Hypertriglyceridemia in adults: Approach to evaluation

Authors:: Robert S Rosenson, MD; Robert H Eckel, MD
Section Editor:: Mason W Freeman, MD
Deputy Editors:: Susan B Yeon, MD, JD; Sara Swenson, MD

Literature review current through: Jan 2024.

This topic last updated: Nov 29, 2021.

INTRODUCTION — Hypertriglyceridemia is a common clinical condition most commonly identified in individuals who have had a lipid profile obtained as part of cardiovascular risk assessment. (See "Screening for lipid disorders in adults", section on 'Choice of tests' and "Atherosclerotic cardiovascular disease risk assessment for primary prevention in adults: Our approach" and "Overview of established risk factors for cardiovascular disease", section on 'Lipids and lipoproteins'.)

This topic reviews the relationship between hypertriglyceridemia and adverse cardiovascular events, the mechanisms by which this might occur, the disorders of triglyceride (TG) metabolism that have been identified, and our approach to the management of hypertriglyceridemia. Other relevant topics include:

●(See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Endogenous pathway of lipid metabolism'.)

●(See "Hypertriglyceridemia-induced acute pancreatitis".)

CLASSIFICATION — We classify fasting serum (or plasma) TG levels according to the following criteria (to convert from mg/dL to mmol/L, divide by 88.5):

●Normal – <150 mg/dL (<1.7 mmol/L)

●Moderate hypertriglyceridemia – 150 to 499 mg/dL (1.7 to 5.6 mmol/L)

●Moderate to severe hypertriglyceridemia – 500 to 999 mg/dL (5.65 to 11.3 mmol/L)

●Severe hypertriglyceridemia – >1000 mg/dL (>11.3 mmol/L)

Guidelines and expert committees have used a variety of classification systems for hypertriglyceridemia. While the consensus of these committees is that a normal level is <150 mg/dL (1.7 mmol/L), committees have used differing terminology and criteria to classify severity of hypertriglyceridemia [1-4]. While hypertriglyceridemia classification systems provide a structure for diagnosis and management (see "Hypertriglyceridemia in adults: Management", section on 'Treatment goals'), these cut-points do not fully capture differences in lipoprotein profiles among individuals, as reflected by the following observations. In moderate hypertriglyceridemia, there are increases in very low-density lipoprotein (VLDL). When fasting serum or plasma TG levels are >500 mg/dL (5.6 mmol/L) but <1000 mg/dL (11.3 mmol/L), some, but not all, patients have chylomicrons present. When fasting TG levels are >1000 mg/dL (11.3 mmol/L), almost all patients have chylomicrons present, in addition to increases in VLDL. (See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Classification'.)

As discussed separately, the major types of dyslipidemia have been classified according to the Fredrickson phenotype (table 1). (See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Clinical classification of dyslipidemias'.)

PREVALENCE — Hypertriglyceridemia is common among adults, with prevalence varying among different populations. The US National Health and Nutrition Examination Surveys (NHANES) from 2007 to 2014 found that the percentages of non-statin-treated adults with TG levels >150 mg/dL (1.7 mmol/L), >200 mg/dL (2.3 mmol/L), >500 mg/dL (5.7 mmol/L), and >1000 mg/dL (11.3 mmol/L) were 24.7, 10.9, 1, and <1 percent, respectively [5]. Serum TG values >1000 mg/dL (11.3 mmol/L) occur in fewer than 1 in 5000 individuals [5]. Racial and ethnic differences have been observed, with non-Hispanic African Americans having lower fasting TG levels than non-Hispanic White and Mexican Americans [6]. The prevalence is higher among individuals with established cardiovascular disease [7].

ETIOLOGY — In most patients with elevated TG levels, genetic (primary) (table 2) and acquired (secondary) disorders coexist [8]. Hypertriglyceridemia results from imbalance in production of TG-rich lipoproteins from liver (VLDL) and intestine (chylomicrons) and lipolytic removal of TG from both these lipoproteins and their remnants. VLDL overproduction frequently contributes. Chylomicron production reflects dietary fat intake. Most lipolysis of circulating TG-rich lipoproteins is mediated by lipoprotein lipase (LPL). Nearly all patients with severe hypertriglyceridemia have a genetic predisposition plus an additional condition or factor known to raise serum TGs (eg, diabetes mellitus, alcohol abuse, or oral estrogen therapy) that lead to saturation kinetics of lipoprotein lipase (LPL) [9-11]. LPL mediates lipolysis of TG in TG-rich lipoproteins, chylomicrons, and VLDL. (See 'Potential mechanisms' below and 'Lipid profile' below and "Lipoprotein classification, metabolism, and role in atherosclerosis".)

