Myasthenia gravis causes: Difference between revisions

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==Overview==
==Overview==
Myasthenia gravis may be caused by thymus abnormalities, genetic and environment.
==Causes==


==Causes==
=== Common Causes ===
Myasthenia gravis may be caused by:
Myasthenia gravis may be caused by:
* Thymus abnormalities:  
* Thymus abnormalities:
Thymus abnormalities including thymic hyperplasia and [[thymoma]] are very common in myasthenia gravis and [[thymectomy]] is one of the treatment of this disease.<ref name="pmid8190158">{{cite journal |vauthors=Drachman DB |title=Myasthenia gravis |journal=N. Engl. J. Med. |volume=330 |issue=25 |pages=1797–810 |date=June 1994 |pmid=8190158 |doi=10.1056/NEJM199406233302507 |url=}}</ref><ref name="pmid12360217">{{cite journal |vauthors=Vincent A |title=Unravelling the pathogenesis of myasthenia gravis |journal=Nat. Rev. Immunol. |volume=2 |issue=10 |pages=797–804 |date=October 2002 |pmid=12360217 |doi=10.1038/nri916 |url=}}</ref> In [[thymus]], we have myoid cells which present intact [[Acetylcholine receptor|AChR]] on their surface. On the other hand thymic epithelial cells produce [[Acetylcholine receptor|AChR]] subunits which activate [[helper T cells]]. These [[T cell|T cells]] attack [[Acetylcholine receptor|AChR]] on the myoid cells and the cascade of [[antibody]] production and [[complement]] activation will begin.<ref name="pmid18567866">{{cite journal |vauthors=Willcox N, Leite MI, Kadota Y, Jones M, Meager A, Subrahmanyam P, Dasgupta B, Morgan BP, Vincent A |title=Autoimmunizing mechanisms in thymoma and thymus |journal=Ann. N. Y. Acad. Sci. |volume=1132 |issue= |pages=163–73 |date=2008 |pmid=18567866 |doi=10.1196/annals.1405.021 |url=}}</ref><ref name="pmid17675582">{{cite journal |vauthors=Leite MI, Jones M, Ströbel P, Marx A, Gold R, Niks E, Verschuuren JJ, Berrih-Aknin S, Scaravilli F, Canelhas A, Morgan BP, Vincent A, Willcox N |title=Myasthenia gravis thymus: complement vulnerability of epithelial and myoid cells, complement attack on them, and correlations with autoantibody status |journal=Am. J. Pathol. |volume=171 |issue=3 |pages=893–905 |date=September 2007 |pmid=17675582 |pmc=1959483 |doi=10.2353/ajpath.2007.070240 |url=}}</ref><ref name="pmid18644632">{{cite journal |vauthors=Hohlfeld R, Wekerle H |title=Reflections on the "intrathymic pathogenesis" of myasthenia gravis |journal=J. Neuroimmunol. |volume=201-202 |issue= |pages=21–7 |date=September 2008 |pmid=18644632 |doi=10.1016/j.jneuroim.2008.05.020 |url=}}</ref>
