Algorithms of modifying therapies in multiple sclerosis: dominant role of interferon beta
Keywords:
multiple sclerosis, algorithms of modifying therapies, interferon beta, efficacy of treatmentAbstract
Background. Algorithms of the disease modifying therapies (DMT's) are mainstream of multiple sclerosis (MS) current treatment. Objective. To classify algorithms and to evaluate the efficacy of the DMT’s algorithms in MS. Method and patients. Analysis of algorithms aiming at improving the DMT's in 5 groups of MS patients was carried out: 1) in patients with worsening disability, 2) with very active disease, 3) showing a non-response to IFN beta, 4) in drug resistant malignant MS, 5) in patients with antibody neutralizing IFN beta (NAB+). Results. The first set of algorithms includes escalating DMT’s for progressive MS. Therapy began from administration of the Ist line drug and ended with combined treatment, plasmapheresis or natalizumab (NAT) alone. Algorithm of induction treatment showed efficacy of mitozantrone (MTX) + methylprednisolone (MP i.v.) with consecutive IFN beta in very active MS. These patients had lower relapse rate, decreased disability and the reduced number of new T2-related lesions than patients receiving IFN beta alone. Third series of the DMT's algorithms depended on change of treatments in non-responders to IFN beta. The improvement ensued after increase of IFN beta dose, sideeffects management, switching of IFN beta to other Ist and 2nd line drugs or NAT. Fourth kind of algorithm included immunoablation with consecutive rituximab or daclizumab in malignant MS. Small group of seropositive patients (NAB+) favourably responded to combined treatment with IFN beta and cyclic MP iv. Conclusions. The efficacy of MS treatment depends to some extent on choice of the proper DMT algorithm. Batter result of the DMT is more likely if algorithm is adapted to severity, clinical course of the disease and to the drug responsiveness.
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Goodin D., Frohman E., Garmany G. i wsp.: Disease modifying therapy in multiple sclerosis. Neurology 2002; 58: 169-178.
Frohman E.: Treatment of patients with relapsingremitting multiple sclerosis [w:] Rudick R., Goodkin D. (red.): Multiple Sclerosis Therapeutics. M. Dunits. London 1999.
Giovannoni G.: Strategies to treat and prevent the development of neutralizing anti-interferon-β antibodies, Neurology 2003; 61: suppl. 5, S13-S17.
Batra N., Ramanathan N., Hojnacki D. i wsp.: Natalizumab use in a large multiple sclerosis centre ascertaining the therapeutic benefit and the cause for treatment discontinuation, Multiple Sclerosis 2008; 14: suppl. 1, S184.
Cendrowski W.: Stwardnienie rozsiane, Państwowe Wydawnictwo Lekarskie. Warszawa 1993.
Rieckmann P.: Escalating immunomodulatory therapy of multiple sclerosis: update (September 2006), Nervenarzt 2006; 77: 1506-1518.
Karussis D., Bierrmann L., Bohlega S. i wsp.: A recommended treatment algorithm in RRMS: reprint of an international consensus meeting, Europ. J. Neurol. 2006; 13: 61-71.
Ramtahal J., Jacob A., Das K. i wsp.: Sequential maintenance treatment with glatiramer acetate after mitoxantrone is safe and can limit exposure to immunosupression in very active RRMS, J. Neurol. 2006; 253: 1160–1164.
Roxburgh R., Seaman S., Masterman Z. i wsp.: Multiple Sclerosis Severity Scale: using disability and disease duration to rate disease severity, Neurology 2005; 64: 1144–1151.
Herbert J.: Rational treatment algorithms for relapsing multiple sclerosis, Multiple Sclerosis 2006; 12: suppl. 1, S81.
Zivadinov R., Rudick R., De Masi R. i wsp.: Long-term effects of intravenous methylprednisolone therapy on brain atrophy in RRMS, J. Neurol. Sci. 2001; 187: suppl. 1, S434.
Fazekas F., Lublin F., Li D. i wsp.: Intravenous immunoglobulin in RRMS, Neurology 2008; 71: 265-271.
Goodkin D., Bailey R., Teetzen M. i wsp.: The efficacy of azathioprine in RR multiple sclerosis, Neurology 1991; 41: 20-25.
Caon Ch., Zvartau-Hind M., Din M. i wsp.: Combination therapy with glatiramer acetate and intravenous methylprednisolone in RRMS patients at high risk of secondary progression, Multiple Sclerosis 2001; 7: supp. 1, S58.
Havrdova E., Krasensky J., Ticha V. i wsp.: Intramuscular interferon beta 1-A in combination with azatioprine and low dose steroids: preliminary results of a doubleblind placebo controlled study, Multiple Sclerosis 2001; 7: suppl. 1, S65.
