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==== Symptomatic treatments ====
==== Symptomatic treatments ====
An oral [[anticholinesterase]] like [[pyridostigmine]] is usually the first drug in [[Myasthenia gravis|MG]] patients.<ref name="pmid27358333">{{cite journal |vauthors=Sanders DB, Wolfe GI, Benatar M, Evoli A, Gilhus NE, Illa I, Kuntz N, Massey JM, Melms A, Murai H, Nicolle M, Palace J, Richman DP, Verschuuren J, Narayanaswami P |title=International consensus guidance for management of myasthenia gravis: Executive summary |journal=Neurology |volume=87 |issue=4 |pages=419–25 |date=July 2016 |pmid=27358333 |pmc=4977114 |doi=10.1212/WNL.0000000000002790 |url=}}</ref> these drugs can reduce the degradation of [[Acetylcholine|Ach]] in the [[synaptic cleft]].<ref name="pmid19260048">{{cite journal |vauthors=Punga AR, Stålberg E |title=Acetylcholinesterase inhibitors in MG: to be or not to be? |journal=Muscle Nerve |volume=39 |issue=6 |pages=724–8 |date=June 2009 |pmid=19260048 |doi=10.1002/mus.21319 |url=}}</ref>   
An oral [[anticholinesterase]] like [[pyridostigmine]] is usually the first drug in [[Myasthenia gravis|MG]] patients.<ref name="pmid27358333">{{cite journal |vauthors=Sanders DB, Wolfe GI, Benatar M, Evoli A, Gilhus NE, Illa I, Kuntz N, Massey JM, Melms A, Murai H, Nicolle M, Palace J, Richman DP, Verschuuren J, Narayanaswami P |title=International consensus guidance for management of myasthenia gravis: Executive summary |journal=Neurology |volume=87 |issue=4 |pages=419–25 |date=July 2016 |pmid=27358333 |pmc=4977114 |doi=10.1212/WNL.0000000000002790 |url=}}</ref> These drugs can reduce the degradation of [[Acetylcholine|Ach]] in the [[synaptic cleft]].<ref name="pmid19260048">{{cite journal |vauthors=Punga AR, Stålberg E |title=Acetylcholinesterase inhibitors in MG: to be or not to be? |journal=Muscle Nerve |volume=39 |issue=6 |pages=724–8 |date=June 2009 |pmid=19260048 |doi=10.1002/mus.21319 |url=}}</ref>   


