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I think there are implications for genetic screening in this patient:
One, it provided a molecular explanation for the phenotype of severe hypercholesterolemia that explains why it is that this patient seems to be more severely affected than the garden variety patient with heterozygous FH.
Two, it successfully identified other family members, particularly on his father's side, who wouldn't normally be diagnosed with heterozygous FH but actually do have a mutation, do have moderate hypercholesterolemia, and probably should be treated.
Third, it has raised some considerations for the testing of his spouse and for prenatal counseling of this couple and perhaps for his sister as well in order to avoid having children with homozygous FH.
And then finally, this patient, by virtue of that fact he has two loss of function mutations in his LDL receptor, would be considered a potential candidate for these new drugs that are coming along, mipomersen and lomitapide, as result of the fact that he does have these 2 mutations and can therefore be considered as having homozygous FH.