학술논문

[Hypertriglyceridemia-induced pancreatitis].
Document Type
Academic Journal
Author
Nagayama D; Center of Diabetes, Endocrinology and Metabolism.; Shirai K
Source
Publisher: Nippon Rinsho Co Country of Publication: Japan NLM ID: 0420546 Publication Model: Print Cited Medium: Print ISSN: 0047-1852 (Print) Linking ISSN: 00471852 NLM ISO Abbreviation: Nihon Rinsho Subsets: MEDLINE
Subject
Language
Japanese
ISSN
0047-1852
Abstract
In Japan, the frequency of acute pancreatitis is 27.7 per 100,000, which includes 1.4 % of hypertriglyceridemia-induced pancreatitis(HTGP). Severity and complication rates with HTGP have been reported as higher in comparison to acute pancreatitis from other etiologies. Havel has suggested that hydrolysis of excessive triglyceride-rich lipoproteins releases high concentrations of free fatty acid(FFA). The FFA micelles injure the vascular endothelium and acinar cells of the pancreas, producing a self-perpetuating ischemic and acidic environment with resultant toxicity. Lipoprotein lipase (LPL) abnormality has been reported to contribute to severe hypertriglyceridemia. However, patients without any LPL abnormality are often encountered clinically, suggesting that other factors may be involved in the development of severe hypertriglyceridemia. In 21 patients with HTGP, 9 patients(42.9 %) with apolipoprotein AV (ApoAV) Gly185-Cys polymorphism were observed, whereas 14.3 % with LPL gene variants. No patient had ApoCII deficiency. These results suggest that in addition to LPL gene variants, ApoAV variant may be numerously involved in HTGP. It is important for clinicians to routinely investigate pathogenesis of hypertriglyceridemia in case with pancreatitis because specific management may be needed.