==== Chronic immunomodulating treatments ====
==== Chronic immunomodulating treatments ====
* glucocorticoids: There are many studies supporting the beneficial effect of [[glucocorticoids]] like oral [[prednisone]] and pulsed [[Intravenous|intravenous (IV)]] [[methylprednisolone]] in [[Myasthenia gravis|MG]] patients. This group of drugs can improve the [[Symptom|symptoms]] in almost 50 percent of patients.<ref name="pmid15846640">{{cite journal |vauthors=Schneider-Gold C, Gajdos P, Toyka KV, Hohlfeld RR |title=Corticosteroids for myasthenia gravis |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD002828 |date=April 2005 |pmid=15846640 |doi=10.1002/14651858.CD002828.pub2 |url=}}</ref><ref name="pmid821005">{{cite journal |vauthors=Mann JD, Johns TR, Campa JF |title=Long-term administration of corticosteroids in myasthenia gravis |journal=Neurology |volume=26 |issue=8 |pages=729–40 |date=August 1976 |pmid=821005 |doi= |url=}}</ref><ref name="pmid6721451">{{cite journal |vauthors=Pascuzzi RM, Coslett HB, Johns TR |title=Long-term corticosteroid treatment of myasthenia gravis: report of 116 patients |journal=Ann. Neurol. |volume=15 |issue=3 |pages=291–8 |date=March 1984 |pmid=6721451 |doi=10.1002/ana.410150316 |url=}}</ref><ref name="pmid4062612">{{cite journal |vauthors=Arsura E, Brunner NG, Namba T, Grob D |title=High-dose intravenous methylprednisolone in myasthenia gravis |journal=Arch. Neurol. |volume=42 |issue=12 |pages=1149–53 |date=December 1985 |pmid=4062612 |doi= |url=}}</ref> the side effects of these drug are: Skin thinning and [[purpura]]<ref name="pmid17501951">{{cite journal |vauthors=Fardet L, Flahault A, Kettaneh A, Tiev KP, Généreau T, Tolédano C, Lebbé C, Cabane J |title=Corticosteroid-induced clinical adverse events: frequency, risk factors and patient's opinion |journal=Br. J. Dermatol. |volume=157 |issue=1 |pages=142–8 |date=July 2007 |pmid=17501951 |doi=10.1111/j.1365-2133.2007.07950.x |url=}}</ref>, [[Cushingoid appearance]] and weight gain<ref name="pmid18684744">{{cite journal |vauthors=Huscher D, Thiele K, Gromnica-Ihle E, Hein G, Demary W, Dreher R, Zink A, Buttgereit F |title=Dose-related patterns of glucocorticoid-induced side effects |journal=Ann. Rheum. Dis. |volume=68 |issue=7 |pages=1119–24 |date=July 2009 |pmid=18684744 |doi=10.1136/ard.2008.092163 |url=}}</ref>, [[Cataract|cataracts]] and [[glaucoma]]<ref name="pmid16107513">{{cite journal |vauthors=Da Silva JA, Jacobs JW, Kirwan JR, Boers M, Saag KG, Inês LB, de Koning EJ, Buttgereit F, Cutolo M, Capell H, Rau R, Bijlsma JW |title=Safety of low dose glucocorticoid treatment in rheumatoid arthritis: published evidence and prospective trial data |journal=Ann. Rheum. Dis. |volume=65 |issue=3 |pages=285–93 |date=March 2006 |pmid=16107513 |pmc=1798053 |doi=10.1136/ard.2005.038638 |url=}}</ref>, [[ischemic heart disease]] and [[heart failure]]<ref name="pmid15545676">{{cite journal |vauthors=Wei L, MacDonald TM, Walker BR |title=Taking glucocorticoids by prescription is associated with subsequent cardiovascular disease |journal=Ann. Intern. Med. |volume=141 |issue=10 |pages=764–70 |date=November 2004 |pmid=15545676 |doi= |url=}}</ref>, [[gastritis]], ulcer formation, and [[gastrointestinal bleeding]]<ref name="pmid6343871">{{cite journal |vauthors=Messer J, Reitman D, Sacks HS, Smith H, Chalmers TC |title=Association of adrenocorticosteroid therapy and peptic-ulcer disease |journal=N. Engl. J. Med. |volume=309 |issue=1 |pages=21–4 |date=July 1983 |pmid=6343871 |doi=10.1056/NEJM198307073090105 |url=}}</ref><ref name="pmid2012355">{{cite journal |vauthors=Piper JM, Ray WA, Daugherty JR, Griffin MR |title=Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs |journal=Ann. Intern. Med. |volume=114 |issue=9 |pages=735–40 |date=May 1991 |pmid=2012355 |doi= |url=}}</ref>, [[Menstrual cycle|menstrual]] irregularities in women and low [[fertility]] in both men and women<ref name="pmid3083749">{{cite journal |vauthors=MacAdams MR, White RH, Chipps BE |title=Reduction of serum testosterone levels during chronic glucocorticoid therapy |journal=Ann. Intern. Med. |volume=104 |issue=5 |pages=648–51 |date=May 1986 |pmid=3083749 |doi= |url=}}</ref><ref name="pmid712726">{{cite journal |vauthors=Crilly R, Cawood M, Marshall DH, Nordin BE |title=Hormonal status in normal, osteoporotic and corticosteroid-treated postmenopausal women |journal=J R Soc Med |volume=71 |issue=10 |pages=733–6 |date=October 1978 |pmid=712726 |pmc=1436218 |doi= |url=}}</ref> and [[psychiatric]] and [[cognitive]] symptoms.<ref name="pmid19906230">{{cite journal |vauthors=Wolkowitz OM, Burke H, Epel ES, Reus VI |title=Glucocorticoids. Mood, memory, and mechanisms |journal=Ann. N. Y. Acad. Sci. |volume=1179 |issue= |pages=19–40 |date=October 2009 |pmid=19906230 |doi=10.1111/j.1749-6632.2009.04980.x |url=}}</ref>
