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A functional SNP in the regulatory region of the decay-accelerating factor gene associates with extraocular muscle pareses in myasthenia gravis
Genes and Immunity, 08/14/09

Heckmann JM et al. – Findings suggest that at critical periods during autoimmune MG, this SNP may result in inadequate DAF upregulation with consequent complement–mediated EOM damage. Susceptible individuals may benefit from anti–complement therapy in addition to immunosuppression.

Exclusive Author Commentary
Associate Professor JM Heckmann, 08/17/09

Extraocular muscles (EOMs) are commonly involved in active myasthenia gravis (MG) and most myasthenics develop fatiguable weakness of one or more EOMs, most likely at disease onset. If MG remains confined to the EOMs for a 2-year period and does not generalize, it is referred to as "ocular MG". In this report we investigated a different group of MG subjects that developed severe EOM pareses (i.e. non-fatiguable); most affected subjects developed this complication after generalized MG was diagnosed and whilst receiving standard immunosuppressive treatment. Further, in these subjects the ophthalmoparesis and ptosis did not respond to increasing prenisone treatment. Our current study results suggest that individuals who have MG and the SNP in the regulatory region of the DAF gene, may be at risk of indadequate DAF upregulation at critical periods during MG, which in turn may require additional anti-complement therapy to prevent EOM damage.

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