Conventional approaches may not lower triglycerides to guideline thresholds in FCS1–4

With conventional triglyceride-lowering approaches (e.g., statins, fibrates, and omega-3 fatty acids), people with Familial Chylomicronaemia Syndrome (FCS) may still face a high risk of acute pancreatitis (AP)1–4

A strict, low-fat diet is the cornerstone of treatment in FCS5

Current FCS management primarily includes the use of an extremely low-fat diet (<15–20 g/day) and avoidance of alcohol to manage high triglycerides.6,7 This remains essential for managing FCS symptoms and reducing the risk of acute pancreatitis, especially as conventional approaches show limited efficacy6

Despite this, in a survey of 166 people with FCS, participants reported the following regarding their restrictive diet:8

81%

reported it as extremely time consuming

70%

reported it as energy draining

53%

reported it as ineffective at stopping all symptoms

CONVENTIONAL TRIGLYCERIDE-LOWERING
APPROACHES are limited1–3

Conventional approaches may not lower the risk of acute pancreatitis in people with extremely high triglyceride levels. While conventional approaches are effective in some lipid disorders, their efficacy is limited in people with FCS due to lipoprotein lipase deficiency1,3,8,9

Limitations of conventional approaches:

Icon of a pill alongside a closed pill bottle. Statins

Statins may be useful in protecting against atherosclerotic cardiovascular disease; however, they show limited efficacy in people with FCS and may not lower acute pancreatitis risk2,3,6,9

Icon of two medication capsules. Fibrates

Fibrates induce triglyceride clearance by activating lipoprotein lipase; however, due to the loss of lipoprotein lipase activity in people with FCS, the clinical benefit of fibrates is minimal3,5,6,9

Icon of a fatty acid. Eicosapentaenoic Acid (EPA)

EPA, an omega-3 fatty acid, has been shown to moderately reduce triglyceride levels caused by other diseases but shows only marginal efficacy for people with FCS3,5,6,9

Why conventional triglyceride-lowering approaches are limited in FCS3,6,10

Tap the green hotspots to learn more

Diagram showing how apolipoprotein C-III inhibits triglyceride breakdown in Familial Chylomicronaemia Syndrome, highlighting lipoprotein lipase-dependent and -independent pathways, leading to high plasma triglycerides and increased risk of acute pancreatitis.
  • Apolipoprotein C-III plays a key role in regulating triglyceride metabolism10,12
  • It inhibits the breakdown of chylomicrons and clearance of subsequent triglycerides via both lipoprotein lipase-dependent and -independent pathways10,12
  • Triglycerides are transported in the blood by chylomicrons and VLDL11,12
  • Lipoprotein lipase catalyses the breakdown of plasma triglycerides. In 80–90% of cases of FCS, there is an absence or impairment of lipoprotein lipase function8
  • The impaired clearance of chylomicrons from the bloodstream leads to chylomicronaemia and increased risk of acute pancreatitis10,12

UNDERSTAND WHY CONVENTIONAL APPROACHES SHOW LIMITED EFFICACY IN FCS

Learn about the mechanisms underlying FCS8,10

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How could achieving the guideline triglyceride level benefit people with FCS?

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Abbreviations

AP, acute pancreatitis; apoC-III, apolipoprotein C-III; FCS, Familial Chylomicronaemia Syndrome; LPL, lipoprotein lipase; MOD, mechanism of disease; TG, triglyceride; TRL, triglyceride-rich lipoprotein; VLDL, very-low-density lipoprotein.

Show References Expand Collapse

  1. Paragh G, Németh Á, et al. Lipids Health Dis. 2022;21:21.
  2. Spagnuolo CM, Hegele RA, et al. Expert Rev Endocrinol Metab. 2024;19(4):299–306.
  3. Gouni-Berthold I. J Endocr Soc. 2020;4(2):bvz037.
  4. Mach F, Baigent C, et al. Eur Heart J. 2020;41(1):111–88.
  5. Shamsudeen I, Hegele RA, et al. Expert Rev Clin Pharmacol. 2022;15(4):395–405.
  6. Stroes E, Moulin P, et al. Atheroscler Suppl. 2017;23:1–7.
  7. Williams L, Rhodes KS, et al. J Clin Lipidol. 2018;12(4):908–19.
  8. Davidson M, Stevenson M, et al. J Clin Lipidol. 2018;12(4):898–907.
  9. Veliadkis N, Stachteas P, et al. Pharmaceuticals (Basel). 2024;17(5):568.
  10. Brinton EA, Eckel RH, et al. Atherosclerosis. 2025;403:119114.
  11. Ginsberg HN, Packard CJ, et al. Eur Heart J. 2021;42(47):4791–806.
  12. Gaudet D, Brisson D, et al. N Engl J Med. 2014. 4;371(23):2200–6.

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