November 12, 2014
Notes: Morimoto, Tsuyoshi
Biomed Rep. 2013 Jul;1(4):651-653. Epub 2013 May 17.
Author Address: Department of Pediatrics, Tokai University School of Medicine, Isehara, Kanagawa 259-1193, Japan.
Reference Type: Journal Article
Record Number: 4727Author: Nagayama, D. and Shirai, K.
Title: [Hypertriglyceridemia-induced pancreatitis]
Journal: Nihon Rinsho
Short Title: [Hypertriglyceridemia-induced pancreatitis]
Alternate Journal: Nihon rinsho. Japanese journal of clinical medicine
ISSN: 0047-1852 (Print)
Accession Number: 24205721
Keywords: Acute Disease
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.