Acquired factors — The following acquired conditions and factors increase the risk of hypertriglyceridemia (in individuals with or without genetic risk factors) [12,13]:

●Insulin resistance is a common phenotype and includes obesity [14], metabolic syndrome [15], type 2 diabetes [16], pregnancy [17], chronic renal failure [18], HIV [19], hepatocellular disease [20], and chronic inflammatory diseases [21,22]. Insulin-resistant conditions lead to an increase in free fatty acid delivery from adipose tissue to the liver and overproduction of VLDL-TG [23] with variable defects in clearance secondary to reductions in LPL [23]. (See "Insulin resistance: Definition and clinical spectrum" and "Metabolic syndrome (insulin resistance syndrome or syndrome X)" and "Pathogenesis of type 2 diabetes mellitus".)

●Renal disease (proteinuria, uremia, or glomerulonephritis). With nephrotic syndrome, hypertriglyceridemia is often associated with hypercholesterolemia [24]. (See "Lipid abnormalities in nephrotic syndrome", section on 'Triglyceride metabolism'.)

●Hypothyroidism is most often associated with hypercholesterolemia [25], but association with hypertriglyceridemia has also been described [26]. (See "Clinical manifestations of hypothyroidism", section on 'Metabolic abnormalities' and "Lipid abnormalities in thyroid disease".)

●Diet with excess calories, high glycemic load, and/or sucrose- or fructose-containing beverages. Total fat intake may also contribute in patients with TG ≥500 mg/dL. (See "Lipid management with diet or dietary supplements".)

●Alcohol consumption above two drinks per day for males and one drink per day for females. (See "Overview of the risks and benefits of alcohol consumption" and "Cardiovascular benefits and risks of moderate alcohol consumption".)

●Pregnancy (particularly in the third trimester). (See "Maternal adaptations to pregnancy: Gastrointestinal tract", section on 'Liver'.)

●Multiple myeloma [27,28]. (See "Multiple myeloma: Clinical features, laboratory manifestations, and diagnosis".)

●Systemic lupus erythematosus [29]. (See "Clinical manifestations and diagnosis of systemic lupus erythematosus in adults".)

●Medications:

•Thiazide diuretics [30]. (See "Antihypertensive drugs and lipids", section on 'Thiazide diuretics'.)

•Glucocorticoids [31]. (See "Major adverse effects of systemic glucocorticoids", section on 'Metabolic and endocrine effects'.)

•Bile-acid sequestrants [32]. (See "Low-density lipoprotein cholesterol lowering with drugs other than statins and PCSK9 inhibitors", section on 'Bile acid sequestrants'.)

•Antiretroviral regimens, especially for HIV [33]. (See "Management of cardiovascular risk (including dyslipidemia) in patients with HIV", section on 'Management of hypertriglyceridemia'.)

•Second-generation antipsychotic medications such as clozapine and olanzapine [34]. (See "Schizophrenia in adults: Guidelines for prescribing clozapine", section on 'Metabolic' and "Bipolar major depression in adults: Efficacy and adverse effects of second-generation antipsychotics", section on 'Metabolic effects'.)

•Most beta blockers [35]. (See "Antihypertensive drugs and lipids".)

•Certain antineoplastic agents (cyclophosphamide and L-asparaginase).

•Certain immunosuppressants (eg, cyclosporine and mechanistic target of rapamycin (mTOR) kinase inhibitors such as everolimus and sirolimus) [36]. (See "Lipid abnormalities after kidney transplantation", section on 'Immunosuppressive agents' and "Heart transplantation: Hyperlipidemia after transplantation", section on 'Causes of hyperlipidemia after transplantation'.)

•Oral estrogens [37]. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Lipid changes and metabolic effects'.)

•Tamoxifen [38], raloxifene [39], clomiphene [40].