* glucocorticoids: There are many studies supporting the beneficial effect of [[glucocorticoids]] like oral [[prednisone]] and pulsed [[Intravenous|intravenous (IV)]] [[methylprednisolone]] in [[Myasthenia gravis|MG]] patients. This group of drugs can improve the [[Symptom|symptoms]] in almost 50 percent of patients.<ref name="pmid15846640">{{cite journal |vauthors=Schneider-Gold C, Gajdos P, Toyka KV, Hohlfeld RR |title=Corticosteroids for myasthenia gravis |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD002828 |date=April 2005 |pmid=15846640 |doi=10.1002/14651858.CD002828.pub2 |url=}}</ref><ref name="pmid821005">{{cite journal |vauthors=Mann JD, Johns TR, Campa JF |title=Long-term administration of corticosteroids in myasthenia gravis |journal=Neurology |volume=26 |issue=8 |pages=729–40 |date=August 1976 |pmid=821005 |doi= |url=}}</ref><ref name="pmid6721451">{{cite journal |vauthors=Pascuzzi RM, Coslett HB, Johns TR |title=Long-term corticosteroid treatment of myasthenia gravis: report of 116 patients |journal=Ann. Neurol. |volume=15 |issue=3 |pages=291–8 |date=March 1984 |pmid=6721451 |doi=10.1002/ana.410150316 |url=}}</ref><ref name="pmid4062612">{{cite journal |vauthors=Arsura E, Brunner NG, Namba T, Grob D |title=High-dose intravenous methylprednisolone in myasthenia gravis |journal=Arch. Neurol. |volume=42 |issue=12 |pages=1149–53 |date=December 1985 |pmid=4062612 |doi= |url=}}</ref> The side effects of these drug are: Skin thinning and [[purpura]]<ref name="pmid17501951">{{cite journal |vauthors=Fardet L, Flahault A, Kettaneh A, Tiev KP, Généreau T, Tolédano C, Lebbé C, Cabane J |title=Corticosteroid-induced clinical adverse events: frequency, risk factors and patient's opinion |journal=Br. J. Dermatol. |volume=157 |issue=1 |pages=142–8 |date=July 2007 |pmid=17501951 |doi=10.1111/j.1365-2133.2007.07950.x |url=}}</ref>, [[Cushingoid appearance]] and weight gain<ref name="pmid18684744">{{cite journal |vauthors=Huscher D, Thiele K, Gromnica-Ihle E, Hein G, Demary W, Dreher R, Zink A, Buttgereit F |title=Dose-related patterns of glucocorticoid-induced side effects |journal=Ann. Rheum. Dis. |volume=68 |issue=7 |pages=1119–24 |date=July 2009 |pmid=18684744 |doi=10.1136/ard.2008.092163 |url=}}</ref>, [[Cataract|cataracts]] and [[glaucoma]]<ref name="pmid16107513">{{cite journal |vauthors=Da Silva JA, Jacobs JW, Kirwan JR, Boers M, Saag KG, Inês LB, de Koning EJ, Buttgereit F, Cutolo M, Capell H, Rau R, Bijlsma JW |title=Safety of low dose glucocorticoid treatment in rheumatoid arthritis: published evidence and prospective trial data |journal=Ann. Rheum. Dis. |volume=65 |issue=3 |pages=285–93 |date=March 2006 |pmid=16107513 |pmc=1798053 |doi=10.1136/ard.2005.038638 |url=}}</ref>, [[ischemic heart disease]] and [[heart failure]]<ref name="pmid15545676">{{cite journal |vauthors=Wei L, MacDonald TM, Walker BR |title=Taking glucocorticoids by prescription is associated with subsequent cardiovascular disease |journal=Ann. Intern. Med. |volume=141 |issue=10 |pages=764–70 |date=November 2004 |pmid=15545676 |doi= |url=}}</ref>, [[gastritis]], ulcer formation, and [[gastrointestinal bleeding]]<ref name="pmid6343871">{{cite journal |vauthors=Messer J, Reitman D, Sacks HS, Smith H, Chalmers TC |title=Association of adrenocorticosteroid therapy and peptic-ulcer disease |journal=N. Engl. J. Med. |volume=309 |issue=1 |pages=21–4 |date=July 1983 |pmid=6343871 |doi=10.1056/NEJM198307073090105 |url=}}</ref><ref name="pmid2012355">{{cite journal |vauthors=Piper JM, Ray WA, Daugherty JR, Griffin MR |title=Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs |journal=Ann. Intern. Med. |volume=114 |issue=9 |pages=735–40 |date=May 1991 |pmid=2012355 |doi= |url=}}</ref>, [[Menstrual cycle|menstrual]] irregularities in women and low [[fertility]] in both men and women<ref name="pmid3083749">{{cite journal |vauthors=MacAdams MR, White RH, Chipps BE |title=Reduction of serum testosterone levels during chronic glucocorticoid therapy |journal=Ann. Intern. Med. |volume=104 |issue=5 |pages=648–51 |date=May 1986 |pmid=3083749 |doi= |url=}}</ref><ref name="pmid712726">{{cite journal |vauthors=Crilly R, Cawood M, Marshall DH, Nordin BE |title=Hormonal status in normal, osteoporotic and corticosteroid-treated postmenopausal women |journal=J R Soc Med |volume=71 |issue=10 |pages=733–6 |date=October 1978 |pmid=712726 |pmc=1436218 |doi= |url=}}</ref> and [[psychiatric]] and [[cognitive]] symptoms.<ref name="pmid19906230">{{cite journal |vauthors=Wolkowitz OM, Burke H, Epel ES, Reus VI |title=Glucocorticoids. Mood, memory, and mechanisms |journal=Ann. N. Y. Acad. Sci. |volume=1179 |issue= |pages=19–40 |date=October 2009 |pmid=19906230 |doi=10.1111/j.1749-6632.2009.04980.x |url=}}</ref>
* immunosuppressive drugs
* immunosuppressive drugs
# Azathioprine: [[Azathioprine]], a [[purine]] analogue which inhibits the [[Nucleic acid|nucleic acids]] synthesis, can cause improvement in about 90 percent of myasthenia gravis patients but the onset of this effect takes at least 6 to 12 month.(13-14-15-16 chronic) [[Azathioprine]] can cause [[macrocytosis]] (increased [[MCV]]) and [[Malignancy|malignancies]] such as [[Non hodgkin lymphoma|non-hodgkin lymphoma]]. (19-20 chronic)  
# Azathioprine: [[Azathioprine]], a [[purine]] analogue which inhibits the [[Nucleic acid|nucleic acids]] synthesis, can cause improvement in about 90 percent of myasthenia gravis patients but the onset of this effect takes at least 6 to 12 month.(13-14-15-16 chronic) [[Azathioprine]] can cause [[macrocytosis]] (increased [[MCV]]) and [[Malignancy|malignancies]] such as [[Non hodgkin lymphoma|non-hodgkin lymphoma]]. (19-20 chronic)  