Jeffery D., Durden D., Burdette J.: Trial of combined mitoxantrone and interferon beta-1B therapy in patients with worsening MS using monthly gadolinium enhanced MRI, Multiple Sclerosis 2001; 7: suppl. 1, S66.
Phillips J., Kappas L., O’Connor P. i wsp.: The effects of natalizumab monotherapy on multiple measures of disability progression in MS patients, Neurology 2006; 66: suppl. 2, A62-A63.
Kozak T., Havrdova A., Trneny M. i wsp.: Immunoablative therapy with autologous hematopoetic stem cell transplantation in the treatment of poor-risk MS. Multiple Sclerosis 2008; 14: suppl. 1, S52.
Krishnan C., Kaplin A., Brodsky R. i wsp.: Reduction of disease activity and disability with high-dose cydophosphamide in patients with aggressive multiple sclerosis, Arch. Neurol. 2008; 65: 1044–1051.
Edan G.: The effectiveness and practicality of immunosuppressive drugs, Int. MS J. 2004; 11: 53–60.
Le Page E., Comi G., Filippi M. i wsp.: Comparison of two therapeutic strategies in aggressive RRMS: mitoxantrone as induction for 6 months followed by interferon-b-1b versus interferon-b-1b. A 3-year randomized trial, Neurology 2008; 70: A227.
Filippi M., Le Page E., Leray E. i wsp.: MRI results of a 3-year randomized trial comparing two therapeutic strategies in aggressive RRMS: mitoxantrone as induction for 6 months followed by interferon-b-1b versus interferon-b-1b, Multiple Sclerosis 2008; 14: suppl. 1, S103.
Handouk Y., Angeleri V., Danni M. i wsp.: Long-term maintance treatment with glatiramer acetate after mitoxantrone in rapidly progressive MS, Multiple Sclerosis 2008; 14: suppl. 1, S46.
Arnold D., Bar-Or A., Campagnolo D. i wsp.: Short-term immunosuppressive with mitoxantrone: followed by longterm glatiramer acetate vs. glatiramer acetate alone: results at 36 months in patients with RRMS, Multiple Sclerosis 2008; 14: suppl. 1, S29.
Perumal J., Hreha S., Caon Ch. i wsp.: Intense immunosuppression as the initial disease-modifying therapy in clinically active relapsing MS, Multiple Sclerosis 2008; 14: suppl. 1, S172.
Goodin D.: The BEYOND Study. The Bayer Schering Satellite Symposium at the 1st World Congress on Controversies in Neurology, Berlin 2007.
Schwid S., Thorpe J., Sharief M. i wsp.: Enhanced benefit of increasing interferon beta-1a dose and frequency in RRMS, Ann. Neurol. 2005; 62: 785-792.
Tellez N., Rio J., Tintoré M. i wsp.: Glatiramer acetate after mitoxantrone in non-responding to interferon-beta, Multiple Sclerosis 2006; 12: suppl. 1, S216–S217.
Fox E., Mayer L., Sullivan H. i wsp.: Two-year results with alemtuzumab in patients with active RRMS who have failed licensed beta interferon therapies, Multiple Sclerosis 2007; 13: suppl. 2, S166-S167.
Pozzilli C., Gasperini C., Mainero C. i wsp.: Methylprednisolone in association with IFN β-1b to supress the development of NAB in RRMS, Multiple Sclerosis 1999; 5: suppl. 1, S13.
Pozzilli C., Borriello G.: Possible strategies to reduce interferon-beta antibody formation: concomitant treatment with steroids. Eur. J. Neurol. 2002; 9: suppl. 2, 233.
Never L., Singer R., Wang H. i wsp.: Daclizumab exhibits efficacy in multiple sclerosis subjects positive for interferon-beta neutralizing antibodies, Multiple Sclerosis 2008; 14: suppl. 1, S169.
Giovanneni G., Goodman D.: Neutralizing and-IFN-β antibodies. How much more evidence do we need to use them in practice? Neurology 2005; 65: 6-8.
Kappos L., Achtnichts L., Wu S.: BEST (Betaferon® in Early Relapsing-remitting MS Surveillance Trial): interim report 2, Multiple Sclerosis 2005; 11: suppl. 1, S154.
Durko A., Singer M., Nicpan A. i wsp.: Ocena kliniczna i rezonansowa chorych na SR w odległym czasie po zakończeniu leczenia interferonem beta, Neur. Neurochir. Pol. 2008; 42: suppl. 4, S340.
Vellings M., Castelijns J., Barkhof F. i wsp.: Postwithdrawal rebound increase in T2 lesions activity in natalizumab treated MS patients. Neurology 2008; 70: 1150-1151.
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