# Hypertriglyceridaemia-Associated Acute Pancreatitis: Risk Stratification, Drivers, and Prevention of Recurrence

**Authors:** Federica Fogacci, Arrigo F. G. Cicero

PMC · DOI: 10.3390/diseases14020047 · 2026-01-30

## TL;DR

This paper reviews how high triglycerides cause acute pancreatitis, how to manage it, and new treatments to prevent recurrence.

## Contribution

The paper provides updated insights into risk factors, management strategies, and emerging therapies for hypertriglyceridaemia-induced pancreatitis.

## Key findings

- Acute pancreatitis risk increases sharply when triglycerides exceed 10 mmol/L.
- Emerging RNA-targeted therapies show promise in preventing pancreatitis recurrence in high-risk patients.

## Abstract

Hypertriglyceridaemia is the third most common aetiology of acute pancreatitis and a leading cause of recurrence in specialized lipid clinics. The risk of acute pancreatitis rises steeply once triglycerides exceed approximately 10 mmol/L (≈885 mg/dL). Still, clinically meaningful risk may occur at lower levels in the presence of chylomicronaemia, metabolic stress, or pregnancy. This mini-review synthesizes contemporary evidence on epidemiology, mechanistic links between triglyceride-rich lipoproteins and pancreatic injury, and the practical distinction between secondary (acquired) and genetic drivers of severe hypertriglyceridaemia. We summarize acute management strategies aimed at rapid triglyceride reduction (including insulin-based approaches and therapeutic plasma exchange in selected scenarios) and focus on long-term prevention of recurrence through lifestyle interventions, correction of secondary contributors, and triglyceride-lowering pharmacotherapy. Finally, we discuss emerging RNA-targeted therapies against apolipoprotein C-III and angiopoietin-like 3, which are reshaping prevention strategies for familial and persistent chylomicronaemia and may reduce pancreatitis burden in the highest-risk phenotypes.

## Linked entities

- **Diseases:** acute pancreatitis (MONDO:0006515)

## Full-text entities

- **Genes:** APOC3 (apolipoprotein C3) [NCBI Gene 345] {aka APOCIII, Apo-C3, ApoC-3}, LPL (lipoprotein lipase) [NCBI Gene 4023] {aka HDLCQ11, LIPD}, ANGPTL3 (angiopoietin like 3) [NCBI Gene 27329] {aka ANG-5, ANGPT5, ANL3, FHBL2}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, PCSK9 (proprotein convertase subtilisin/kexin type 9) [NCBI Gene 255738] {aka FH3, FHCL3, HCHOLA3, LDLCQ1, NARC-1, NARC1}, PNLIP (pancreatic lipase) [NCBI Gene 5406] {aka PL, PNLIPD, PTL}, LMF1 (lipase maturation factor 1) [NCBI Gene 64788] {aka C16orf26, HMFN1876, JFP11, TMEM112, TMEM112A}, APOA5 (apolipoprotein A5) [NCBI Gene 116519] {aka APOAV, RAP3}, APOC2 (apolipoprotein C2) [NCBI Gene 344] {aka APO-CII, APOC-II}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, GPIHBP1 (glycosylphosphatidylinositol anchored high density lipoprotein binding protein 1) [NCBI Gene 338328] {aka GPI-HBP1, HYPL1D}
- **Diseases:** type 2 diabetes (MESH:D003924), miscarriage (MESH:D000022), organ dysfunction (MESH:D009102), obesity (MESH:D009765), renal disease (MESH:D007674), prematurity (MESH:C536271), diabetic ketoacidosis (MESH:D016883), ischaemia (MESH:D007511), autosomal recessive disorder (MESH:D030342), metabolic dysfunction (MESH:D008659), ketosis (MESH:D007662), necrosis (MESH:D009336), PC (MESH:D008072), Hypertriglyceridemia (MESH:D015228), injury to (MESH:D014947), persistent (MESH:D000088562), inflammation (MESH:D007249), fetal growth restriction (MESH:D005317), critically ill (MESH:D016638), deaths (MESH:D003643), hypothyroidism (MESH:D007037), mitochondrial dysfunction (MESH:D028361), nephrotic syndrome (MESH:D009404), infection (MESH:D007239), eruptive xanthomata (MESH:D003875), cardiovascular disease (MESH:D002318), diabetic (MESH:D003920), thrombocytopenia (MESH:D013921), FCS (MESH:D011125), toxicity (MESH:D064420), abdominal pain (MESH:D015746), weight loss (MESH:D015431), chronic kidney disease (MESH:D051436), HTG-AP (MESH:D010195), insulin deficiency (MESH:D007333)
- **Chemicals:** fructose (MESH:D005632), MCT (MESH:C000709826), FFA (MESH:D005230), lipid (MESH:D008055), Fibrates (MESH:D058607), retinoids (MESH:D012176), propofol (MESH:D015742), oligonucleotides (MESH:D009841), alcohol (MESH:D000438), heparin (MESH:D006493), icosapent ethyl (MESH:C035276), volanesorsen (MESH:C000593612), LDL-C (-), fat (MESH:D005223), TG (MESH:D013866), sugars (MESH:D000073893), Ezetimibe (MESH:D000069438), Omega-3 fatty acids (MESH:D015525), bempedoic acid (MESH:C581236), Triglyceride (MESH:D014280), evinacumab (MESH:C000621590), carbohydrates (MESH:D002241)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12939449/full.md

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Source: https://tomesphere.com/paper/PMC12939449