** Thymus abnormalities including thymic hyperplasia and [[thymoma]] are very common in myasthenia gravis and [[thymectomy]] is one of the treatment of this disease.<ref name="pmid8190158">{{cite journal |vauthors=Drachman DB |title=Myasthenia gravis |journal=N. Engl. J. Med. |volume=330 |issue=25 |pages=1797–810 |date=June 1994 |pmid=8190158 |doi=10.1056/NEJM199406233302507 |url=}}</ref><ref name="pmid12360217">{{cite journal |vauthors=Vincent A |title=Unravelling the pathogenesis of myasthenia gravis |journal=Nat. Rev. Immunol. |volume=2 |issue=10 |pages=797–804 |date=October 2002 |pmid=12360217 |doi=10.1038/nri916 |url=}}</ref>  
* Genetic:  
** In [[thymus]], we have myoid cells which present intact [[Acetylcholine receptor|AChR]] on their surface. On the other hand thymic epithelial cells produce [[Acetylcholine receptor|AChR]] subunits which activate [[helper T cells]]. These [[T cell|T cells]] attack [[Acetylcholine receptor|AChR]] on the myoid cells and the cascade of [[antibody]] production and [[complement]] activation will begin.<ref name="pmid18567866">{{cite journal |vauthors=Willcox N, Leite MI, Kadota Y, Jones M, Meager A, Subrahmanyam P, Dasgupta B, Morgan BP, Vincent A |title=Autoimmunizing mechanisms in thymoma and thymus |journal=Ann. N. Y. Acad. Sci. |volume=1132 |issue= |pages=163–73 |date=2008 |pmid=18567866 |doi=10.1196/annals.1405.021 |url=}}</ref><ref name="pmid17675582">{{cite journal |vauthors=Leite MI, Jones M, Ströbel P, Marx A, Gold R, Niks E, Verschuuren JJ, Berrih-Aknin S, Scaravilli F, Canelhas A, Morgan BP, Vincent A, Willcox N |title=Myasthenia gravis thymus: complement vulnerability of epithelial and myoid cells, complement attack on them, and correlations with autoantibody status |journal=Am. J. Pathol. |volume=171 |issue=3 |pages=893–905 |date=September 2007 |pmid=17675582 |pmc=1959483 |doi=10.2353/ajpath.2007.070240 |url=}}</ref><ref name="pmid18644632">{{cite journal |vauthors=Hohlfeld R, Wekerle H |title=Reflections on the "intrathymic pathogenesis" of myasthenia gravis |journal=J. Neuroimmunol. |volume=201-202 |issue= |pages=21–7 |date=September 2008 |pmid=18644632 |doi=10.1016/j.jneuroim.2008.05.020 |url=}}</ref>
# [[MHC|The Major Histocompatibility Complex]]: In genetic etiology of most of the [[autoimmune diseases]] including [[Myasthenia gravis|MG]], [[MHC]] genes play the most important role.<ref name="pmid4544224">{{cite journal |vauthors=Feltkamp TE, van den Berg-Loonen PM, Nijenhuis LE, Engelfriet CP, van Rossum AL, van Loghem JJ, Oosterhuis HJ |title=Myasthenia gravis, autoantibodies, and HL-A antigens |journal=Br Med J |volume=1 |issue=5899 |pages=131–3 |date=January 1974 |pmid=4544224 |pmc=1633001 |doi= |url=}}</ref>
 
