Which medications in the drug class Corticosteroids are used in the treatment of Myasthenia Gravis?

Updated: Aug 27, 2018
  • Author: Abbas A Jowkar, MBBS; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL  more...
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Corticosteroids are anti-inflammatory and immunomodulating agents used to treat idiopathic and acquired autoimmune disorders. They were among the first immunomodulating agents used to treat MG and still are used frequently and effectively. They are typically used in moderate or severe cases that do not respond adequately to AChE inhibitors and thymectomy. Long-term treatment with corticosteroids is effective and may induce remission or cause marked to moderate improvement in most patients.

Transient worsening might occur initially; clinical improvement then shows after 2-4 weeks with maximal effect in 5-6 months. These agents are usually given over 1 or 2 years before tapering is begun. Remissions are noted in 30% and marked improvement in 40%.

Corticosteroids act in both ocular MG and generalized MG. They can be combined with other immunosuppressive medications for better effect with lesser dose and shorter duration of administration. Pulsed IV steroids might be beneficial in refractory patients.

Prednisone (Deltasone, Rayos)

Prednisone is most commonly used corticosteroid in the United States. Some experts believe that the long-term administration of prednisone is beneficial, but others use the drug only during acute exacerbations to limit the adverse effects of chronic steroid use.

Prednisone is effective in decreasing the severity of MG exacerbations by suppressing the formation of autoantibodies. However, clinical effects often are not seen for several weeks. Significant improvement, which may be associated with a decreased antibody titer, usually occurs in 1-4 months. An alternate-day regimen may minimize adverse effects. A trial of steroid withdrawal may be attempted, but most patients on long-term corticosteroid therapy relapse and require re-institution of steroids.

Chronic administration of corticosteroids is associated with numerous serious side effects. The risk of infection, diabetes mellitus, hypotension, glaucoma, osteoporosis, steroid myopathy, and aseptic necrosis of the joints are some examples. It is prudent to obtain chest X-ray, PPD skin test, and a detailed history of exposure to tuberculosis, strongyloides, or other organisms that may grow as a result of the chronic administration of corticosteroids. Measurement of DEXA at baseline and every 6-12 months while the patient is on corticosteroids is recommended. If the bone density shows evidence of osteopenia or osteoporosis, calcium supplementation  (1 g/day), vitamin D (400-800 IU daily), and biphosphonates are started prophylactically for steroid-induced osteoporosis. Prophylactic treatment with histamine-H2 receptor blockers are usually not required.

BP monitoring, periodic eye exam to check for glaucoma and cataracts is recommended.  Fasting blood glucose, serum potassium levels should be periodically checked. Potassium may be supplemented if the patient becomes hypokalemic.

High dose steroids and lack of physical activity can lead to type 2 muscle fiber atrophy with proximal muscle weakness. Distinction from myasthenic weakness is important and is challenging. Patients who become weaker during a prednisone taper, and show craniobulbar, and upper extremity muscle weakness, and demonstrate worsening of their decremental response on RNS are more likely to experience worsening of their myasthenia gravis symptoms.  In contrast, patients who are continued on high doses of corticosteroids, normal RNS, and other evidence of steroid induced toxicity (i.e., Cushingoid features), increasing leg weakness, or have type 2 muscle fiber atrophy could benefit from physical therapy and steroid dose reduction.

Methylprednisolone (Solu-Medrol, Medrol, A-Methapred)

Methylprednisolone may be used in place of prednisone in patients who are intubated and in those unable to tolerate oral intake. It decreases inflammation by suppressing the migration of polymorphonuclear (PMN) leukocytes and reversing increased capillary permeability.

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