title: [Current treatment of multiple sclerosis].
abstract: Multiple sclerosis (MS) is an autoimmune and degenerative disorder. In the past decades, the introduction of parenteral immunomodulatory therapies brought significant progress. These agents increase the number of relapses (shubs) by about 30%, and some of them has been shown to halter the accumulation of neurological symptoms and the development of disability. As first-line agents, interferon beta and glatiramer acetate (consisting of amino acids) can be used. Some new therapeutic strategies have been developed as a result of biotechnological development. The advantage of humanised monoclonal antibodies is that they affect the autoimmune inflammatory process more selectively. Among monoclonal antibodies, natalizumab, which binds to alpha-4-beta-1 integrin receptors and inhibits the migration of T-lymphocytes into the central nervous system, is available from February 2010 in Hungary, recommended as second-line treatment. The efficacy of natalizumab in decreasing relapse rate is > 60%. However, its use is associated with progressive multifocal leukoencephalopathy (PML) in one out of 1000 treated patient. Currently it is recommended as second-line treatment, if the patient has active disease despite immunomodulatory therapy. Among orally administered agents, a preparation containing fingolimod is expected to become available next year, and another pill, cladribin has been also found to be efficient in randomised, controlled phase III trials. Fingolimod acts on sphingosine 1-phosphate receptors-1 (S1P1). Cladribine is a purine nucleotide analogue, and its efficacy is based on long-term reduction of CD4+ and CD8+ lymphocytes. Further promising oral immunomodulatory agents are laquinimod and BG000012 (dimethylfumarate), which are currently being tested in phase III clinical trials in relapsing-remitting MS. The most efficient treatment should be chosen on the basis of the activity, aetiology and the posited pathomechanism of the disease. With the increasing number of therapeutic options, choosing the treatment that is optimal for the patient while also considering side effects might be challenging for both the patients and physicians.
authors.affiliation: Debreceni Egyetem Orvos- és Egészségtudományi Centrum, Neurológiai Klinika/University of Debrecen, Medical and Health Science Center, Department of Neurology; H-4032 Debrecen, Móricz Zsigmond krt. 22. csepany@dote.hu
authors.forename: Tünde
authors.initials: T
authors.lastname: Csépány
mesh_terms: D000284:Administration, Oral; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D017338:Cladribine / Q000627:therapeutic use; D000069462:Dimethyl Fumarate; D004334:Drug Administration Schedule; D000068876:Fingolimod Hydrochloride; D005650:Fumarates / Q000627:therapeutic use; D000068717:Glatiramer Acetate; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D016899:Interferon-beta / Q000627:therapeutic use; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000188:drug therapy; D000069442:Natalizumab; D010455:Peptides / Q000627:therapeutic use; D011409:Propylene Glycols / Q000627:therapeutic use; D015363:Quinolones / Q000627:therapeutic use; D013110:Sphingosine / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D005650:Fumarates; D007166:Immunosuppressive Agents; D000069442:Natalizumab; D010455:Peptides; D011409:Propylene Glycols; D015363:Quinolones; D017338:Cladribine; D000068717:Glatiramer Acetate; D016899:Interferon-beta; C476223:laquinimod; D000069462:Dimethyl Fumarate; D000068876:Fingolimod Hydrochloride; D013110:Sphingosine