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Interferons In Multiple Sclerosis

  1. Rationale for early treatment with Interferon-ß in MS
    Clin Ther 1997 Sep;19(5):868-882

  2. Acute and chronic NeuroEndocrine effects of Interferon-ß-1a in Multiple Sclerosis
    Clin Endocrinol (Oxf) 2007 Feb;66(2):295-303

  3. Twenty-four-month comparison of ImmunoModulatory treatments - a retrospective open label study in 308 RRMS patients treated with Interferon-beta or Glatiramer Acetate (Copaxone)
    Eur J Neurol 2005 Jun;12(6):425-31

  4. The effects of Interferon-ß on InterLeukin-10 in Multiple Sclerosis
    Eur J Neurol 2005 Mar;12(3):208-11

  5. Bulk Listing
    Newest,   Newer,   Older,   Oldest

  6. Bulk Listing
    Neutralizing AntiBodies to Interferon-beta treatments in MS
    #1   #2   #3

  7. Bulk Listing
    Interferon-ß-1a (Rebif) treatment trial results

  8. Bulk Listing
    Interferon-ß-1a (Avonex) treatment trial results

  9. Bulk Listing
    Pentoxifylline eases Interferon's side effects

  10. Bulk Listing
    Glycosylation in MS Interferon treatments

  11. Bulk Listing Must Read
    Adhesion Molecules in Multiple Sclerosis

  12. Bulk Listing Must Read
    Cytokines and T-Helper Cells in Multiple Sclerosis
    #1   #2

  13. Neutralizing AntiBodies reduce the efficacy of IFN-ß during treatment of Multiple Sclerosis
    Neurology 2004 Jun 8;62(11):2031-7

  14. ElectroPhysiological, NeuroPsychological and clinical findings in Multiple Sclerosis patients receiving Interferon-ß-1b: A 1-year follow-up
    Eur Neurol 2000 Nov;44(4):205-209

  15. Longitudinal study of T1 HypoIntense Lesions in Relapsing MS: MSCRG trial of Interferon-ß-1a
    Neurology 2000 Jul 25;55 (2):185-92

  16. Differential susceptibility of human Th1 versus Th 2 Cells to induction of Anergy and Apoptosis by ECDI/Antigen-coupled Antigen Presenting Cells
    Int Immunol 2000 Jan;12(1):57-66

  17. Interferon-beta inhibits activated Leukocyte migration through the Blood-Brain Barrier
    Lab Invest 1999 Aug;79(8):1015-25

  18. Interferon-gamma (gamma) secretion correlation with disease phase
    Ann Neurol 1999 Feb;45(2):247-50

  19. Interferon gamma receptor binding in Interferon-ß-1b-treated patients
    Arch Neurol 1999;56:217-222

  20. How ß Interferon protects the CNS
    Ann Neurol 43: 384-7 (1998)

  21. Interferon-ß effective against Secondary/Progressive MS
    Lancet 1998 Nov 7;352(9139):1491-7

  22. Interferon-ß effective against R/R & S/P Multiple Sclerosis
    Lancet 1998;352:1486-1487,1491-1504

  23. All-trans Retinoic Acid augments Suppressor cell function in MS
    Arch Neurol 55: 315-21 (1998)

  24. Pretreatment of Astrocytes with Interferon-alpha ß prevents Neuronal Mitochondrial Respiratory Chain Damage
    J NeuroChem 1998 Jan;70(1):432-434

  25. Decreased Type-I Interferons & InterLeukin-2 in Multiple Sclerosis
    J Neurol Sci 1997;149:87-93. 07/21/97

  26. Interferon-ß interferes with MBP-specific Helper T-Cells
    Neurology 1997 Aug;49(2):385-92

  27. MRI changes with Interferon-ß-1a: A short term study in Relapsing/Remitting Multiple Sclerosis
    J Neurol NeuroSurg Psychiatry 1996 Sep;61(3):251-8

  28. LymphoBlastoid Interferon therapy in C/P Multiple Sclerosis
    Neurology 1990 Mar;40(3 Pt 1):479-86



WWW Links

  1. Advances in Multiple Sclerosis Management
    54th Annual Meeting of the American Academy of Neurology

  2. A Global Perspective on Multiple Sclerosis
    Patricia K. Coyle, MD & Syed Rizvi, MD, MBBS

  3. Have Interferons Proven to be the Breakthrough Patients With Multiple Sclerosis Hoped For?
    Drug & Ther Perspect 14(8):1-5, 1999. 1999 Adis International Limited




Rationale for Early Treatment
With Interferon-ß-1a in
R/R Multiple Sclerosis

Munschauer FE 3rd, Stuart WH
Clin Ther 1997 Sep;19(5):868-882
State Univ of New York at Buffalo, William C. Baird Multiple Sclerosis Research Center, School of Medicine and Biomedical Sciences, Buffalo, NY; USA
UI# 98046586
Abstract

Disease-modifying therapies are now available for the treatment of Relapsing/Remitting Multiple Sclerosis (RR/MS).

These drugs have transformed the management of RR/MS from simply treating symptomatic disease to providing effective but incomplete prophylaxis against further disease activity.

Our ability to modify disease activity is limited to reducing exacerbations and delaying progression of disability.

No intervention has yet been shown to reverse disability once it is established. To prevent disability, therapy should be initiated early in the course of the illness. The rationale for early treatment is as follows:

  1. A high percentage of patients with Clinically Definite RR/MS progress from isolated attacks to Neurologic impairment and then to disability within a short time.

  2. Survival in MS is directly related to Disability, so delaying the onset of disability could be expected to influence survival.

  3. Interferon-ß-1a (IFN) has been shown to slow the progression of disability when given to RR/MS patients with impairment or mild disability.

  4. Magnetic Resonance Imaging studies indicate that MS patients frequently have evidence of Central Nervous System Inflammation without overt clinical symptoms (Clinically Silent MS lesions).

  5. It has been postulated that treatment of subclinical disease as identified by Magnetic Resonance Imaging may improve long-term outcome.

  6. IFN-ß reduces the number of new T2-weighted Lesions, as well as the number and volume of Gadolinium-Enhanced Lesions.

Aggressive early treatment with IFN ß-1a is recommended, particularly for patients with risk factors suggesting an unfavorable prognosis.



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