Key result
Hypertriglyceridemia contributes to acute pancreatitis pathogenesis through complex mechanisms including lipid metabolism, calcium signal transduction, inflammatory mediators, and oxidative stress.
Why the study?
Hypertriglyceridemia pancreatitis incidence is increasing and associated with severe complications, yet its underlying pathogenic mechanisms are not fully understood.
This comprehensive review outlines the complex mechanisms underlying acute hypertriglyceridemic pancreatitis to facilitate the development of targeted pharmacological interventions.
Does not alter management of hypertriglyceridemic pancreatitis; leaves open targeted therapies pending clinical validation.
The incidence rate of hypertriglyceridemia pancreatitis (HTGP) has experienced a notable increase in recent years, with eclipsing alcohol as the second leading cause of acute pancreatitis (AP). HTGP is often associated with more severe local and systemic complications. Recognized as a metabolic disorder hypertriglyceridemia (HTG), it holds significant relevance in the pathogenesis of HTGP, yet its mechanisms are not fully understood. Both primary (genetic) and secondary (acquired) factors contribute to elevated triglyceride (TG) levels, which concurrently influence the progression of HTGP. This article presents a comprehensive review of the evolving research on HTGP pathogenesis, encompassing lipid synthesis and metabolism, calcium signal transduction, inflammatory mediators, endoplasmic reticulum stress, autophagy, mitochondrial injury by fatty acids, oxidative stress response, genetic factors, and gene mutations. By unraveling the intricate mechanisms underlying HTGP, this article aims to enhance physicians' understanding of the disease and facilitate the development of potential targeted pharmacological interventions for patients.
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Meng et al. (2024) conducted a review in Acute Hypertriglyceridemic Pancreatitis. Hypertriglyceridemia was evaluated. Hypertriglyceridemia contributes to acute pancreatitis pathogenesis through complex mechanisms including lipid metabolism, calcium signal transduction, inflammatory mediators, and oxidative stress.
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