# The [[CHRNA1]] [[Locus]]: The [[Translation (genetics)|translation]] product of this [[gene]] is the alpha subunit of [[Acetylcholine receptor|AChR]], which is the target of many [[autoantibodies]] in myasthenia gravis patients.<ref name="pmid9700504">{{cite journal |vauthors=Tzartos SJ, Barkas T, Cung MT, Mamalaki A, Marraud M, Orlewski P, Papanastasiou D, Sakarellos C, Sakarellos-Daitsiotis M, Tsantili P, Tsikaris V |title=Anatomy of the antigenic structure of a large membrane autoantigen, the muscle-type nicotinic acetylcholine receptor |journal=Immunol. Rev. |volume=163 |issue= |pages=89–120 |date=June 1998 |pmid=9700504 |doi= |url=}}</ref>
* Genetic:
# The [[PTPN22]] [[Gene]]: This [[gene]] is responsible for producing an intracellular protein phosphatase [[PTPN22]]. The impaired binding of this protein to protein tyrosine kinase Csk occurs as a result of a missense polymorphism which replace [[arginine]] with [[tryptophan]]. Activity of [[PTPN22]] will increase and inhibits [[T cell]] activation and [[interleukin 2]] production which leads to predisposition to [[autoimmunity]].<ref name="pmid15004560">{{cite journal |vauthors=Bottini N, Musumeci L, Alonso A, Rahmouni S, Nika K, Rostamkhani M, MacMurray J, Meloni GF, Lucarelli P, Pellecchia M, Eisenbarth GS, Comings D, Mustelin T |title=A functional variant of lymphoid tyrosine phosphatase is associated with type I diabetes |journal=Nat. Genet. |volume=36 |issue=4 |pages=337–8 |date=April 2004 |pmid=15004560 |doi=10.1038/ng1323 |url=}}</ref><ref name="pmid17277778">{{cite journal |vauthors=Yamanouchi J, Rainbow D, Serra P, Howlett S, Hunter K, Garner VE, Gonzalez-Munoz A, Clark J, Veijola R, Cubbon R, Chen SL, Rosa R, Cumiskey AM, Serreze DV, Gregory S, Rogers J, Lyons PA, Healy B, Smink LJ, Todd JA, Peterson LB, Wicker LS, Santamaria P |title=Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity |journal=Nat. Genet. |volume=39 |issue=3 |pages=329–37 |date=March 2007 |pmid=17277778 |pmc=2886969 |doi=10.1038/ng1958 |url=}}</ref>
** [[MHC|The Major Histocompatibility Complex]]: In genetic etiology of most of the [[autoimmune diseases]] including [[Myasthenia gravis|MG]], [[MHC]] genes play the most important role.<ref name="pmid4544224">{{cite journal |vauthors=Feltkamp TE, van den Berg-Loonen PM, Nijenhuis LE, Engelfriet CP, van Rossum AL, van Loghem JJ, Oosterhuis HJ |title=Myasthenia gravis, autoantibodies, and HL-A antigens |journal=Br Med J |volume=1 |issue=5899 |pages=131–3 |date=January 1974 |pmid=4544224 |pmc=1633001 |doi= |url=}}</ref>
# The [[FCGR2A|FCGR2]] [[Locus]]: Some studies investigated the relationship between [[Polymorphisms|polymorphism]] of FC receptors [[gene]] and [[Myasthenia gravis|MG]] and suggested that R arginine variant in type 2 (FCGR2) can be related to this disease.<ref name="pmid9521619">{{cite journal |vauthors=Raknes G, Skeie GO, Gilhus NE, Aadland S, Vedeler C |title=FcgammaRIIA and FcgammaRIIIB polymorphisms in myasthenia gravis |journal=J. Neuroimmunol. |volume=81 |issue=1-2 |pages=173–6 |date=January 1998 |pmid=9521619 |doi= |url=}}</ref><ref name="pmid14597109">{{cite journal |vauthors=van der Pol WL, Jansen MD, Kuks JB, de Baets M, Leppers-van de Straat FG, Wokke JH, van de Winkel JG, van den Berg LH |title=Association of the Fc gamma receptor IIA-R/R131 genotype with myasthenia gravis in Dutch patients |journal=J. Neuroimmunol. |volume=144 |issue=1-2 |pages=143–7 |date=November 2003 |pmid=14597109 |doi= |url=}}</ref>
** The [[CHRNA1]] [[Locus]]: The [[Translation (genetics)|translation]] product of this [[gene]] is the alpha subunit of [[Acetylcholine receptor|AChR]], which is the target of many [[autoantibodies]] in myasthenia gravis patients.