•Retinoic acid derivatives: isotretinoin [41], acitretin [42], and bexarotene [43]. (See "Oral isotretinoin therapy for acne vulgaris", section on 'Hyperlipidemia'.)

Genetic factors — Among patients with hypertriglyceridemia, polygenic determinants (causing complex genetic susceptibility) are much more common than monogenic disorders; some clinical syndromes are caused by the combined effects of complex genetic susceptibility and monogenic mutations (table 2). Clinical syndromes of primary causes (polygenic and/or monogenic) of hyperlipidemia are discussed below. (See 'Clinical syndromes of primary causes' below.)

CLINICAL MANIFESTATIONS

Symptoms and signs — Patients with hypertriglyceridemia generally have no symptoms or signs with the following exceptions:

●Xanthomas – Some patients with moderate or severe hypertriglyceridemia have xanthomas (picture 1). The type of xanthoma varies among different types of lipoprotein disorder (table 3). (See "Cutaneous xanthomas".)

●Chylomicronemia syndrome – Patients with severe hypertriglyceridemia (polygenic or monogenic) may develop chylomicronemia syndrome. Manifestations of this disorder include short-term memory loss, hepatosplenomegaly, abdominal pain and/or pancreatitis, dyspnea, flushing with alcohol, lipemia retinalis, and xanthomas [44,45].

Blood lipids

Appearance of blood specimen — The appearance of an overnight refrigerated plasma sample may suggest the presence of very high levels of VLDL and/or chylomicrons (table 1). The plasma in patients with severe hypertriglyceridemia may appear opalescent due to an increase in VLDL; at higher levels, it may be milky due to hyperchylomicronemia (picture 2).

●With monogenic chylomicronemia syndrome (formerly known as type 1 hyperlipoproteinemia phenotype) the supernatant appears creamy due to chylomicrons and the infranatant is clear. (See 'Severe hypertriglyceridemia' below.)

●With type 5 hyperlipoproteinemia (chylomicrons and VLDL), the supernatant appears milky due to chylomicrons and the infranatant is cloudy due to VLDL particles. (See 'Severe hypertriglyceridemia' below.)

Lipid profile — Hypertriglyceridemia is commonly accompanied by other abnormalities in serum lipid levels (table 1):

●LDL-C – Most patients with hypertriglyceridemia have elevated serum low-density lipoprotein (LDL) particle concentrations (and correspondingly high apolipoprotein B levels). High TG levels are associated with small, dense cholesterol-depleted LDL particles that may not be captured by the LDL-cholesterol (LDL-C) measurement [46-49]. LDL-C levels thus may underrepresent cardiovascular risk in this population. (See "Inherited disorders of LDL-cholesterol metabolism other than familial hypercholesterolemia", section on 'Small dense LDL (LDL phenotype B)' and "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Triglyceride-rich lipoprotein remnants and cardiovascular disease'.)

Therapies that lower TGs also lower LDL-C. (See "Hypertriglyceridemia in adults: Management", section on 'Treatment goals'.)

●Non-HDL-C and apolipoprotein B – In patients with hypertriglyceridemia, non-high-density lipoprotein-cholesterol (non-HDL-C) and apoprotein B levels are elevated. These are better measures of excess concentrations of atherogenic lipoproteins than LDL-C in patients with hypertriglyceridemia [13]. (See "Measurement of blood lipids and lipoproteins", section on 'Non-HDL cholesterol'.)

●HDL-C – Most patients with hypertriglyceridemia have low levels of HDL-C [50-58]. Lipoprotein lipase (LPL) is important in the generation of more buoyant cholesterol-enriched HDL particles, and when LPL activity is reduced, plasma TGs increase, and the production of these HDL particles is reduced [59]. In addition, when hypertriglyceridemia is present, HDL particles are more TG-enriched, replacing cholesteryl ester with TG in the lipoprotein core [60], and TG-enriched HDLs are more rapidly catabolized by lipid-processing enzymes and cleared [61].

While changes in plasma TG and HDL-C levels are generally inversely related, the following conditions are exceptions: moderate alcohol consumption (increases both), sex steroid hormones (eg, oral estrogen raises both), active weight loss (both may decrease), and thyroid disease (eg, hypothyroidism may increase both). (See "Menopausal hormone therapy and cardiovascular risk" and "Clinical manifestations of hypothyroidism" and "Measurement of blood lipids and lipoproteins" and "Hematologic complications of alcohol use" and "Cardiovascular benefits and risks of moderate alcohol consumption".)

