A review paper of all of the medications and treatments that may interfere with MG is at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457047/pdf/fnmol-13-00156.pdf   

It attempts to explain why these are a problem and where in our neuromuscular junction the problem comes.  It is a comprehensive review and a reference article for folks with MG.  These review summaries are useful to get the big picture and what is known at the current time. 

So, for example, Magnesium  

An electrolyte-related impairment of NMJ function may be caused by electrolyte imbalances, most typically by an excess of magnesium. Magnesium competitively blocks the entry of calcium into the presynaptic nerve terminal – a process that is crucial for the release of ACh into the synaptic cleft. The subsequent magnesium-induced reduction of ACh release eventually impairs neuromuscular transmission (Krendel, 1990). Accordingly, the pathophysiological mechanisms of hypermagnesemia resemble LEMS, in which Abs are directed against the presynaptic VGCC. Investigations of nerve and muscle tissue showed that endplate potential amplitudes evoked by nerve stimulation were reduced in the presence of magnesium, which could be reversed by adding calcium. This finding corroborates a presynaptic mechanism as the key mode of action. A slight decrease in sensitivity of the motor endplate to ACh was also observed, potentially suggesting a mild additional postsynaptic effect (del Castillo and Engbaek, 1954).

  (a simple interpretation is that magnesium reduces the amount of neurotransmitter made and so decreases the communication from nerves to muscles).  

Statins

Statins, the most commonly used class of lipid-lowering drugs, also show a variety of immunomodulatory properties such as increasing the serum levels of multiple Th2 interleukins (Youssef et al., 2002). Well-fitting, studies in animals and humans indicate that Th2 cytokines may generally be crucial in the development of MG (Milani et al., 2003). Therefore, these changes may be responsible for inducing de novo MG (Gale and Danesh-Meyer, 2014). Another pathomechanism potentially underlying statin-induced myasthenia is the depletion of coenzyme Q10, which may result in mitochondrial dysfunction (Evans and Rees, 2002; Vaklavas et al., 2009). This is particularly relevant, as presynaptic endings and the postsynaptic junction have a high density of mitochondria.

In contrast to new-onset MG, non-inflammatory myopathy is a well-known side effect of statins, potentially explaining the case reports that suggest an aggravation of pre-existing MG (Parmar et al., 2002; Cartwright et al., 2004; Purvin et al., 2006). A small case series reported worsening of symptoms in 6 patients with MG receiving statins (11% of the small analyzed cohort), predominantly affecting oculo-bulbar muscles with symptom onset between 1 week and 4 months after initiating treatment (Oh et al., 2008). This latency appears too long for a mechanism directly related to NMJ function. Some reported patients had no previous history of myasthenic symptoms, indicating that statins may have the potential to trigger or unmask myasthenia in previously healthy individuals (Purvin et al., 2006; Khalid et al., 2016)

(simplified-- read the last sentence).  

Russ