HDL was reduced from 1.0 ± 0.2 mmol/L pre- to 0.5 ± 0.1 mmol/L post-apheresis (p = 0.03). It increased following apheresis and then remained constant throughout the evolocumab treatment. Lp(a) decreased from 484 ± 76 mg/L pre- to 142 ± 15 mg/L post-apheresis (P = 0.02), but there was a small increase from week 1 to week 7 (p < 0.01) during evolocumab therapy. There was a non-significant trend towards an increase in perceived health status (week 0; 57 ± 21, week three; 65 ± 9 and week seven; 77 ± 10).

The researchers reported that treatment with evolocumab was safe and well tolerated. Liver enzymes, bilirubin, liver function, creating kinase (CK), renal function, hematologic profile, and thyroid tests “were controlled at all sampling times, without deviations from normal values at any time.”

They noted that, on average, HDL cholesterol is reduced by 10% to 20% during apheresis. They acknowledge that there is no obvious explanation from this, but suggested that some patients with FH also have low levels of HDL and reduced cholesterol efflux capacity. In the current study, HDL cholesterol, which was reduced after LDL apheresis, returned to pre-apheresis levels in week 1 and remained at that level during evolocumab treatment. This could be “beneficial, with regards to cardiovascular disease,” they said. However, they cautioned, “this finding should be explored in further studies.”

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One limitation of the study is that it is observational, the researchers noted. Moreover, the number of participants was low, which limited generalizability. And the effects observed when converting from LDL apheresis to PCSK9 inhibition “may not necessarily reflect effects in apheresis-naïve patients.” Nevertheless, they concluded that their study demonstrated reductions in LDL-C, triglycerides and Lp(a)when switching from LDL apheresis to evolocumab.

The researchers added that this was the first trial to study changes in lipoproteins during transitions from long-term LDL apheresis to self-administered PCSK9 inhibition.


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