<ref name="pmid9700504">{{cite journal |vauthors=Tzartos SJ, Barkas T, Cung MT, Mamalaki A, Marraud M, Orlewski P, Papanastasiou D, Sakarellos C, Sakarellos-Daitsiotis M, Tsantili P, Tsikaris V |title=Anatomy of the antigenic structure of a large membrane autoantigen, the muscle-type nicotinic acetylcholine receptor |journal=Immunol. Rev. |volume=163 |issue= |pages=89–120 |date=June 1998 |pmid=9700504 |doi= |url=}}</ref>
# The [[CTLA-4|CTLA4]] [[Locus]]: This [[gene]] is known to be responsible for many [[autoimmune diseases]].<ref name="pmid11196709">{{cite journal |vauthors=Kristiansen OP, Larsen ZM, Pociot F |title=CTLA-4 in autoimmune diseases--a general susceptibility gene to autoimmunity? |journal=Genes Immun. |volume=1 |issue=3 |pages=170–84 |date=February 2000 |pmid=11196709 |doi=10.1038/sj.gene.6363655 |url=}}</ref>
** The [[PTPN22]] [[Gene]]: This [[gene]] is responsible for producing an intracellular protein phosphatase [[PTPN22]]. The impaired binding of this protein to protein tyrosine kinase Csk occurs as a result of a missense polymorphism which replace [[arginine]] with [[tryptophan]]. Activity of [[PTPN22]] will increase and inhibits [[T cell]] activation and [[interleukin 2]] production which leads to predisposition to [[autoimmunity]].<ref name="pmid15004560">{{cite journal |vauthors=Bottini N, Musumeci L, Alonso A, Rahmouni S, Nika K, Rostamkhani M, MacMurray J, Meloni GF, Lucarelli P, Pellecchia M, Eisenbarth GS, Comings D, Mustelin T |title=A functional variant of lymphoid tyrosine phosphatase is associated with type I diabetes |journal=Nat. Genet. |volume=36 |issue=4 |pages=337–8 |date=April 2004 |pmid=15004560 |doi=10.1038/ng1323 |url=}}</ref><ref name="pmid17277778">{{cite journal |vauthors=Yamanouchi J, Rainbow D, Serra P, Howlett S, Hunter K, Garner VE, Gonzalez-Munoz A, Clark J, Veijola R, Cubbon R, Chen SL, Rosa R, Cumiskey AM, Serreze DV, Gregory S, Rogers J, Lyons PA, Healy B, Smink LJ, Todd JA, Peterson LB, Wicker LS, Santamaria P |title=Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity |journal=Nat. Genet. |volume=39 |issue=3 |pages=329–37 |date=March 2007 |pmid=17277778 |pmc=2886969 |doi=10.1038/ng1958 |url=}}</ref>
* environment:
** The [[FCGR2A|FCGR2]] [[Locus]]: Some studies investigated the relationship between [[Polymorphisms|polymorphism]] of FC receptors [[gene]] and [[Myasthenia gravis|MG]] and suggested that R arginine variant in type 2 (FCGR2) can be related to this disease.<ref name="pmid9521619">{{cite journal |vauthors=Raknes G, Skeie GO, Gilhus NE, Aadland S, Vedeler C |title=FcgammaRIIA and FcgammaRIIIB polymorphisms in myasthenia gravis |journal=J. Neuroimmunol. |volume=81 |issue=1-2 |pages=173–6 |date=January 1998 |pmid=9521619 |doi= |url=}}</ref><ref name="pmid14597109">{{cite journal |vauthors=van der Pol WL, Jansen MD, Kuks JB, de Baets M, Leppers-van de Straat FG, Wokke JH, van de Winkel JG, van den Berg LH |title=Association of the Fc gamma receptor IIA-R/R131 genotype with myasthenia gravis in Dutch patients |journal=J. Neuroimmunol. |volume=144 |issue=1-2 |pages=143–7 |date=November 2003 |pmid=14597109 |doi= |url=}}</ref>
# Drugs: Drugs such as [[D-penicillamine]]<ref name="pmid9046891">{{cite journal |vauthors=Wittbrodt ET |title=Drugs and myasthenia gravis. An update |journal=Arch. Intern. Med. |volume=157 |issue=4 |pages=399–408 |date=February 1997 |pmid=9046891 |doi= |url=}}</ref>, [[fludarabine]]<ref name="pmid16019566">{{cite journal |vauthors=Fujimaki K, Takasaki H, Koharazawa H, Takabayashi M, Yamaji S, Baba Y, Kanamori H, Ishigatsubo Y |title=Idiopathic thrombocytopenic purpura and myasthenia gravis after fludarabine treatment for chronic lymphocytic leukemia |journal=Leuk. Lymphoma |volume=46 |issue=7 |pages=1101–2 |date=July 2005 |pmid=16019566 |doi=10.1080/10428190500063054 |url=}}</ref>, [[lithium carbonate]]<ref name="pmid10874911">{{cite journal |vauthors=Ronzière T, Auzou P, Ozsancak C, Magnier P, Sénant J, Hannequin D |title=[Myasthenic syndrome