Incidence of pancreatitis, secondary causes, and treatment of patients referred to a specialty lipid clinic with severe hypertriglyceridemia: a retrospective cohort study

Lipids in Health and Disease

Gordon A Francis²  Jiri Frohlich¹  Catalin Taraboanta²  Ahmad Al-Sarraf¹  Supna Sandhu² 

[1] Department of Pathology and Laboratory Medicine, Healthy Heart Program Prevention Clinic, UBC James Hogg Research Centre, Providence Heart + Lung Institute, St. Paul's Hospital, University of British Columbia, 1081 Burrard St., Vancouver, BC V6Z 1Y6 Canada;Department of Medicine, Healthy Heart Program Prevention Clinic, UBC James Hogg Research Centre, Providence Heart + Lung Institute, St. Paul's Hospital, University of British Columbia, 1081 Burrard St., Vancouver, BC V6Z 1Y6 Canada

关键词: fibrates;    diabetes;    dysglycemia;    pancreatitis;    triglycerides;    Hypertriglyceridemia;   

Others  :  1212522
DOI  :  10.1186/1476-511X-10-157

 received in 2011-07-18, accepted in 2011-09-11,  发布年份 2011

【 摘 要 】

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.

【 授权许可】

   
2011 Sandhu et al; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

【 参考文献 】

• [1]Alberti KG, Zimmet P, Shaw J: The metabolic syndrome--a new worldwide definition. Lancet 2005, 366:1059-1062.
• [2]Brunzell JD, Deeb SS: Familial lipoprotein lipase deficiency, apo CII deficiency and hepatic lipase deficiency. In The Metabolic and Molecular Bases of Inherited Disease. 8th edition. Edited by Scriver CR, Beaudet AL, Sly WS, Valle D. New York: McGraw-Hill; 2001:2789-2816.
• [3]Yuan G, Al-Shali KZ, Hegele RA: Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007, 176:1113-1120.
• [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.
• [5]Johansen CT, Wang J, Lanktree MB, Cao H, McIntyre AD, Ban MR, Martins RA, Kennedy BA, Hassell RG, Visser ME, et al.: Excess of rare variants in genes identified by genome-wide association study of hypertriglyceridemia. Nat Genet 2010, 42:684-687.
• [6]Truninger K, Schmid PA, Hoffmann MM, Bertschinger P, Ammann RW: Recurrent acute and chronic pancreatitis in two brothers with familial chylomicronemia syndrome. Pancreas 2006, 32:215-219.
• [7]Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III) JAMA 2001, 285:2486-2497.
• [8]Fortson MR, Freedman SN, Webster PD: Clinical assessment of hyperlipidemic pancreatitis. Am J Gastroenterol 1995, 90:2134-2139.
• [9]Lloret Linares C, Pelletier AL, Czernichow S, Vergnaud AC, Bonnefont-Rousselot D, Levy P, Ruszniewski P, Bruckert E: Acute pancreatitis in a cohort of 129 patients referred for severe hypertriglyceridemia. Pancreas 2008, 37:13-12.
• [10]Leaf DA: Chylomicronemia and the chylomicronemia syndrome: a practical approach to management. Am J Med 2008, 121:10-12.
• [11]McPherson R, Frohlich J, Fodor G, Genest J, Canadian Cardiovascular S: Canadian Cardiovascular Society position statement--recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease. Can J Cardiol 2006, 22:913-927.
• [12]Verges BL: Dyslipidaemia in diabetes mellitus. Review of the main lipoprotein abnormalities and their consequences on the development of atherogenesis. Diabetes Metab 1999, 25(Suppl 3):32-40.
• [13]Barter PJ, Rye KA: Cardioprotective properties of fibrates: which fibrate, which patients, what mechanism? Circulation 2006, 113:1553-1555.
• [14]Oh R: Practical applications of fish oil (Omega-3 fatty acids) in primary care. J Am Board Fam Pract 2005, 18:28-36.
• [15]Jones PH, Davidson MH, Stein EA, Bays HE, McKenney JM, Miller E, Cain VA, Blasetto JW: Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial). Am J Cardiol 2003, 92:152-160.
• [16]Ginsberg HN, Elam MB, Lovato LC, Crouse JR, Leiter LA, Linz P, Friedewald WT, Buse JB, Gerstein HC, Probstfield J, et al.: Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med 2010, 362:1563-1574.