Revision as of 18:42, 21 June 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Medical Therapy

The mainstays of medical therapy for myasthenia gravis are:

Symptomatic treatments

An oral anticholinesterase like pyridostigmine is usually the first drug in MG patients.[1] These drugs can reduce the degradation of Ach in the synaptic cleft.[2]

Chronic immunomodulating treatments

  1. Azathioprine: Azathioprine, a purine analogue which inhibits the nucleic acids synthesis, can cause improvement in about 90 percent of myasthenia gravis patients but the onset of this effect takes at least 6 to 12 month.(13-14-15-16 chronic) Azathioprine can cause macrocytosis (increased MCV) and malignancies such as non-hodgkin lymphoma. (19-20 chronic)
  2. Mycophenolate: Mycophenolate mofetil, a purine synthesis blocker in lymphocytes, is proven to be effective in reducing the symptoms of MG patients and their need to glucocorticoids.(25-26)
  3. Cyclosporine: Cyclosporine, an immunomodulatory agent which blocks the production of interleukin-2 and inhibits the function of T helper cells, can cause improvement in about 90 percent of MG patients after 1 to 2 months of start but the maximum effect will appear after 7 months.(32-33-34 chronic) This drug can cause nephrotoxicity (37), tremor, nausea, myalgias, gingival hyperplasia, hypertrichosis and malignancies such as squamous cell skin cancer and lymphoma.(34)
  4. Tacrolimus: Tacrolimus, an immunosuppressive macrolid can significantly reduce the requirement to prednisolone and MG symptoms in almost 67 to 87 percent of patients with less nephrotoxicity than cyclosporine.(37-38-40 ta44 chronic) the side effects of this drug include hyperglycemia, hypomagnesemia, paresthesias and tremor.(45)
  5. Rituximab: Rituximab, a monoclonal antibody against B cell membrane marker CD20 can be used in refractory myasthenia gravis. This drug is also effective in patients with anti MuSK antibody.(46-47-48-49-50 chronic)
  6. Methotrexate: Methotrexate is an immunosuppressant agent which suggested to be effective as a second line immunosuppressant for MG patients.(51-52)
  7. Etanercept: Etanercept is made of TNF receptor linked to Fc portion of human IgG1. This drug can inhibit TNF-alpha which is a proinflammatory cytokine, and improve the symptoms of MG patients.(53)
  8. Cyclophosphamide: Cyclophosphamide is an alkylating agent which inhibits the proliferation of B and T cells. Monthly high dose intravenous administration of this drug is proved to be more effective than daily oral type.(54) the side effects of this drug include anorexia, nausea and vomiting, leukopenia, alopecia and hemorrhagic cystitis and it can also increase the risk of malignancies.(54-55)

