1. Hypertriglyceridemia http://emedicine.medscape.com/article/126568-overview
Author: Elena Citkowitz, MD, PhD, FACP; Chief Editor: George T Griffing, MD more...
Updated: Jan 5, 2010
Background
Hypertriglyceridemia (hTG), a condition in which triglyceride levels are elevated, is a common disorder in the United
States. It is often caused or exacerbated by uncontrolled diabetes mellitus, obesity, and sedentary habits, all of which
are more prevalent in industrialized societies than in developing nations. In epidemiologic and interventional studies,
hypertriglyceridemia is a risk factor for coronary artery disease (CAD).
Hyperlipidemia (elevation of cholesterol levels and/or triglyceride levels) has been defined by the Fredrickson
classification, which is based on a beta-quantification, a process involving ultracentrifugation followed by
electrophoresis.[1] In this system, all categories except type IIa are forms of hTG.
Table 1. Fredrickson Classification of Hyperlipoproteinemia (Open Table in a new window)
Type Serum elevation Lipoprotein elevation
I Cholesterol and triglycerides Chylomicrons
IIa Cholesterol LDL*
IIb Cholesterol and triglycerides LDL, VLDL**
III Cholesterol and triglycerides IDL***
IV Triglycerides VLDL
V Cholesterol and triglycerides VLDL, chylomicrons
*LDL (low-density lipoprotein)
**VLDL (very low-density lipoprotein)
***IDL (intermediate-density lipoprotein)
Type I is a rare disorder characterized by severe elevations in chylomicrons and extremely elevated triglycerides,
always reaching well above 1000 mg/dL and not infrequently rising as high as 10,000 mg/dL or more. It is caused by
mutations of either the lipoprotein lipase gene (LPL), which is critical for the metabolism of chylomicrons and very
low-density lipoprotein (VLDL), or of the gene's cofactor, apolipoprotein (apo) C-II.
Counterintuitively, despite exceedingly high elevations of triglyceride and, in some cases, of total cholesterol, these
mutations do not appear to confer an increased risk of atherosclerotic disease. This fact may have contributed to the
unfounded belief that hypertriglyceridemia is not a risk factor for atherosclerotic disease. Although chylomicrons
contain far less cholesterol than other triglyceride-rich lipoproteins do, when serum triglyceride levels are severely
elevated, cholesterol levels can also be quite high.
Type IIb is the classic mixed hyperlipidemia (high cholesterol and triglyceride levels), caused by elevations in LDL and
VLDL.
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2. Hypertriglyceridemia http://emedicine.medscape.com/article/126568-overview
Type III is known as dysbetalipoproteinemia, remnant removal disease, or broad-beta disease (see
Dysbetalipoproteinemia). Typically, patients with this condition have elevated total cholesterol and triglyceride levels
and are easily confused with patients with type IIb hyperlipidemia. Patients with type III hyperlipidemia have elevations
in intermediate-density lipoprotein (IDL), a VLDL remnant, and a significant risk for developing coronary artery disease.
Type IV is characterized by abnormal elevations of VLDL, and triglyceride levels are almost always less than 1000
mg/dL. Serum cholesterol levels are normal.
Type V is characterized by elevations of chylomicrons and VLDL. Triglyceride levels are invariably greater than 1000
mg/dL, and total cholesterol levels are always elevated. The LDL cholesterol level is usually low. Given the rarity of
type I disease, when triglyceride levels above 1000 mg/dL are noted, the most likely cause is type V hyperlipidemia.
Triglyceride levels greater than 1000 mg/dL increase the risk of acute pancreatitis, and because triglycerides are so
labile, levels of 500 mg/dL or greater must be the primary focus of therapy. If a patient also has a high risk for a
cardiovascular event, LDL-lowering therapy should be considered.
Pathophysiology
Triglycerides are fats consisting of 3 fatty acids covalently bonded to a glycerol molecule. Triglycerides are
synthesized by the liver or, in the case of those derived from dietary sources, are ingested by the liver (as described
below); they are subsequently transported throughout the circulation by triglyceride-rich lipoproteins.
By dry weight, triglycerides make up approximately 86%, 55%, and 23% of chylomicrons, VLDLs, and IDLs,
respectively, as represented in the image below. Triglycerides are present in LDL and high-density lipoprotein (HDL),
but in much smaller quantities of 10% or less.
Composition of triglyceride-rich proteins is shown below.
Composition of triglyceride-rich lipoproteins.
