Key result
Statin-fenofibrate therapy cuts triglycerides ~66% in type V hyperlipoproteinemia but leaves persistent hypertriglyceridemia.
Why the study?
Hypertriglyceridemia is a risk-enhancing factor for atherosclerotic cardiovascular disease, but real-world data on managing type V hyperlipoproteinemia were needed.
How do lipid profile responses and persistent hypertriglyceridemia compare at 6 months between patients with type V hyperlipoproteinemia and those with type IV hyperlipoproteinemia receiving real-world lipid-lowering therapy?
Cohort (n=90)
No
How do lipid profile responses and persistent hypertriglyceridemia compare at 6 months between patients with type V hyperlipoproteinemia and those with type IV hyperlipoproteinemia receiving real-world lipid-lowering therapy?
Even with aggressive combination statin and fenofibrate therapy, patients with type V hyperlipoproteinemia experience persistent hypertriglyceridemia, a paradoxical rise in LDL-C, and minimal apoB reduction, underscoring an unmet need for novel triglyceride-lowering therapies and dedicated clinical guidelines.
Answers are grounded in this paper and cite their sources.
Persistent hypertriglyceridemia despite combination therapy supports caution in type V management; leaves open need for targeted agents in this phenotype.
Hypertriglyceridemia (HTG) remains a risk-enhancing factor of atherosclerotic cardiovascular disease. We aimed to report real-world data on the management of patients with type V hyperlipoproteinemia (HLP5), an uncommon phenotype of dyslipidemia characterized by fasting chylomicronemia and severe HTG. Between July 2018 and May 2021, 90 patients with HTG, including 83 patients with type IV hyperlipoproteinemia (HLP4) and 7 patients with HLP5, were identified by plasma apolipoprotein B (apoB) and lipoprotein electrophoresis. Patients with HLP5 were younger, had higher total cholesterol (TC) (264.9 ± 26.7 mg/dL vs. 183.9 ± 26.1 mg/dL; p < 0.01) and higher triglyceride (TG) (1296.7 ± 380.5 mg/dL vs. 247.6 ± 96.1 mg/dL; p < 0.01), and had lower high-density lipoprotein cholesterol (HDL-C) (30.6 ± 4.8 mg/dL vs. 40.5 ± 8.7 mg/dL; p < 0.01) and lower low-density lipoprotein cholesterol (LDL-C) (62.9 ± 16.4 vs. 103.0 ± 21.1 mg/dL; p < 0.01) compared with patients with HLP4. Despite an aggressive use of statin and fenofibrate with greater reductions in TG (-65.9 ± 13.7% vs. -27.9 ± 30.5%; p < 0.01) following 6 months of treatment, patients with HLP5 had persistent HTG (440.1 ± 239.0 mg/dL vs. 173.9 ± 94.8 mg/dL; p < 0.01) and an increase in LDL-C (28.3 ± 57.2% vs. -19.5 ± 32.0%; p < 0.01) compared with patients with HLP4. Our findings highlight that the lack of novel TG-lowering medications and management guidelines remains an unmet medical need in patients with HLP5. Closely monitoring lipid profiles, full assessment of individual’s risk of cardiovascular disease, and emphasis on medication adherence are of clinical importance.
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Chang et al. (2022) conducted a cohort in Hypertriglyceridemia (Type V vs. Type IV hyperlipoproteinemia) (n=90). Type V hyperlipoproteinemia (HLP5) phenotype treated with statin and fenofibrate vs. Type IV hyperlipoproteinemia (HLP4) phenotype on lipid-lowering therapy was evaluated on Fasting plasma triglyceride (TG) level and percentage change at 6 months (p=<0.01). Patients with type V hyperlipoproteinemia had greater 6-month triglyceride reductions on statin and fenofibrate than type IV patients, but retained persistent HTG and increased LDL-C.
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