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Did you know? Generalized myasthenia gravis (gMG) is driven by pathogenic IgG autoantibodies—primarily anti-AChR—that impair neuromuscular transmission. FcRn inhibition accelerates IgG catabolism, rapidly reducing pathogenic autoantibody titers. This mechanism offers a novel therapeutic target distinct from acetylcholinesterase inhibitors or broad immunosuppression.
How do you currently assess disease burden and treatment response in your gMG patients?
How do you currently assess disease burden and treatment response in your gMG patients?
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JOEL WASHINSKY3wOne has to look at subjective QOL, functional status.
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Mike Shirk2moI look at a patients functional status. What activities of daily living do they have problems with. What activities are they no longer doing. And then at follow up see if there has been improvement in any functions
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SHABNAM SACHDEVA2moTreatment response is typically judged by improvements in function, reduction in symptom fluctuations, decreased need for rescue therapies, corticosteroid-sparing effects, and overall quality of life. FcRN targeted therapies improve function and quality of life for these patients
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SACHINKUMAR PANCHAL2mosuch as the MG-ADL, QMG, patient-reported outcomes, functional status, or biomarkers—most influence your treatment decisions and evaluation of therapeutic response.
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Steven Seller2moevery patient evaluated individually based on their current disease state