Disease Modifying Therapies

It is generally held that disease-modifying therapy should be initiated immediately on the diagnosis of MS (Coyle and Hartung, 2002). Disease-modifying therapy has been shown to be more effective in preventing new lesion formation than repairing old lesions. These therapies include interferon beta-1b (Betaseron), interferon beta-1a (Avonex, Rebif), and glatiramer acetate (Copaxone). The beta interferons are immunomodulating medications that also have antiviral activities. They have been shown to reduce relapses in patients with the relapsing-remitting form of MS. Betaseron is given as an alternating-day subcutaneous (SC) injection, Rebif is a three-times-weekly SC injection, and Avonex is administered as a weekly intramuscular injection. All have similar side effects, including injection site reactions, influenza-like symptoms, and worsening of preexisting depression. Bone marrow suppression and transient elevation of liver enzymes may also occur.

Glatiramer (Copaxone) is a synthetic polypeptide consisting of four amino acids. It is thought to lead to the induction of antigen-specific suppressor T cells. It is administered as a daily SC injection and has been shown to reduce relapses by approximately 30% (Comi et al., 2001). Side effects include postinjection reactions and occasionally a reaction involving flushing, chest pain, anxiety, and dyspnea. The reaction is self-limited and does not require discontinuation of the medication.

Two other disease-modifying drugs for MS are mitoxan-trone and natalizumab. Mitoxantrone is a synthetic anthra-cenedione given by IV infusion once every 3 months. It has been shown to reduce MS relapses by 67% (Hartung et al., 2002). Mitoxantrone is blue and can lead to transient bluish discoloration of the sclera and urine. It also can cause car-diotoxicity and as a chemotherapeutic agent, should only be prescribed for worsening cases of MS not responding to firstline agents. Also, only experienced health care professionals should prescribe mitoxantrone.

Natalizumab is a monoclonal antibody that blocks a4-integrin. This molecule is involved in moving circulating leukocytes into the brain in response to inflammation. It is administered as a 1-hour infusion every 4 weeks. Natalizumab has been shown to reduce clinical relapses, slow the progression of disability, and reduce the development of new brain lesions (Polman et al., 2006). Complications that limit its use include a hypersensitivity reaction up to an hour after infusion. Natalizumab has also been associated with progressive multifocal leukoencephalopathy, a destructive brain infection caused by JC virus. Therefore the distribution and use of natalizumab is closely monitored, and it can be administered only by registered physicians.

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