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Myasthenia gravis (MG) is a disorder of the neuromuscular junction mediated by the actions of autoantibodies directed against one of several proteins expressed on the postjunction muscle membrane. For the large majority of MG patients the target for the autoantibodies is the acetylcholine receptor (AChR) (1) that interacts with acetylcholine, the transmitter released by the motor nerve, to trigger muscle contraction.
The Thymus in Myasthenia Gravis
There is a well-known association between abnormalities in the thymus, the central immune organ for development of T cell-mediated immune system and the site of central immune regulation during development (1⇓–3), and the AChR form of MG. The most common abnormality consists of atypical follicular germinal centers in the thymic medulla, so-called thymic hyperplasia, occurring in ∼60 to 75% of patients. In 10 to 15% of patients, neoplastic changes (thymoma) occur, and the remainder of patients exhibit normal involution (1, 4). The etiologic connection between the thymic changes and MG is uncertain (5). For many years there have been series reporting improvement after thymectomy. Recently a prospective single-blinded controlled study demonstrated that thymectomy in patients already receiving corticosteroid therapy is superior to corticosteroids both at 3 y (6) and confirmed at 5 y (7). The improvement was …
↵1To whom correspondence may be addressed. Email: rlisak{at}med.wayne.edu.
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Thymectomy and myasthenia gravis
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- Immunology and Inflammation
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