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The acute pancreatitis critical threshold
  • Risk of acute pancreatitis increases exponentially with increasing TG levels, with clinical significance above 880 mg/dL (10 mmol/L)1-3
  • The severity and outcomes of acute pancreatitis are known to worsen with increasing TG levels4-6

Preventing the first episode of acute pancreatitis reduces the risk of subsequent events7

  • HTG-associated acute pancreatitis is a medical emergency that may require hospitalisation and, in 5–8% of cases, can be fatal1,8,9
  • Preventing an initial episode of acute pancreatitis in patients with sHTG is associated with a lower risk of recurrent episodes and of developing chronic acute pancreatitis7,10

24%

Once a parient with sHTG has had an episode of AP, their risk for a second can be as high as 24%7

49%

After 2 or more episodes, the risk for another can increase to nearly 49%7

How accumulation of chylomicrons in sHTG can lead to acute pancreatitis

  • The mechanisms by which sHTG leads to acute pancreatitis have not been completely elucidated1,11-13

Two potential mechanisms:

1

Chylomicrons accumulate in pancreatic capillaries, leading to ischaemia, acidosis and pancreatic autodigestion

Chylomicrons mechanism illustration

2

Free fatty acids generated by pancreatic lipase trigger the inflammatory cascade that leads to acute pancreatitis

Chylomicrons mechanism illustration

Adapted from Chyzhyk & Brown 2020.

Acute pancreatitis can lead to serious consequences

  • HTG-associated acute pancreatitis is a medical emergency that may require hospitalisation and, in 5–8% of cases, can be fatal1,8,9
Pancreatitis can lead to serious consequences
  • sHTG is the third most commonly identified cause of acute pancreatitis and may be more serious than acute pancreatitis from other causes5,14

In patients who recover from HTG-induced acute pancreatitis:

45%

develop pancreatic and/or peripancreatic necrosis8

~9%

develop new-onset chronic acute pancreatitis post-acute pancreatitis8

Up to 40%

develop type 2 diabetes during an average 3 years follow-up9

Clinical outcomes of HTG-associated acute pancreatitis worsen with increasing TG levels:5

Risk of clinical outcomes of HTG-related acute pancreatitis at different TG levels (Odds Ratio [95% CI])5

TG level
(mg/dL)		Persistent
organ failure
(POF)		Multiple organ
dysfunction
syndrome (MODS)		Pancreatic
necrosis		Newly diagnosed
diabetes
mellitus		Mortality
500–10001.48 [0.84, 2.61]1.29 [0.46, 3.57]1.27 [0.69, 2.34]3.66 [1.54, 8.70]1.92 [0.62, 5.99]
≥10002.92 [1.78, 4.77]3.89 [1.77, 8.56]1.80 [1.06, 3.04]5.11 [2.39, 10.94]4.02 [1.55, 10.46]
  • Need for hospitalisation and long-term consequences of acute pancreatitis put serious economic burden on healthcare systems15-18

Guidelines recommend action to prevent acute pancreatitis

  • European and American guidelines recommend treatment of elevated TG levels to prevent acute pancreatitis19-21
  • Preventing an initial episode of acute pancreatitis in patients with severely elevated TGs is associated with a lower risk of recurrent episodes and of developing chronic pancreatitis7,10
  • According to the 2019 ESC/EAS Guidelines for the management of dyslipidaemias: in sHTG ≥880 mg/dL (10 mmol/L), risk of pancreatitis is clinically significant and actions to prevent acute pancreatitis are mandatory19
  • Triglyceride levels should be determined in all cases of acute pancreatitis, as sHTG may contribute even when the primary cause is obvious22

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References

  1. Javed F, et al. J Clin Lipid. 2025;19:382-403.
  2. Patel RS, et al. Cardiovascular Diabetology. 2022;21:102.
  3. Moulin P, et al. Atherosclerosis. 2018;275:265-272.
  4. Pothoulakis I, et al. Digestion. 2021;102(5):809-813.
  5. Zhang R, et al. HPB (Oxford). 2019;21(9):1240-1249.
  6. Nawaz H, Am J Gastroenterol. 2015;110(10):1497–1503.
  7. Sanchez RJ, et al. Lipids in Health and Disease. 2021;20:72.
  8. Vipperla, J Clin Gastroenterol 2017;51:77–85.
  9. Subramanian S, Eur J Intern Med. 2025 Dec;145:106648.
  10. Gagyi EB, et al. Ther Adv Gastroenterol. 2024;17:17562848241258671.
  11. Chyzhyk V, Brown AS. Trends Cardiovasc Med. 2020;30(2):80-85.
  12. Valdivielso P, et al. Eur J Intern Med. 2014;25(8):689-694.
  13. Berglund L, et al. J Clin Endocrinol Metab. 2012;97(9):2969-2989.
  14. Bálint ER , et al. Sci Rep. 2020;10(1):17936.
  15. Kessler AS, et al. J Clin Lipidol 2025; S1933-2874(25)00268-5.
  16. Pahomeanu MR, et al. Healthcare (Basel). 2023;11(18):2482.
  17. Andersson B, et al. Scand J Gastroenterol. 2013;48(12):1459-65.
  18. Hall T, et al. J Eval Clin Pract. 2014;20(3):203-207.
  19. Mach F, et al. European Heart Journal. 2020;41(1):111-188.
  20. Blumenthal RS, et al. Circulation. 2026;153(17):e1154–e1276.
  21. Newman C, et al. J Clin Endocrinol Metab. 2020;105(12):dgaa674.
  22. Laufs U, et al. Eur Heart J. 2020;41(1):99-109.
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