About sHTG | Disease Overview

As triglyceride levels rise across the sHTG spectrum, so do the risks

Expert guidelines highlight the urgency in lowering triglyceride levels that are ≥500 mg/dL to reduce associated risks, including acute pancreatitis.1-4

Infographic

Postprandial spikes can push patients into the acute pancreatitis (AP) danger zone.1,5,9,10

sHTG=severe hypertriglyceridemia.

Triglycerides are dynamic and can surge dramatically after meals9,10

Estimated triglyceride kinetics for average US male with normal triglycerides (122 mg/dL) following the typical Western dietary pattern9*†
Chart showing estimated triglycerides kinetics for average US male with normal triglycerides following typical Western dietary pattern

For people with

sHTG, how high can triglycerides rise over
a typical day of eating?

Postprandial triglyceride elevations could potentially be increasing the risk of AP and ASCVD.1,5,8,9

*Estimate based on average US male who consumes approximately 2400 kcal/day, 35% of which are from fat, over 4 to 5 meals and snacks. These averages equate to consumption of approximately 93 g of fat each day, approximately 23 g per meal if divided across 4 meals. Figure adapted from Keirns BH, et al. J Nutr Sci. 2021.9 
Normal triglycerides are defined as <150 mg/dL.11

ASCVD=atherosclerotic cardiovascular disease.

sHTG, defined as fasting triglyceride levels ≥500 mg/dL, includes metabolic and genetic forms such as familial chylomicronemia syndrome (FCS)1,12

Genetic and metabolic drivers lead to a shared biological threat: impaired clearance and accumulation of triglyceride-rich lipoproteins (TRLs).1,12

Genetic burden1,12

Ranging from a broad polygenic background to rare, biallelic pathogenic variants in genes such as LPL, APOC2, and APOA5

Metabolic triggers1,12

Environmental and secondary factors (eg, obesity, insulin resistance, diabetes, and alcohol consumption)

Impaired clearance and accumulation1,6,13,14

Impaired lipolytic activity 
(LPL-dependent and LPL-independent) 

Toxic accumulation of TRLs
(VLDL and chylomicrons)

Increased risk for acute pancreatitis and ASCVD

ApoC-III acts as a pivotal regulator of triglyceride metabolism, inhibiting LPL activity and impairing the hepatic clearance of TRLs.12

apo=apolipoprotein; LPL=lipoprotein lipase; VLDL=very low-density lipoprotein.

The real threats of elevated triglycerides ≥500 mg/dL

sHTG puts millions of adults at risk of potentially life-threatening AP and ASCVD.1,6,11,15-17


Triglycerides fluctuate more than other lipids, complicating accurate assessment of risk.9,10

  • The additive effect of multiple meals can cause a substantial postprandial triglyceride peak, with levels elevated for most of the day


Chylomicrons, VLDL, and their remnants contribute to these risks.1,6

  • Chylomicrons (marked by apolipoprotein B-48) and VLDL (marked by apolipoprotein B-100) contribute to acute pancreatitis risk
  • VLDL and their remnant cholesterol contribute to ASCVD
threat of elevated levels

Not a real patient; actor portrayal.