PCSK9, alirocumab, evolocumab, allergy
The proprotein convertase subtilisin/kexin type 9 (PCSK9) gene and gain-of-function mutations were first described in 2003. The gain-of-function mutations observed were associated with low-density lipoprotein-cholesterol (LDL-C) levels in the 400’s, in addition to premature cardiovascular disease. Subsequent loss-of-function experiments conducted in mice demonstrated marked reductions in plasma cholesterol levels in the absence of PCSK9. Physiologically, PCSK9 serves as a chaperone protein and functions to reduce low-density lipoprotein (LDL) receptor recycling; consequently, less LDL-C is removed from circulation and serum lipid concentrations become elevated. Inhibition of PCSK9 prevents LDL receptor degradation and preserves receptor recycling to the hepatocyte surface; this in turn results in reduced LDL-C levels. We report a lack of cross-sensitivity following the administration of evolocumab after an allergic reaction to alirocumab.
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