Azathioprine for Multiple Sclerosis
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Multiple sclerosis (MS) is a complex central nervous system (CNS) disease in which several pathophysiological mechanisms are involved such as inflammation, demyelination, axonal damage, and repairing. MS is currently believed to be an autoimmune disease mediated by a combined attack of both innate and acquired immune responses directed against myelin proteins, because of the failure of self-tolerance. It is widely accepted that this coordinated immune reaction is orchestrated by autoreactive CD4+ T cells secreting T helper 1 (Th1)-type pro-inflammatory cytokines that traffic across the blood–brain barrier and infiltrate the CNS after activation. The involvement of both cellular and humoral mechanisms is widely recognized. MS usually affects young adults, predominantly women. About 80% of MS patients begin with an initial relapsing–remitting (RR) course that, in most cases, evolves into a secondary progressive (SP) phase. Less often (15–20%), a primary progressive (PP) form represents the onset of the disease. Data currently available indicate that reversible deficit mainly results from inflammation and edema, persistent clinical signs from demyelination and axonal damage, whereas progression is attributable to axonal degeneration.
Abstract
Keywords
Multiple sclerosis, immunosuppressive drugs, azathioprine
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