Why the study?
Do MTP gene variants impact the lipid-lowering response to lomitapide in patients with homozygous familial hypercholesterolemia?
Do MTP gene variants impact the lipid-lowering response to lomitapide in patients with homozygous familial hypercholesterolemia?
Specific MTP gene variants may predict hyper-response to lomitapide in patients with homozygous familial hypercholesterolemia, suggesting a potential pharmacogenomic approach to therapy.
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MTP variants may influence lomitapide response in HoFH; leaves open whether genotyping should guide therapy.
Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder, which leads to premature cardiovascular diseases. Microsomal triglyceride transport protein (MTP) inhibitors, such as lomitapide, offer a new therapeutic approach for treating these patients. We evaluated the lipid lowering (LL) efficacy of lomitapide according to several gene variants in MTP. Four clinically and/or molecularly defined HoFH patients were treated with lomitapide in addition to conventional high intensity LL therapy and regular lipoprotein apheresis. Two patients responded to the therapy, with a significant reduction of LDL cholesterol (LDL-C>50%, hyper-responders). Sequencing of all exonic and intronic flanking regions of the MTP gene in all patients revealed 36 different variants. The hyper-responders to lomitapide shared six common variants: rs17533489, rs79194015, rs745075, rs41275715, rs1491246, and rs17533517, which were not seen in hypo-responders (reduction in LDL-C<50%). We suggest that in HoFH variants in the MTP gene may impact on the therapeutic response to lomitapide, but this requires further investigation.
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Kolovou et al. (2016) studied this question.
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