induced by lithium] |language=French |journal=Presse Med |volume=29 |issue=19 |pages=1043–4 |date=2000 |pmid=10874911 |doi= |url=}}</ref> and [[botulinum toxin]]<ref name="pmid16175373">{{cite journal |vauthors=Iwase T, Iwase C |title=Systemic effect of local and small-dose botulinum toxin injection to unmask subclinical myasthenia gravis |journal=Graefes Arch. Clin. Exp. Ophthalmol. |volume=244 |issue=3 |pages=415–6 |date=March 2006 |pmid=16175373 |doi=10.1007/s00417-005-0130-4 |url=}}</ref> can induce [[Myasthenia gravis|MG]], and drugs such as [[curare]], [[aminoglycosides]], [[Macrolide|macrolides]], [[fluoroquinolones]], [[quinine]], [[quinidine]], [[procainamide]], magnesium salts, [[Calcium channel blocker|calcium channel blockers]], [[beta blockers]], [[Iodinated contrast|iodinated contrast agents]] and [[statins]] can worsen [[Myasthenia gravis|MG]].<ref name="pmid18720505">{{cite journal |vauthors=de Sousa E, Howard J |title=More evidence for the association between statins and myasthenia gravis |journal=Muscle Nerve |volume=38 |issue=3 |pages=1085–6 |date=September 2008 |pmid=18720505 |doi=10.1002/mus.21072 |url=}}</ref><ref name="pmid9046891">{{cite journal |vauthors=Wittbrodt ET |title=Drugs and myasthenia gravis. An update |journal=Arch. Intern. Med. |volume=157 |issue=4 |pages=399–408 |date=February 1997 |pmid=9046891 |doi= |url=}}</ref>  
** The [[CTLA-4|CTLA4]] [[Locus]]: This [[gene]] is known to be responsible for many [[autoimmune diseases]].<ref name="pmid11196709">{{cite journal |vauthors=Kristiansen OP, Larsen ZM, Pociot F |title=CTLA-4 in autoimmune diseases--a general susceptibility gene to autoimmunity? |journal=Genes Immun. |volume=1 |issue=3 |pages=170–84 |date=February 2000 |pmid=11196709 |doi=10.1038/sj.gene.6363655 |url=}}</ref>
# Infections: Infections such as [[hepatitis C]]<ref name="pmid9952242">{{cite journal |vauthors=Eddy S, Wim R, Peter VE, Tanja R, Jan T, Werner VS |title=Myasthenia gravis: another autoimmune disease associated with hepatitis C virus infection |journal=Dig. Dis. Sci. |volume=44 |issue=1 |pages=186–9 |date=January 1999 |pmid=9952242 |doi= |url=}}</ref>, [[Herpes simplex virus|HSV]]<ref name="pmid16197809">{{cite journal |vauthors=Ercolini AM, Miller SD |title=Role of immunologic cross-reactivity in neurological diseases |journal=Neurol. Res. |volume=27 |issue=7 |pages=726–33 |date=October 2005 |pmid=16197809 |doi=10.1179/016164105X49508 |url=}}</ref>, [[Epstein Barr virus|EBV]]<ref name="pmid2837902">{{cite journal |vauthors=McGuire LJ, Huang DP, Teoh R, Arnold M, Wong K, Lee JC |title=Epstein-Barr virus genome in thymoma and thymic lymphoid hyperplasia |journal=Am. J. Pathol. |volume=131 |issue=3 |pages=385–90 |date=June 1988 |pmid=2837902 |pmc=1880705 |doi= |url=}}</ref>, [[Cytomegalovirus infection|CMV]]<ref name="pmid16236323">{{cite journal |vauthors=Mori M, Kuwabara S, Nemoto Y, Tamura N, Hattori T |title=Concomitant chronic inflammatory demyelinating polyneuropathy and myasthenia gravis following cytomegalovirus infection |journal=J. Neurol. Sci. |volume=240 |issue=1-2 |pages=103–6 |date=January 2006 |pmid=16236323 |doi=10.1016/j.jns.2005.08.013 |url=}}</ref>, [[HTLV-1|HTLV1]]<ref name="pmid17117410">{{cite journal |vauthors=Lalive PH, Allali G, Truffert A |title=Myasthenia gravis associated with HTLV-I infection and atypical brain lesions |journal=Muscle Nerve |volume=35 |issue=4 |pages=525–8 |date=April 2007 |pmid=17117410 |doi=10.1002/mus.20694 |url=}}</ref> and [[West nile virus|west Nile virus]]<ref name="pmid15610703">{{cite journal |vauthors=Leis AA, Stokic DS |title=Neuromuscular Manifestations of Human West Nile Virus Infection |journal=Curr Treat Options Neurol |volume=7 |issue=1 |pages=15–22 |date=January 2005 |pmid=15610703 |doi= |url=}}</ref> are suggested to have a relationship with myasthenia gravis disease.
 
