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Association between myasthenia gravis (MG) and excess iron.
Based on the search results, the association between myasthenia gravis (MG) and iron appears complex, but current research predominantly points towards iron deficiency or altered iron metabolism rather than excess iron being common in MG patients.

Here’s a breakdown of the findings:

Iron Deficiency is More Commonly Reported:

Multiple studies found that non-anemic, immunotherapy-naive MG patients had significantly lower serum iron (SI) and transferrin saturation (TS) levels compared to healthy individuals.
Iron deficiency was found to be prevalent in MG patients (one study reported a 73.68% deficiency rate).
Lower serum iron levels were negatively correlated with levels of acetylcholine receptor antibodies (AChR-Ab) and Interleukin-6 (IL-6), suggesting that lower iron might be associated with higher disease activity or inflammation.
Iron inadequacy seems particularly common in premenopausal female patients with MG.
Anemia in MG:

Anemia, often iron-deficiency anemia, is frequently observed in female MG patients (one study found 40% had a history of anemia post-diagnosis).
This anemia was associated with greater MG severity, more frequent use of immunosuppressive treatments (which might contribute to iron metabolism issues), and poorer quality of life.
Altered Iron Metabolism:

While outright excess iron isn’t typically reported, some studies note alterations in iron metabolism markers. For instance, higher ferritin levels (an iron storage protein that can also be elevated during inflammation) were associated with more severe generalized disease in one study. This suggests inflammation-related dysregulation rather than simple overload.
Research is exploring the role of iron-dependent cell death (ferroptosis) and mitochondrial function in the pathogenesis of MG, indicating iron’s involvement at a cellular level, but this doesn’t equate to systemic iron overload.
Context for Iron Overload/Sensitivity:

There is a case report of a patient with MG and red cell aplasia who developed hepatic iron overload, but this was potentially secondary to the aplasia or hereditary hemochromatosis, not necessarily MG itself.
A letter to the editor discussed potential exacerbation of MG symptoms following intravenous iron administration, suggesting a sensitivity in some individuals rather than an underlying state of excess iron.
In conclusion: While iron metabolism is clearly relevant in MG, current evidence does not support the idea that MG is generally associated with excess iron. Instead, research highlights a tendency towards iron deficiency and altered iron regulation, which may be linked to disease activity, inflammation, and potentially treatment side effects.

I have about 20 US patents related to the normalization of iron metabolim.