Clinical syndromes of primary causes — The following clinical syndromes are associated with primary causes (polygenic and/or monogenic) of hypertriglyceridemia (table 2). Nomenclature for these syndromes has varied, as noted.

Moderate or moderate to severe hypertriglyceridemia — Most patients with moderate (150 to 499 mg/dL; 1.7 to 5.6 mmol/L) or moderate to severe (500 to 999 mg/dL; 5.65 to 11.3 mmol/L) hypertriglyceridemia have polygenic determinants (table 2) along with environmental influences [12,13] (see 'Acquired factors' above). Complex genetic susceptibility in moderate hypertriglyceridemia results from the cumulative effects of common and rare variants in multiple of the 30 or more genes related to TG metabolism that have modest but additive effects on plasma TG levels [62,63].

●Multifactorial or polygenic hypertriglyceridemia (also known as primary hypertriglyceridemia, hyperlipoproteinemia type 4, or familial hypertriglyceridemia) has an estimated prevalence of 5 to 10 percent. It is caused by complex genetic susceptibility and is associated with increased production of TG-rich VLDL particles. Serum TG levels can range from 200 to 1000 mg/dL (although generally ≤885 mg/dL), and total cholesterol and apolipoprotein B concentrations are normal.

●Combined hyperlipoproteinemia (also known as hyperlipoproteinemia type 2B or familial combined hyperlipidemia) has an estimated prevalence of 1 to 2 percent. It is caused by complex genetic susceptibility plus accumulation of common small effect LDL-C-raising polymorphisms and is associated with increased production of apolipoprotein B and associated lipoproteins. A variety of criteria have been used to define this disorder, which is associated with elevated apolipoprotein B level (eg, >90^th percentile) accompanied by elevated triglyceride level (eg, >150 or 200 mg/dL) and/or elevated total cholesterol levels (eg, >200 or 240 mg/dL) [64]. This disorder is frequently associated with type 2 diabetes mellitus and is associated with high risk of ASCVD.

●Dysbetalipoproteinemia (also known as hyperlipoproteinemia type 3) is a rare cause of moderate hypertriglyceridemia. This disorder occurs in the setting of complex genetic susceptibility plus a monogenic disorder (generally homozygosity for autosomal recessive apoE2, with only 10 percent of cases caused by autosomal dominant apoE mutations) along with an acquired cause of overproduction of VLDL, most frequently insulin-resistant disorders such as type 2 diabetes [65,66]. The apoE2 protein causes impaired clearance of chylomicron and VLDL remnants due to low binding affinity to the LDL receptor [67]. This condition is associated with similar TG and total cholesterol levels (both usually 300 to 500 mg/dL). Premature coronary heart disease and peripheral vascular disease are common. Physical findings include tuberoeruptive xanthomas (picture 3) and xanthomas of the palmar creases (ie, xanthomata palmare striatum) (picture 4 and table 3).

Severe hypertriglyceridemia — Most patients with severe hypertriglyceridemia (>1000 mg/dL; 11.3 mmol/L) have polygenic determinants (table 2) [62,63] along with environmental influences [12,13]; rare cases are caused by a monogenic condition.

●Multifactorial chylomicronemia (also known as hyperlipoproteinemia type 5) is caused by complex genetic susceptibility including heterozygous rare large-effect gene variants for monogenic chylomicronemia and/or accumulated common small-effect TG-raising polymorphisms, often along with acquired factors. In this condition there is elevation in VLDL and chylomicrons levels but no deficiency in LPL or its activator, apo C-II [68,69]. The underlying defect in this disorder is uncertain, but apoE4, which is a ligand for the hepatic chylomicron and VLDL remnant receptor, may play a role [69]. Some patients with this condition have clinical characteristics of monogenic chylomicronemia.

These primary forms of type 5 hyperlipoproteinemia differ from partial LPL deficiency, in which the type 5 phenotype is brought out by one of the exacerbating acquired factors discussed above.

