I tried to upload the file, but even with breaking it up, it is too big to load. I will try to cut and paste it.

kathie

format:
type receptor abbrev reference link comment
muscle Acethylcholine blocking mACH MG http://www.myasthenia.org/HealthProf...rviewofMG.aspx may impair binding of acetylcholine to the receptor, leading to poor muscle contraction

muscle Acethylcholine binding mACH MG http://cdn.intechweb.org/pdfs/20680.pdf can activate complement mediated membrane damage and lead to loss of AChR.

muscle Acethylcholine modulating mACH MG http://www.hindawi.com/journals/ad/2011/740583/ causes receptor endocytosis (accelerated degredation) resulting in loss of AChR expression, which correlates with clinical severity of disease

neuronal Acethylcholine nACH AAG/ POTS/ AGID http://www.ncbi.nlm.nih.gov/pubmed/10514242 , http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153777/, http://www.neurology.org/content/50/6/1806.short , http://lib.bioinfo.pl/pmid:14732619 , http://www.mayomedicallaboratories.c...nit_code=89886 Autoimmune autonomic ganglionopathy, Autoimmune gastrointestinal dysmotility (AGID)

Muscle specific kinease Musk MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1739764/ , http://neuromuscular.wustl.edu/mtime/mgthy.html predominantly female with more prominent facial and bulbar involvement and more frequent crises. Disease onset tended to be earlier. lack of improvement with, anticholinesterase agents. Somewhat better response was observed with steroids and plasma exchange

titin striated muscle antibody SM Ab MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139883/ Anti-titin antibodies are a sensitive marker of thymoma associated with MG in patients 60 years and younger, seen in other immune disorders. Seen in rippling muscle syndrome which may proceed a MG diagnosis, Respiratory difficulties at MG onset

actnin striated muscle antibody MG http://emedicine.medscape.com/article/1171206-workup also seen in celiac disease

ryanodine striated muscle antibody RyR MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139883/ more common in MG with thymoma, increases the risk for severe MG, highest rate of bulbar, respiratory and neck involvement at MG onset, distinctive non-limb MG symptom profile

Kv1.4 /KCNA4 Voltage-gated K channel VGKC MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139883/ Issacs syndrome, severe MG, thymoma, and concomitant myocarditis and/or myositis

voltage-gated calcium channel VGCC LEMS http://www.privatemdlabs.com/lp/VGCCA_Test.php Lambert-Eaton myasthenic syndrome

low-density lipoprotein receptor-related protein 4 LRP4 MG http://www.ncbi.nlm.nih.gov/pubmed/21814823 , http://www.ncbi.nlm.nih.gov/pubmed/22941261 50% of seronegatice MG have LRP4 antibody

rapsyn MG http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1851878/ , http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2442426/ congenital myasthenic syndrome

collapsin response mediator protein 5 CRMP5 http://www.ncbi.nlm.nih.gov/pubmed/19151024 , http://www.ncbi.nlm.nih.gov/pubmed/18931014 more than twice as frequent, and the antibody levels are higher in patients with thymoma and MG

Transient receptor potential canonical-3 TRPC3 http://www.sciencedirect.com/science...65572808001835 detected in thymoma-associated MG patients

GLUTAMIC ACID DECARBOXYLASE GAD65 http://www.mayomedicallaboratories.c...Overview/81596 , http://www.mayomedicallaboratories.c...rpretive/81596 autoimmune diabetes, stiff‐person syndrome and also in other neurological syndromes, including cerebellar ataxia and epilepsy

Antineuronal nuclear autoantibody-type 1 (ANNA-1) ANNA-1 http://neurology.org/content/59/6/929.abstract Autoimmune gastrointestinal dysmotility (AGID), Seropositive patients usually present with subacute neurological symptoms and signs such as encephalopathy; cerebellar ataxia; myelopathy; radiculopathy; plexopathy; or sensory, sensorimotor, or autoimmune neuropathy, with or without a neuromuscular transmission disorder: Lambert-Eaton syndrome, myasthenia gravis, or neuromuscular hyper-excitability

Wow, thanks, Kathie. I wish we knew more about the different effects of the various antibodies (for example, MuSK tends to have bulbar symptoms and doesn't respond to Mestinon--how about the others?).

This post should be encouraging to seronegative patients who are trying to get a diagnosis. There are a lot of other possibilities besides AChR.

Abby

Heat for me is anything over 80:rolleyes:

I find the best articles under the clinical research:

Annals of the New York Academy of Sciences
© The New York Academy of Sciences, June 2008,
Volume 1132 Myasthenia Gravis and Related Disorders 11th International Conference
Pages 84-92 ,Myasthenia Gravis Seronegative for Acetylcholine Receptor Antibodies

There was a great article where they tested sseronegative ACHR and MUSK MGers by adding Rapsyn ( the thing that makes ACHR receptors cluster) and 60% of the seronegative showed low affinity binding for ACHR antibodies. That means seronegative fit the clinical profile for ACHR Mgers. The test is faulty or not sensitive enough and does not taken into account the heavy clustering of ACHR receptors in the body.

Rapsyn is under investigation as a future treatment for MG. If the ACHR receptors cluster more it is easier to get a muscle action potential and our muscles will work better. At least that is the theory.

I also found another interesting article, I can't find the link now. But it did not consider ACHR antibody a definitive test for MG. It considered, SFEMG, tensilon etc, the definitive test. It said that the antibody tests should be used to profile and subtype the MG to anticipate clinical presentation and treatment response. I think this is a great approach. I wish more neuros used it.

Hope this helps,
kathie

Here is another good article that talks about pain and MG. https://research.wsulibs.wsu.edu/xml...pdf?sequence=1. I know all the common sites say there is not pain with MG, but I have a lot of muscle pain with MG.

There is also another very important point buried around pages 15-16. MG affects skeletal ACHR. But there is also ganglionic and neuronal ACHR which controls the autonomic nervous system like digestion, temperature regulation, hearing etc. In the article it says that after 5 or more years of skeletal antibody production there is some cross-reactivity with ganglionic ACHR. I think this explains my GI symptoms, constant tinitis, dizziness, profuse sweating etc, I think they refer to this as AGID and AAG on my earlier post.

Sorry for the over-analysis, but I am analyst by profession. I need to dig to know the "why".

kathie

I can't handle the heat lol but I'm handling the spring ok. Once it gets to 85/90 degrees, and that lovely humidity kicks in, I'm done, and ready for the AC. My problem maybe more humidity than just being warm, but I do "wilt" a bit in warm weather.