Triglyceride-rich lipoproteins come from 2 sources, often described as the endogenous and exogenous pathways. In
the exogenous pathway, dietary fats (triglycerides) are hydrolyzed to free fatty acids (FFAs) and monoglycerides and
are absorbed, with cholesterol, by intestinal cells. They are then reesterified and combined with apolipoproteins and
phospholipids to form a nascent chylomicron, a process requiring microsomal triglyceride transfer protein (MTP). The
initial apolipoproteins are apo A, which are soluble and can transfer to HDL; and apolipoprotein B48, a structural
apolipoprotein that is not removed during catabolism of the chylomicron. Chylomicrons enter the plasma via the
thoracic duct, where they acquire two other soluble apolipoproteins, apo C and apo E, from high-density lipoprotein
(HDL).
VLDLs are produced by a process analogous to the exogenous pathway. Triglycerides may derive from de novo free
fatty acid synthesis in the liver or from the uptake of remnant chylomicrons, VLDL, or free fatty acids from the plasma.
Precursor VLDL combines triglycerides, the structural apolipoprotein apo B100, and phospholipids, as well as
cholesterol and some apo Cs and Es. The formation of the immature VLDL requires MTP. Once secreted into the
plasma, VLDLs acquire more apo Cs and Es.
Any disturbance that causes increased synthesis of chylomicrons and/or VLDLs or decreased metabolic breakdown
causes elevations in triglyceride levels. That disturbance may be as common as dietary indiscretion or as unusual as a
genetic mutation of an enzyme in the lipid metabolism pathway.
As shown in the images below, chylomicrons and VLDLs are initially metabolized by lipoprotein lipase (LPL), which
hydrolyzes the triglycerides, releasing free fatty acids; these fatty acids are stored in fat and muscle. With normal LPL
activity, the half-lives of chylomicrons and VLDLs are about 10 minutes and 9 hours, respectively. Because of the large
size of unmetabolized chylomicrons, they are unlikely to be taken up by macrophages, which are the precursors of
foam cells. Foam cells promote fatty streak formation, the precursor of atherosclerotic plaque. LPL activity produces
chylomicron remnants that are small enough to take part in the atherosclerotic process. Chylomicron remnants are
taken up by the LDL receptor or the LDL receptor-related protein.[2]
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3. Hypertriglyceridemia http://emedicine.medscape.com/article/126568-overview
Lipoprotein lipase (LPL) releases free fatty acids from chylomicrons and produces chylomicron remnants that are small enough to take
part in the atherosclerotic process.
Once very low-density lipoprotein (VLDL) has been metabolized by lipoprotein lipase, VLDL remnants in the form of intermediate-density
lipoprotein (IDL) can be metabolized by hepatic lipase, producing LDL, or they can be taken up by the LDL receptor via either
apolipoprotein B (apo B) or apo E.
VLDL remnants have 1 of 2 fates: they can be metabolized by hepatic lipase, which further depletes triglycerides,
producing LDL, or they can be taken up by the LDL receptor via either apo B or apo E. VLDL remnants are not only
triglyceride-poor, they are also cholesterol enriched, having acquired cholesterol ester from HDL via the action of
cholesterol ester transfer protein (CETP), which facilitates the exchange of VLDL triglycerides for cholesterol in HDL.
This pathway may promote HDL's reverse cholesterol transport activity, but only if VLDL and LDL return cholesterol to
the liver. If these lipoproteins are taken up by macrophages, the CETP transfer results in increased atherogenesis.
Chylomicron remnants, VLDL, VLDL remnants, and LDL are all atherogenic.
Epidemiology
Frequency
United States
The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) defined elevated triglycerides
as 150 mg/dL and higher.[2] Using that criterion, the Third National Health and Nutrition Examination Survey (NHANES)
found that the prevalence of hypertriglyceridemia in US adults age 20 years and older was approximately 35% in men
and 25% in women. Triglyceride levels in African American men and women were 21% and 14%, respectively; 40%
and 35% in Mexican American men and women, respectively; and in 37% and 25% in white American men and
women, respectively.
Prevalence of severe hypertriglyceridemia, defined as triglycerides greater than 2000 mg/dL, is estimated to be to be
1.8 cases per 10,000 white adults, with a higher prevalence in patients with diabetes or alcoholism.
The most severe form of hypertriglyceridemia, LPL deficiency, occurs in approximately 1 case per 1 million; the
frequency of apo C-II deficiency is even lower.
International
The worldwide incidence of LPL deficiency is similar to that in the United States with the exception of small
populations such as in Quebec, Canada, where the number is significantly higher, probably due to the founder effect.
Apo C-II is infrequent in all populations studied to date.
