Dottie, Thanks for the info.
I don't think MG is as "easy" to understand as some people say it is! So many things can affect MG, make it worse (or better), etc.
Dr. Angela Vincent works at Oxford University in England. She has a great article on MG and the AChR antibodies (below in PDF form). They are mainly IgG subclass 1 and subclass 3. There are four total subclasses of IgG. If you have a deficiency of one of these subclasses - like I do - your antibodies may not show up when the tests are done. Just like in Celiac Disease if you have an IgA deficiency, antibodies may not show up in the blood tests.
Also, if you are on another drug like Advair before you go through diagnostic testing for MG, it may make the antibodies disappear or SFEMG appear negative.
I think equating disease process with either the antibodies or the SFEMG is deceptive. There are articles that say that even in those who supposedly have only ocular MG, they can look at the neuromuscular junction in other muscle groups and "see" damage. It may not be enough for frank weakness but there's damage just the same.
I don't know how anyone can say that an autoimmune process is not or cannot be progressive. We can slow it down or stop it with drugs. We can lessen it with treating infections, reducing stress, etc. (like Dottie was talking about). I kind of see antibodies like locusts, eating as much of our NMJ as they possibly can!
Bottom line is to do whatever we can to calm the disease down and make our immune systems happy. We may never have a definitive answer to this question.
Annie
Here's the explanation for the thumbnail.
Figure 2
Effector mechanisms of anti-AChR Abs. (A) Ab binding to the AChR activates the complement cascade, resulting in the formation of membrane attack complex (MAC) and localized destruction of the postsynaptic NMJ membrane. This ultimately leads to a simplified, altered morphology of the postsynaptic membrane of the NMJ of MG patients, which lacks the normal deep folds and has a relatively flat surface. (B) Abs cross-link AChR molecules on the NMJ postsynaptic membrane, causing endocytosis of the cross-linked AChR molecules and their degradation (antigenic modulation). This ultimately leads to a reduced number of AChR molecules on the postsynaptic membrane. (C) Ab binding the ACh-binding sites of the AChR causes functional block of the AChR by interfering with binding of ACh released at the NMJ. This results in failure of neuromuscular transmission.