Author:
Sandhu Supna,Al-Sarraf Ahmad,Taraboanta Catalin,Frohlich Jiri,Francis Gordon A
Abstract
Abstract
Background
Severe hypertriglyceridemia (HTG) is one cause of acute pancreatitis, yet the level of plasma triglycerides likely to be responsible for inducing pancreatitis has not been clearly defined.
Methods and Results
A retrospective cohort study was conducted on patients presenting non-acutely to the Healthy Heart Program Lipid Clinic at St. Paul's Hospital with a TG level > 20 mM (1772 mg/dl) between 1986 and 2007. Ninety-five patients with TG > 20 mM at the time of referral were identified, in who follow up data was available for 84. Fifteen patients (15.8%), with a mean outpatient TG level of 38.1 mM, had a history of acute pancreatitis. Among 91 additional patients with less severe HTG, none had a history of pancreatitis when TG were between 10 and 20 mM. Among patients with TG > 20 mM on presentation, 8 (8.5%), with a mean TG level of 67.8 mM, exhibited eruptive xanthomata. A diet high in carbohydrates and fats (79%) and obesity (47.6%) were the two most frequent secondary causes of HTG at initial visit. By 2009, among patients with follow up data 53% exhibited either pre-diabetes or overt Type 2 diabetes mellitus. Upon referral only 23 patients (24%) were receiving a fibrate as either monotherapy or part of combination lipid-lowering therapy. Following initial assessment by a lipid specialist this rose to 84%, and remained at 67% at the last follow up visit.
Conclusions
These results suggest hypertriglyceridemia is unlikely to be the primary cause of acute pancreatitis unless TG levels are > 20 mM, that dysglycemia, a diet high in carbohydrates and fats, and obesity are the main secondary causes of HTG, and that fibrates are frequently overlooked as the drug of first choice for severe HTG.
Publisher
Springer Science and Business Media LLC
Subject
Biochemistry, medical,Clinical Biochemistry,Endocrinology,Endocrinology, Diabetes and Metabolism
Reference16 articles.
1. Alberti KG, Zimmet P, Shaw J: The metabolic syndrome--a new worldwide definition. Lancet. 2005, 366: 1059-1062. 10.1016/S0140-6736(05)67402-8
2. Brunzell JD, Deeb SS: Familial lipoprotein lipase deficiency, apo CII deficiency and hepatic lipase deficiency. The Metabolic and Molecular Bases of Inherited Disease. Edited by: Scriver CR, Beaudet AL, Sly WS, Valle D. 2001, 2789-2816. New York: McGraw-Hill, 8.
3. Yuan G, Al-Shali KZ, Hegele RA: Hypertriglyceridemia: its etiology, effects and treatment. CMAJ. 2007, 176: 1113-1120. 10.1503/cmaj.060963
4. Wang J, Ban MR, Kennedy BA, Anand S, Yusuf S, Huff MW, Pollex RL, Hegele RA: APOA5 genetic variants are markers for classic hyperlipoproteinemia phenotypes and hypertriglyceridemia. Nat Clin Pract Cardiovasc Med. 2008, 5: 730-737. 10.1038/ncpcardio1326
5. Johansen CT, Wang J, Lanktree MB, Cao H, McIntyre AD, Ban MR, Martins RA, Kennedy BA, Hassell RG, Visser ME: Excess of rare variants in genes identified by genome-wide association study of hypertriglyceridemia. Nat Genet. 2010, 42: 684-687. 10.1038/ng.628
Cited by
130 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献