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Approach to the patient with hypertriglyceridemia

Robert S Rosenson, MD
Section Editor
Mason W Freeman, MD
Deputy Editor
Gordon M Saperia, MD, FACC


Lipid disorders can occur as either a primary event or secondary to some underlying disease [1] (see "Secondary causes of dyslipidemia"). The primary dyslipidemias are associated with overproduction and/or impaired removal of lipoproteins (table 1). The latter defect can be induced by an abnormality in either the lipoprotein itself or in the lipoprotein receptor. Lipoprotein lipase (LPL) hydrolyzes triglycerides contained in the core of chylomicrons and very low density lipoprotein (VLDL); it also facilitates cholesterol transfer from these lipoproteins to high density lipoprotein (HDL) (figure 1 and figure 2). The hydrolysis of triglycerides releases free fatty acids that are then used as an energy source, converted to triglyceride, or stored in adipose tissue. (See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Endogenous pathway of lipid metabolism'.)

One definition of dyslipidemia is total cholesterol, low density lipoprotein-cholesterol (LDL-C), triglyceride, apolipoprotein (apo)-B, or Lp(a) levels above the 90th percentile or high density lipoprotein-cholesterol (HDL-C) or apo A-I levels below the 10th percentile for the general population (table 2). Lipoprotein metabolism and the function of the different apolipoproteins is discussed separately. (See "Lipoprotein classification, metabolism, and role in atherosclerosis".)

This topic reviews the evidence that hypertriglyceridemia contributes to the development of atherosclerosis, the mechanisms by which this might occur, the disorders of triglyceride metabolism that have been identified, and recommendations for the management of hypertriglyceridemia. The pathways involved in normal triglyceride synthesis and metabolism are discussed separately (see "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Endogenous pathway of lipid metabolism'). The management of patients with hypertriglyceridemia who have acute or prior pancreatitis is also discussed separately. (See "Hypertriglyceridemia-induced acute pancreatitis".)

Disorders of LDL and HDL metabolism and the management of lipids for primary and secondary prevention are also discussed separately:

(See "Inherited disorders of LDL-cholesterol metabolism".)


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