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

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.

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.

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