Rapid immunomodulating treatments

References

  1. ↑ Sanders DB, Wolfe GI, Benatar M, Evoli A, Gilhus NE, Illa I, Kuntz N, Massey JM, Melms A, Murai H, Nicolle M, Palace J, Richman DP, Verschuuren J, Narayanaswami P (July 2016). "International consensus guidance for management of myasthenia gravis: Executive summary". Neurology. 87 (4): 419–25. doi:10.1212/WNL.0000000000002790. PMC 4977114. PMID 27358333.
  2. ↑ Punga AR, Stålberg E (June 2009). "Acetylcholinesterase inhibitors in MG: to be or not to be?". Muscle Nerve. 39 (6): 724–8. doi:10.1002/mus.21319. PMID 19260048.
  3. ↑ Schneider-Gold C, Gajdos P, Toyka KV, Hohlfeld RR (April 2005). "Corticosteroids for myasthenia gravis". Cochrane Database Syst Rev (2): CD002828. doi:10.1002/14651858.CD002828.pub2. PMID 15846640.
  4. ↑ Mann JD, Johns TR, Campa JF (August 1976). "Long-term administration of corticosteroids in myasthenia gravis". Neurology. 26 (8): 729–40. PMID 821005.
  5. ↑ Pascuzzi RM, Coslett HB, Johns TR (March 1984). "Long-term corticosteroid treatment of myasthenia gravis: report of 116 patients". Ann. Neurol. 15 (3): 291–8. doi:10.1002/ana.410150316. PMID 6721451.
  6. ↑ Arsura E, Brunner NG, Namba T, Grob D (December 1985). "High-dose intravenous methylprednisolone in myasthenia gravis". Arch. Neurol. 42 (12): 1149–53. PMID 4062612.
  7. ↑ Fardet L, Flahault A, Kettaneh A, Tiev KP, Généreau T, Tolédano C, Lebbé C, Cabane J (July 2007). "Corticosteroid-induced clinical adverse events: frequency, risk factors and patient's opinion". Br. J. Dermatol. 157 (1): 142–8. doi:10.1111/j.1365-2133.2007.07950.x. PMID 17501951.
  8. ↑ Huscher D, Thiele K, Gromnica-Ihle E, Hein G, Demary W, Dreher R, Zink A, Buttgereit F (July 2009). "Dose-related patterns of glucocorticoid-induced side effects". Ann. Rheum. Dis. 68 (7): 1119–24. doi:10.1136/ard.2008.092163. PMID 18684744.
  9. ↑ Da Silva JA, Jacobs JW, Kirwan JR, Boers M, Saag KG, Inês LB, de Koning EJ, Buttgereit F, Cutolo M, Capell H, Rau R, Bijlsma JW (March 2006). "Safety of low dose glucocorticoid treatment in rheumatoid arthritis: published evidence and prospective trial data". Ann. Rheum. Dis. 65 (3): 285–93. doi:10.1136/ard.2005.038638. PMC 1798053. PMID 16107513.
  10. ↑ Wei L, MacDonald TM, Walker BR (November 2004). "Taking glucocorticoids by prescription is associated with subsequent cardiovascular disease". Ann. Intern. Med. 141 (10): 764–70. PMID 15545676.
  11. ↑ Messer J, Reitman D, Sacks HS, Smith H, Chalmers TC (July 1983). "Association of adrenocorticosteroid therapy and peptic-ulcer disease". N. Engl. J. Med. 309 (1): 21–4. doi:10.1056/NEJM198307073090105. PMID 6343871.
  12. ↑ Piper JM, Ray WA, Daugherty JR, Griffin MR (May 1991). "Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs". Ann. Intern. Med. 114 (9): 735–40. PMID 2012355.
  13. ↑ MacAdams MR, White RH, Chipps BE (May 1986). "Reduction of serum testosterone levels during chronic glucocorticoid therapy". Ann. Intern. Med. 104 (5): 648–51. PMID 3083749.
  14. ↑ Crilly R, Cawood M, Marshall DH, Nordin BE (October 1978). "Hormonal status in normal, osteoporotic and corticosteroid-treated postmenopausal women". J R Soc Med. 71 (10): 733–6. PMC 1436218. PMID 712726.
  15. ↑ Wolkowitz OM, Burke H, Epel ES, Reus VI (October 2009). "Glucocorticoids. Mood, memory, and mechanisms". Ann. N. Y. Acad. Sci. 1179: 19–40. doi:10.1111/j.1749-6632.2009.04980.x. PMID 19906230.

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