[Article in Russian]
Krylova NV, Leonova GN.
Suppressing effect of tick-borne encephalitis (TBE) virus on expression of lymphocyte subpopulation receptors has been demonstrated in vitro. Effects of 14 immunomodulators on expression of T lymphocyte receptors under the effect of TBE virus have been compared. Anti-TBE immunoglobulin, 4-iodantipyrin, and leukinferon had the highest protective effect after a preventive injection. Thymalin and leukinferon in combination with human leukocytic interferon were the most effective within the treatment protocols. Further studies of sensitivity of immunoregulator cells to immunomodulators is recommended with the aim of adding these drugs to therapy of TBE patients.
PMID: 11233283 [PubMed - indexed for MEDLINE]
1: Pharmacol Biochem Behav. 1994 Apr;47(4):901-5. Related Articles, Links
Reversible cognitive decline during high-dose alpha-interferon treatment.
Poutiainen E, Hokkanen L, Niemi ML, Farkkila M.
Department of Neurology, University of Helsinki, Finland.
The cognitive effects of high-dose human leukocyte alpha-interferon (IFN-alpha) treatment were evaluated among 15 patients with the newly diagnosed spinal form of amyotrophic lateral sclerosis (ALS). To confirm the earlier findings showing reversible effects on cognitive performance and to exclude confounding effects, a randomized blinded placebo controlled study was conducted. Twelve patients with continuous intravenous IFN-alpha-infusion treatment over five days and 3 placebo control patients were neuropsychologically evaluated. The neuropsychological examination included tests of intelligence, memory, complex mental processing, visuoconstructional skills, writing, and calculation. A clear difference in the performance profiles of the placebo and the IFN-alpha-treated patient groups was detected: The IFN-alpha group showed significant deterioration during treatment in the digit span backwards task, logical verbal memory task, calculation ability, and writing time, while improvement was seen after treatment. Concomitant fever did not explain the findings. In the placebo group an improvement indicating a learning effect in the three consecutive measurements was found. The reversible cognitive deterioration indicates a clear CNS effect during the IFN-alpha treatment.
PMID: 8029260 [PubMed - indexed for MEDLINE] : J Neuroimmunol. 2005 Aug;165(1-2):83-91. Related Articles, Links
Effective combination of minocycline and interferon-beta in a model of multiple sclerosis.
Giuliani F, Fu SA, Metz LM, Yong VW.
Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada.
The objective of the current study was to investigate whether minocycline improves the effect of an existing multiple sclerosis (MS) medication, interferon-beta, on experimental autoimmune encephalomyelitis (EAE) in mice. When used at sub-optimal doses, neither medication affected EAE but their combination at these doses led to the significant alleviation of EAE disease severity scores and histological outcomes. In culture, the toxicity of T cells to neurons was alleviated by their prior exposure to minocycline or interferon-beta and their combination further attenuated neuronal death. Collectively, these results suggest the utility of the combination of minocycline and interferon-beta in MS.
PMID: 15958276
---------------------------------------------------------------------------�----- 1: Neurology. 2000 Jan 25;54(2):469-74. Related Articles, Links
A randomized controlled trial of recombinant interferon beta-1a in ALS. Italian Amyotrophic Lateral Sclerosis Study Group.
Beghi E, Chio A, Inghilleri M, Mazzini L, Micheli A, Mora G, Poloni M, Riva R, Serlenga L, Testa D, Tonali P.
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
OBJECTIVE: To evaluate the efficacy of recombinant interferon beta (IFNbeta)-1a in the treatment of ALS. BACKGROUND: It has been proposed that IFNs affect the progression of ALS by interfering with putative immune mechanisms involved in the pathogenesis of the disease. METHODS: Patients (n = 61) 40 to 70 years of age with a 6- to 24-month history of confirmed ALS with mild to moderate disability received IFNbeta-1a, 12 mIU (n = 31), or placebo (n = 30) subcutaneously three times a week for 6 months and were followed up for an additional 6 months. Patients were assessed after 4, 12, 24, 36, and 48 weeks. Medical Research Council scale, Norris scale, and bulbar scores as well as forced vital capacity were used to assess disability. Selected electrophysiologic measures (latency, amplitude, and duration of the compound muscle action potential) were also used. RESULTS: Twenty patients randomized to IFNbeta-1a and 17 patients given placebo completed the study. A total of 16 patients receiving IFNbeta-1a became non-self-supporting compared with 16 on placebo (52% versus 53%). There were no significant differences between the two treatment groups for any of the measures of disease progression and disability. Deaths were reported in six patients treated with IFNbeta-1a and four patients on placebo. Adverse events were reported more frequently with IFNbeta-1a (77% of patients) compared with placebo (57%), with flu-like symptoms and local erythema being the commonest complaints. CONCLUSIONS: This pilot study suggests that IFNbeta-1a is not effective in the treatment of ALS.
Publication Types: Clinical Trial Multicenter Study Randomized Controlled Trial
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When I experience a major herx or relapse, what if this is a MS type relaspe that is doing more nerve damage?