Mortality/Morbidity
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4. Hypertriglyceridemia http://emedicine.medscape.com/article/126568-overview
Hypertriglyceridemia is correlated with an increased risk of cardiovascular disease (CVD), particularly in the
setting of low HDL cholesterol (HDL-c) levels and/or elevated LDL cholesterol (LDL-c) levels. When low HDL-c
levels are controlled for, some studies demonstrate that elevated triglycerides do not correlate with risk of
cardiovascular disease. Others suggest that high triglyceride levels are an independent risk factor. Because
metabolism of the triglyceride-rich lipoproteins (chylomicrons, VLDL) and metabolism of HDL are
interdependent and because of triglycerides are very labile, the independent impact of hypertriglyceridemia on
cardiovascular disease risk is difficult to confirm. However, randomized clinical trials using triglyceride-lowering
medications have demonstrated decreased coronary events in both the primary and secondary coronary
prevention populations.
An understanding of lipoprotein catabolism provides an explanation for the absence of increased risk of
cardiovascular disease in patients with the most severe form of hypertriglyceridemia, type I
hyperlipoproteinemia. The atherogenicity correlated with elevated triglyceride levels is thought to be secondary
to increased levels of chylomicron and VLDL remnants. Remnants are smaller, richer in cholesterol, and more
readily taken up by macrophages, which are converted to plaque-forming foam cells. The chylomicrons in
patients with type I disease cannot be converted to remnants and, therefore, should not be atherogenic.
Extreme elevations of triglycerides, usually well above 1000 mg/dL, may cause acute pancreatitis and all the
sequelae of that condition (see Pancreatitis, Acute). The NCEP ATP III guidelines stipulate that if triglycerides
are ≥500 mg/dL, the initial management should be to lower the triglycerides to prevent pancreatitis. Only when
the triglyceride level is below 500 should LDL-lowering be addressed.
The chylomicronemia syndrome[3, 4] is an often unrecognized and less severe condition than pancreatitis that is
usually caused by triglyceride levels greater than 1000 mg/dL. Abdominal pain is the most common presenting
symptom, but chest pain and dyspnea may sometimes occur. Amylase and lipase are minimally, if at all,
elevated. Symptoms resolve when triglyceride levels decrease well below 1000.
Race
Triglycerides are lower in African Americans than in whites.
Racial predisposition has been not described for LPL deficiency or apo C-II deficiency.
Sex
In the Prospective Cardiovascular Munster study (PROCAM), a large observational study, mild
hypertriglyceridemia (triglycerides >200 mg/dL) was more prevalent in men (18.6%) than in women (4.2%).[5]
Genetic mutations in both LPL and apo C-II affect males and females in equal numbers.
Age
Triglycerides increase gradually in men until about age 50 years and then decline slightly. In women, they
continue to increase with age.
Mild hypertriglyceridemia (triglycerides >150 mg/dL) is slightly more prevalent in men beginning at age 30 years
and women starting at age 60 years.
LPL deficiency and apo C-II deficiency are caused by homozygous autosomal recessive genes present at
conception. The manifestations of LPL and apo C-II deficiency (severe hypertriglyceridemia) usually are
detected in childhood, although defective apo C-II sometimes presents in early adulthood.
Contributor Information and Disclosures
Author
Elena Citkowitz, MD, PhD, FACP Clinical Professor of Medicine, Yale University School of Medicine; Director,
Cholesterol Management Center, Director, Cardiac Rehabilitation, Department of Medicine, Hospital of St Raphael
Elena Citkowitz, MD, PhD, FACP is a member of the following medical societies: American College of Physicians,
American Heart Association, National Lipid Association, and Sigma Xi
Disclosure: Nothing to disclose.
Specialty Editor Board
Steven R Gambert, MD, MACP Chairman, Department of Medicine, Physician-in-Chief, Sinai Hospital of
Baltimore; Professor of Medicine, Program Director, Internal Medicine Program, Johns Hopkins University School
of Medicine
Steven R Gambert, MD, MACP is a member of the following medical societies: Alpha Omega Alpha, American
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5. Hypertriglyceridemia http://emedicine.medscape.com/article/126568-overview
College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of
Professors of Medicine, Endocrine Society, and Gerontological Society of America
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: eMedicine Salary Employment
Yoram Shenker, MD Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief,
Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism,
University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society
for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.
Mark Cooper, MBBS, PhD, FRACP Head, Diabetes & Metabolism Division, Baker Heart Research Institute,
Professor of Medicine, Monash University
Disclosure: Nothing to disclose.
Chief Editor
George T Griffing, MD Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement
of Science, American College of Medical Practice Executives, American College of Physician Executives,
American College of Physicians, American Diabetes Association, American Federation for Medical Research,
American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for
Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
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