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MYASTHENIA GRAVIS

Iron deficiency may be a causative factor in Myasthenia Gravis.
 
Colle R, Maiolini E, Ceschia T, Colatutto A, Torresin L.
Myasthenia gravis associated with atrophic gastritis type A and iron deficiency.
Haematologica. 1986 Jul-Aug;71(4):352. No abstract available.
PMID: 3096829; UI: 87055414
 
Albahary C, Homberg JC, Guillaume J, Martin S, Boulangiez JP.
[Thymoma, myasthenia and auto-immune hemolytic anemia].
Nouv Presse Med. 1972 Jul 22;1(29):1931-4. French. No abstract available.
PMID: 4559761; UI: 72261340
 
Krishnan K, Trobe JD, Adams PT.
Myasthenia gravis following iron chelation therapy with intravenous desferrioxamine.
Eur J Haematol. 1995 Aug;55(2):138-9. No abstract available.
PMID: 7628591; UI: 95354819

D-penicillamine is a copper chelator.  Thus the following study suggests that chelating copper may induce Myasthenia Gravis.

Weinzierl M, Kruis W, Eisenburg J.
[Myasthenia syndrome in D-penicillamine therapy in primary biliary cirrhosis].
Internist (Berl). 1981 Feb;22(2):93-5. German. No abstract available.
PMID: 7012074; UI: 81167379
 
J Neuroimmunol 1999 Jun 1;97(1-2):146-53

T cell responses to D-penicillamine in drug-induced myasthenia gravis: recognition of modified DR1:peptide complexes.

Hill M, Moss P, Wordsworth P, Newsom-Davis J, Willcox N

Neurosciences Group, Institute of Molecular Medicine, The John Radcliffe Hospital, Headington, Oxford, UK.

The anti-rheumatoid drug D-penicillamine (D-pen) has a reactive sulfhydryl group capable of modifying self antigens, and can provoke typical autoantibody-mediated myasthenia gravis (MG), especially in DR1+ individuals. We have selected T cell clones from one such patient that were highly specific for D-pen but not its L-isomer or D-cysteine. Moreover, they were restricted to HLA-DR1, had a Th1 phenotype and used TCR V alpha4.1, V beta6.1. They responded well to blood mononuclear cells prepulsed with D-pen either in the absence of serum or after chloroquine treatment, but not to autologous D-pen-pulsed B cell lines. Thus, D-pen may directly couple to distinctive peptides resident in surface DR1 molecules on circulating macrophages or dendritic cells.

PMID: 10408968, UI: 99314664

Autoimmune Thyroid Dysfunction Rare in Myasthenia Gravis

A DGReview of :"Clinical significance of autoimmune thyroid disease in myasthenia gravis"
Experimental and Clinical Endocrinology & Diabetes

04/11/2000
By Mark Greener

Some myasthenia gravis patients develop autoimmune thyroid disease. However, autoimmune-induced thyroid dysfunction is rare, a new paper concludes.

The authors enrolled patients with 74 myasthenia gravis and 50 controls with no known thyroid disease. Of the myasthenia gravis patients, 86 per cent showed eye involvement and 56 per cent concurrent thymomas.

Only one myasthenia gravis patient suffered from overt thyroid disease. Another patient had a history of Hashimoto's disease and positive thyroid autoantibodies. A third patient, who underwent partial thyroidectomy but who did not take replacement therapy, showed mildly elevated thyroid stimulating hormone (TSH) levels.

Five per cent of the myasthenia gravis patients showed antibodies against thyroglobulin, while 15 per cent expressed antibodies against thyroid microsomes. Among controls, the prevalence was 4 and 6 per cent, respectively. (The latter difference did not reach statistical significance.) Neither patients nor controls showed antibodies against TSH receptors.
The authors conclude that autoimmune thyroid disease is associated with myasthenia gravis in some patients. However, autoimmune-induced thyroid dysfunction is "a very rare phenomenon" among myasthenia gravis patients, they write.