●Monogenic chylomicronemia (also known as type 1 hyperlipoproteinemia (table 1) or familial chylomicronemia) is characterized by TG levels above the 99^th percentile (885 mg/dL or 10 mmol/L) [12,68-70]. This extremely rare autosomal recessive condition (estimated prevalence of one in one million) is most frequently due to LPL deficiency [71]. LPL activity is reduced due to either mutations in both alleles of the LPL gene or in both alleles of other genes encoding proteins supporting its activity (apo C-II, lipoprotein maturation factor 1, apolipoprotein 5, or glycosylphosphatidylinositol-anchored HDL-binding protein 1) [44,72-74].

●Lipodystrophic syndromes – Severe hypertriglyceridemia also occurs in individuals with lipodystrophic syndromes (generalized or partial). Lipodystrophic syndromes can occur as congenital monogenic disorders or as acquired conditions. These syndromes are discussed separately. (See "Lipodystrophic syndromes" and "Epidemiology, clinical manifestations, and diagnosis of HIV-associated lipodystrophy".)

Associated conditions — Hypertriglyceridemia is a cause of pancreatitis and is associated with increased risk of ASCVD, although hypertriglyceridemia has not been established as a cause of ASCVD.

Pancreatitis — The risk of acute pancreatitis increases progressively with serum TG levels over 500 mg/dL (5.6 mmol/L) and markedly with recent history of acute pancreatitis [75]. In a United States ambulatory database study of 7,119,195 patients with TG levels, the annualized incidence rate of acute pancreatitis for TG levels of >500 to 880 mg/dL (>5.65 to 9.94 mmol/L) was 0.23 percent and for TGs >11.29 mmol/L (>1000 mg/dL) was 1.21 percent [76]. The overall annualized incidence rate of acute pancreatitis among individuals with no acute pancreatitis in the past year was low (0.7 percent) and much higher among those with one acute pancreatitis event in the past year (10.16 percent) and two or more acute pancreatitis events in the past year (29.98 percent). The diagnosis and management of hypertriglyceridemia-induced acute pancreatitis is discussed separately. (See "Hypertriglyceridemia-induced acute pancreatitis".)

Atherosclerotic cardiovascular disease

Observed associations — Hypertriglyceridemia is associated with risk of ASCVD, but a causal relationship has not been established [55,77-87]. Elevated fasting plasma TG levels are associated with ASCVD burden and events such as myocardial infarction and stroke [77,88-97]. The risk of ASCVD events rises with TG levels above 150 mg/dL (1.7 mmol/L) [98-100]. However, when levels of TG are adjusted for other related variables (eg, components of the metabolic syndrome), the relationship is weakened if not absent. Thus, TG levels are not generally included in ASCVD risk prediction models.

Mendelian randomization studies suggest, but do not prove, a causal relationship between TG and ASCVD [77]. As described above, some primary (genetic) causes of hypertriglyceridemia are associated with ASCVD, but some are not. (See 'Clinical syndromes of primary causes' above.)

Hypertriglyceridemia is associated with a number of conditions that predispose to atherosclerosis or are associated with increased cardiovascular disease risk. These include:

●Lipid abnormalities (high LDL-C and low HDL-C levels) associated with ASCVD risk.

●Insulin resistance [101,102].

●Prothrombotic states, including enhanced platelet aggregation, increases in fibrinogen, plasminogen activator inhibitor-1, and viscosity [103-105]. TG-mediated hyperviscosity may contribute to endothelial dysfunction, tissue ischemia, and the chylomicronemia syndrome (See 'Symptoms and signs' above.) [105].

●Inflammation [106,107], an important contributor to the atherosclerotic state [108,109].

The effects of specific triglyceride lowering agents on ASCVD risk are discussed separately. (See "Hypertriglyceridemia in adults: Management", section on 'Specific agents'.)

