By J. Pruitt
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Additional info for A Look Into Myasthenia Gravis
1999). Cyclosporine induced cancer progression by a cell-autonomous mechanism. 6719, pp. 530–534, ISSN 0028-0836 Myasthenia Gravis – Current Treatment Standards and Emerging Drugs 39 Jacobs, C. ; Smith, C. A. (1997) Methods of lowering active TNF-α levels in mammals using tumor necrosis factor receptor. M. (2005). Autoimmune myasthenia gravis: recommendations for treatment and immunologic modulation. 1, pp. M. (2007) Myasthenia gravis. 1, pp. D. (1989). Cyclosporine. 25, pp. K. (2008) Treatment of a patient with myasthenia gravis using antibodies against CD25.
3. Corticosteroids Since a corticosteroid treatment is efficient in many autoimmune diseases, they are also used in the MG treatment, although their mechanism of action is not fully explained (SchneiderGold 2005). Their interference with the immune system leads to anti-inflammatory, antiallergic and anti-proliferative effect. Additionally, an increased expression and stabilization of acetylcholine receptors was observed in a long term administration of corticosteroids (Braun 1993). The corticosteroids belong to the standard treatment of MG moderate forms and MG mild forms insufficiently responding to the treatment with AChEIs.
9, pp. A. (2003) Treatment of autoimmune myasthenia gravis. 12, pp. 1652–1661, ISSN 0893-0341 Rovin, J. (2008) Etanercept treatment in myasthenia gravis. 1, pp. H. (1972). Histomeric study of neuromuscular junction ultrastructure I. Myasthenia gravis. 1, pp. J. (2004). Management of myasthenia gravis. 1, pp. 41–48, ISSN 0271-8235 Schmid, O. (1957) Bis-carbamic acid ester compounds, and a process of making same. ; Aziz-Aloya R. B. et al. (1995). Synaptic and epidermal accumulations of human acetylcholinesterase are encoded by alternative 3’terminal exons.