# Trauma: Few reports suggest that [[Myasthenia gravis|MG]] can appear after cardiothoracic [[bypass surgery]] and insulting the remaining [[thymus]].
* Environment:
** Drugs: Drugs such as [[D-penicillamine]]<ref name="pmid9046891">{{cite journal |vauthors=Wittbrodt ET |title=Drugs and myasthenia gravis. An update |journal=Arch. Intern. Med. |volume=157 |issue=4 |pages=399–408 |date=February 1997 |pmid=9046891 |doi= |url=}}</ref>, [[fludarabine]]<ref name="pmid16019566">{{cite journal |vauthors=Fujimaki K, Takasaki H, Koharazawa H, Takabayashi M, Yamaji S, Baba Y, Kanamori H, Ishigatsubo Y |title=Idiopathic thrombocytopenic purpura and myasthenia gravis after fludarabine treatment for chronic lymphocytic leukemia |journal=Leuk. Lymphoma |volume=46 |issue=7 |pages=1101–2 |date=July 2005 |pmid=16019566 |doi=10.1080/10428190500063054 |url=}}</ref>, [[lithium carbonate]]<ref name="pmid10874911">{{cite journal |vauthors=Ronzière T, Auzou P, Ozsancak C, Magnier P, Sénant J, Hannequin D |title=[Myasthenic syndrome induced by lithium] |language=French |journal=Presse Med |volume=29 |issue=19 |pages=1043–4 |date=2000 |pmid=10874911 |doi= |url=}}</ref> and [[botulinum toxin]]<ref name="pmid16175373">{{cite journal |vauthors=Iwase T, Iwase C |title=Systemic effect of local and small-dose botulinum toxin injection to unmask subclinical myasthenia gravis |journal=Graefes Arch. Clin. Exp. Ophthalmol. |volume=244 |issue=3 |pages=415–6 |date=March 2006 |pmid=16175373 |doi=10.1007/s00417-005-0130-4 |url=}}</ref> can induce [[Myasthenia gravis|MG]], and drugs such as [[curare]], [[aminoglycosides]], [[Macrolide|macrolides]], [[fluoroquinolones]], [[quinine]], [[quinidine]], [[procainamide]], magnesium salts, [[Calcium channel blocker|calcium channel blockers]], [[beta blockers]], [[Iodinated contrast|iodinated contrast agents]] and [[statins]] can worsen [[Myasthenia gravis|MG]].<ref name="pmid18720505">{{cite journal |vauthors=de Sousa E, Howard J |title=More evidence for the association between statins and myasthenia gravis |journal=Muscle Nerve |volume=38 |issue=3 |pages=1085–6 |date=September 2008 |pmid=18720505 |doi=10.1002/mus.21072 |url=}}</ref><ref name="pmid9046891">{{cite journal |vauthors=Wittbrodt ET |title=Drugs and myasthenia gravis. An update |journal=Arch. Intern. Med. |volume=157 |issue=4 |pages=399–408 |date=February 1997 |pmid=9046891 |doi= |url=}}</ref>  
** Infections: Infections such as [[hepatitis C]]<ref name="pmid9952242">{{cite journal |vauthors=Eddy S, Wim R, Peter VE, Tanja R, Jan T, Werner VS |title=Myasthenia gravis: another autoimmune disease associated with hepatitis C virus infection |journal=Dig. Dis. Sci. |volume=44 |issue=1 |pages=186–9 |date=January 1999 |pmid=9952242 |doi= |url=}}</ref>, [[Herpes simplex virus|HSV]]<ref name="pmid16197809">{{cite journal |vauthors=Ercolini AM, Miller SD |title=Role of immunologic cross-reactivity in neurological diseases |journal=Neurol. Res. |volume=27 |issue=7 |pages=726–33 |date=October 2005 |pmid=16197809 |doi=10.1179/016164105X49508 |url=}}</ref>, [[Epstein Barr virus|EBV]]<ref name="pmid2837902">{{cite journal |vauthors=McGuire LJ, Huang DP, Teoh R, Arnold M, Wong K, Lee JC |title=Epstein-Barr virus genome in thymoma and