A patient has severely elevated plasma triglycerides (>2000 mg/dL), eruptive xanthomas, recurrent pancreatitis, and creamy plasma on refrigeration. Lipoprotein lipase (LPL) activity in post-heparin plasma is absent. Which lipoprotein class is most elevated, and why does HDL remain paradoxically low?

• A VLDL; LPL normally converts VLDL to IDL which then becomes HDL
• B LDL; LPL deficiency blocks LDL receptor recycling
• C IDL; intermediate density lipoproteins accumulate due to failed LPL clearance
• D Chylomicrons; LPL normally transfers surface components to HDL during chylomicron catabolism — blocked LPL prevents this HDL 'loading' ✓

Explanation

LPL deficiency (Fredrickson Type I hyperlipoproteinemia) leads to massive chylomicron accumulation since LPL normally hydrolyzes TG in chylomicrons and VLDL. The characteristic creamy plasma and floating layer on refrigeration is due to chylomicrons. As LPL catabolizes TG-rich lipoproteins, surface phospholipids, cholesterol, and apolipoproteins (especially apoA-I, apoC) are transferred to HDL, 'building up' HDL. Without LPL, this transfer doesn't occur, explaining paradoxically low HDL despite massive hypertriglyceridemia.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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