Potential mechanisms — The development of ASCVD in individuals with hypertriglyceridemia is likely more closely related to the cholesterol content of TG-rich lipoproteins and their remnants (eg, intermediate-density lipoproteins, chylomicron remnants, and VLDL remnants) than to their TG content [110,111]. Not all TG-containing lipoproteins are atherogenic, as large TG-rich particles such as chylomicrons secreted by the intestine are unable to penetrate the vessel wall [13]. Nascent VLDL and chylomicrons are categorized as TG-rich lipoproteins because most of their core is TG, not cholesterol. The TG cores of these large particles are hydrolyzed by LPL to produce remnants [112]. The action of LPL markedly reduces the TG content of VLDL and chylomicrons, so their remnants are cholesterol-enriched. Lipoproteins that access the subintimal space (VLDL, chylomicron remnants, and LDL) are retained after entry and serve as the source of cholesterol for esterification in atherosclerotic plaque [113,114]. The lipid-rich atherosclerotic plaque in the arterial wall is mostly cholesteryl ester, not TG [115]. This provides an explanation for why some patients with severe hypertriglyceridemia (eg, patients with familial chylomicronemia syndrome) have no ASCVD [116].

This hypothesis is supported by the pathophysiology and clinical course of dysbetalipoproteinemia (formerly hyperlipoproteinemia type 3), in which there is impaired remnant clearance and premature ASCVD. (See 'Moderate or moderate to severe hypertriglyceridemia' above.)

DIAGNOSIS AND EVALUATION

Indications for measurement — The most common indications for measuring fasting TG levels include:

●As a component of screening for lipid disorders. An initial lipid panel may be obtained in a fasting or nonfasting state. If a nonfasting lipid profile reveals a serum (or plasma) TG level ≥400 mg/dL (4.5 mmol/L), a repeat profile should be performed to assessing fasting TG level and LDL-C [1]. (See "Measurement of blood lipids and lipoproteins".)

●A fasting lipid panel including TG level is a component of the evaluation of patients with cutaneous xanthomas (other than verruciform xanthomas) (table 3), as discussed separately. (See "Cutaneous xanthomas", section on 'Laboratory evaluation'.)

●Screening family members for familial forms of hypertriglyceridemia. A fasting TG level is suggested in first-degree relatives of patients with TG levels >500 mg/dL (5.7 mmol/L) without a disorder known to raise serum TG levels (such as obesity, diabetes, or hypothyroidism). (See 'Clinical syndromes of primary causes' above.)

●Establishing the etiology of acute pancreatitis. (See "Hypertriglyceridemia-induced acute pancreatitis", section on 'Diagnosis'.)

●Monitoring treatment of hypertriglyceridemia. (See "Hypertriglyceridemia in adults: Management", section on 'Monitoring therapy'.)

The laboratory measurement of TG is discussed elsewhere. (See "Measurement of blood lipids and lipoproteins", section on 'Triglycerides'.)

Diagnostic evaluation

●Diagnostic criteria – Hypertriglyceridemia is generally diagnosed at a fasting serum (or plasma) TG level of ≥150 mg/dL (1.7 mmol/L) as cardiovascular risk begins to increase significantly above a TG level of 150 mg/dL (1.7 mmol/L). For patients with a fasting TG level of ≥150 mg/dL (1.7 mmol/L) we suggest repeating the level since fasting TG levels fluctuate in response to a variety of conditions (including alcohol consumption, evening meal before the fast, and exercise). If TG elevation is detected in the setting of a temporary condition that causes hypertriglyceridemia (eg, sepsis or with total parenteral nutrition with lipid emulsions), the measurement should be repeated after condition has resolved [1].

●Identify cause – For all patients who are found to have an elevated TG level, an attempt should be made to identify contributing factors. (See 'Acquired factors' above.)

In patients with hypertriglyceridemia, secondary causes (including diabetes mellitus, nephrotic syndrome, and hypothyroidism) should be excluded. Following history and physical examination, the following tests are performed as warranted by clinical judgment: serum blood glucose or hemoglobin A1c, creatinine and thyroid-stimulating hormone (TSH), and a urinalysis (ie, albumin/protein). Although a TSH is an important screening test for acquired causes of hypercholesterolemia, hypothyroidism has a much more limited impact on plasma TG [26]. If no secondary cause is evident, the patient likely has a hereditary cause.

●Assess complications – In patients with hypertriglyceridemia, a history of prior pancreatitis or risk factors for ASCVD impacts management.

●Genetic testing – We reserve genetic testing for patients with suspected monogenic chylomicronemia and patients with hypertriglyceridemia with first-degree relatives with hypertriglyceridemia-induced acute pancreatitis. (See 'Severe hypertriglyceridemia' above and "Hypertriglyceridemia-induced acute pancreatitis".)