thymic lymphoid hyperplasia |journal=Am. J. Pathol. |volume=131 |issue=3 |pages=385–90 |date=June 1988 |pmid=2837902 |pmc=1880705 |doi= |url=}}</ref>, [[Cytomegalovirus infection|CMV]]<ref name="pmid16236323">{{cite journal |vauthors=Mori M, Kuwabara S, Nemoto Y, Tamura N, Hattori T |title=Concomitant chronic inflammatory demyelinating polyneuropathy and myasthenia gravis following cytomegalovirus infection |journal=J. Neurol. Sci. |volume=240 |issue=1-2 |pages=103–6 |date=January 2006 |pmid=16236323 |doi=10.1016/j.jns.2005.08.013 |url=}}</ref>, [[HTLV-1|HTLV1]]<ref name="pmid17117410">{{cite journal |vauthors=Lalive PH, Allali G, Truffert A |title=Myasthenia gravis associated with HTLV-I infection and atypical brain lesions |journal=Muscle Nerve |volume=35 |issue=4 |pages=525–8 |date=April 2007 |pmid=17117410 |doi=10.1002/mus.20694 |url=}}</ref> and [[West nile virus|west Nile virus]]<ref name="pmid15610703">{{cite journal |vauthors=Leis AA, Stokic DS |title=Neuromuscular Manifestations of Human West Nile Virus Infection |journal=Curr Treat Options Neurol |volume=7 |issue=1 |pages=15–22 |date=January 2005 |pmid=15610703 |doi= |url=}}</ref> are suggested to have a relationship with myasthenia gravis disease.
** Trauma: Few reports suggest that [[Myasthenia gravis|MG]] can appear after cardiothoracic [[bypass surgery]] and insulting the remaining [[thymus]].<ref name="pmid12588942">{{cite journal |vauthors=Scoppetta C, Onorati P, Eusebi F, Fini M, Evoli A, Vincent A |title=Autoimmune myasthenia gravis after cardiac surgery |journal=J. Neurol. Neurosurg. Psychiatry |volume=74 |issue=3 |pages=392–3 |date=March 2003 |pmid=12588942 |pmc=1738331 |doi= |url=}}</ref><ref name="pmid16427886">{{cite journal |vauthors=Resatoglu AG, Tok M, Yemisci M, Yener N, Yener A |title=Autoimmune myasthenia gravis after coronary artery bypass surgery |journal=Ann. Thorac. Surg. |volume=81 |issue=2 |pages=725–6 |date=February 2006 |pmid=16427886 |doi=10.1016/j.athoracsur.2004.10.027 |url=}}</ref>
 
===Less Common Causes===
Less common causes of [disease name] include:
*[Cause1]
*[Cause2]
*[Cause3]
 
===Genetic Causes===
*[Disease name] is caused by a mutation in the [gene name] gene.


==References==
==References==

Latest revision as of 14:18, 15 August 2019

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

Overview

Myasthenia gravis may be caused by thymus abnormalities, genetic and environment.

Causes

Common Causes

Myasthenia gravis may be caused by:

  • Thymus abnormalities:
    • Thymus abnormalities including thymic hyperplasia and thymoma are very common in myasthenia gravis and thymectomy is one of the treatment of this disease.[1][2]
    • In thymus, we have myoid cells which present intact AChR on their surface. On the other hand thymic epithelial cells produce AChR subunits which activate helper T cells. These T cells attack AChR on the myoid cells and the cascade of antibody production and complement activation will begin.[3][4][5]

Less Common Causes

Less common causes of [disease name] include:

  • [Cause1]
  • [Cause2]
  • [Cause3]

Genetic Causes

  • [Disease name] is caused by a mutation in the [gene name] gene.

References

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