Immunomodulatory Treatments for Myasthenia Gravis: Plasma Exchange, Intravenous Immunoglobulins and Semiselective Immunoadsorption

Myasthenia Gravis (MG) is an autoimmune disorder characterized clinically by fluctuating muscle weakness and fatigability on exertion. The disease is caused by specific autoantibodies against proteins of the neuromuscular junction (NMJ) (Conti-Fine et al, 2002; Sanders & Meriggioli, 2009). Two different autoantibodies are routinely detectable, i.e. antibodies against the acetylcholine receptor (AChR) or to a muscle specific tyrosine kinase (MuSK) (Hoch et al., 2001). Anti acetylcholine receptor autoantibodies are detected in about 80-85% of patients with generalized Myasthenia Gravis. Myasthenia Gravis patients without antibodies to either acetylcholine receptor or MuSK are now defined as affected with “seronegative Myasthenia Gravis”. A recent study reported that a proportion of seronegative patients has low-affinity antibodies to acetylcholine receptor, antibodies that cannot be detected by common radioimmunoassay (Leite et al., 2008).