We generally do not perform genetic testing in other patients, as results do not influence management.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Lipid disorders in adults".)

SUMMARY AND RECOMMENDATIONS

●Classification – A normal fasting triglyceride (TG) level is defined as <150 mg/dL (1.7 mmol/L). We classify fasting TG levels from 150 to 499 mg/dL (1.7 to 5.6 mmol/L) as moderate hypertriglyceridemia, 500 to 999 mg/dL (5.65 to 11.3 mmol/L) as moderate to severe hypertriglyceridemia, and >1000 mg/dL (>11.3 mmol/L) as severe. (See 'Classification' above.)

●Prevalence – Hypertriglyceridemia is common among adults (occurring in approximately one-quarter of adults in the United States), with prevalence varying among different populations. (See 'Prevalence' above.)

●Etiology – Among patients with moderate or severe hypertriglyceridemia, genetic (primary) (table 2) and acquired (secondary) disorders generally coexist. Polygenic determinants are much more common than monogenic disorders. Some clinical syndromes are caused by the combined effects of complex genetic susceptibility and monogenic mutations. (See 'Etiology' above and 'Clinical syndromes of primary causes' above.)

●Clinical presentation

•Symptoms and signs – Patients with hypertriglyceridemia generally have no symptoms or signs associated with the biochemical abnormality, except some patients have xanthomas (table 3 and picture 3 and picture 5 and picture 6 and picture 4 and picture 1) and some patients with severe hypertriglyceridemia have chylomicronemia syndrome, which is associated with short-term memory loss, hepatosplenomegaly, abdominal pain and/or pancreatitis, dyspnea, flushing with alcohol, lipemia retinalis, and xanthomas. (See 'Symptoms and signs' above and "Cutaneous xanthomas".)

•Lipid profile – Hypertriglyceridemia is generally associated with high levels of low-density lipoprotein-cholesterol (LDL-C) and low levels of high-density lipoprotein-cholesterol (HDL-C). (See 'Lipid profile' above.)

•Associated conditions – Hypertriglyceridemia is a cause of pancreatitis and is associated with increased risk of atherosclerotic cardiovascular disease (ASCVD), although hypertriglyceridemia has not been established as a cause of ASCVD. The risk of acute pancreatitis increases progressively with serum TG levels over 500 mg/dL (5.6 mmol/L) and markedly with recent history of acute pancreatitis. (See 'Associated conditions' above.)

●Indications for TG measurement – Fasting TG levels are most commonly measured as a component of routine lipid profile screening in adults. Other indications include screening first-degree relatives of patients with TG levels >500 mg/dL (5.7 mmol/L) without a disorder known to raise serum TG levels (such as obesity, diabetes, or hypothyroidism), evaluation of individuals with cutaneous xanthomas (other than verruciform xanthomas) (table 3), establishing the etiology of acute pancreatitis, and monitoring treatment of hypertriglyceridemia. (See 'Indications for measurement' above and "Cutaneous xanthomas", section on 'Laboratory evaluation' and "Hypertriglyceridemia-induced acute pancreatitis", section on 'Diagnosis' and "Hypertriglyceridemia in adults: Management".)

●Diagnosis – Hypertriglyceridemia is generally diagnosed at a fasting serum (or plasma) TG level of ≥150 mg/dL (1.7 mmol/L), as cardiovascular risk begins to increase significantly at this level. For patients with a fasting TG level of ≥150 mg/dL (1.7 mmol/L) we suggest repeating the level since fasting TG levels fluctuate in response to a variety of conditions (including alcohol consumption, evening meal before the fast, and exercise). (See 'Diagnostic evaluation' above.)

●Evaluation – Evaluation of hypertriglyceridemia includes identifying contributing factors, assessing complications, and selective genetic testing (for patients with suspected familial chylomicronemia and evaluation of individuals with hypertriglyceridemia with first-degree relatives with hypertriglyceridemia-induced pancreatitis). (See 'Diagnostic evaluation' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff would like to thank John J P Kastelein, MD, PhD, FESC, who contributed to earlier versions of this topic review.

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Topic 132419 Version 8.0

خرید پکیج

Hypertriglyceridemia in adults: Approach to evaluation

References