Triglyceride: Test Overview, Indication, Normal and Abnormal Value, Nursing Considerations


To evaluate triglyceride (TG) levels to assess cardiovascular disease risk and evaluate the effectiveness of therapeutic interventions.

There are no activity or medication restrictions unless by medical direction. Instruct the patient to fast for 12 hr before specimen collection; fasting is required prior to measurement of TG levels. Ideally, the patient should be on a stable diet for 3 wk and avoid alcohol consumption for 3 days before specimen collection; alcohol increases TG levels. Protocols may vary among facilities.


ClassificationConventional UnitsSI Units (Conventional Units × 0.0113)
NormalLess than 150 mg/dL Less than 1.7 mmol/L
Borderline high 150–199 mg/dL 1.7–2.2 mmol/L
High 200–499 mg/dL 2.2–5.6 mmol/L
Very high Greater than 500 mg/dL Greater than 5.6 mmol/L


(Study type: Blood collected in a gold-, red-, red/gray-, or green-top [heparin] tube; related body system: Circulatory system.) Fat or adipose is an important source of energy. TGs are a combination of three fatty acids and one glycerol molecule. 

Much of the fatty acids used in various metabolic processes come from dietary sources. However, the body also generates fatty acids, from available glucose and amino acids, that are converted into glycogen or stored energy by the liver. Beyond TG, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol values, other important risk factors must be considered. For additional information regarding screening guidelines for atherosclerotic cardiovascular disease (ASCVD), refer to the study titled “Cholesterol, Total and Fractions.” Evidence-based risk factors include age, sex, ethnicity, total cholesterol, HDLC, LDLC, blood pressure, blood pressure treatment status, diabetes, and current use of tobacco products. TG levels vary by age, sex, weight, and ethnicity:

  • Levels increase with age.
  • Levels are higher in men than in women (among women, those who take oral contraceptives have levels that are 20 to 40 mg/dL higher than those who do not).
  • Levels are higher in overweight and obese people than in those with normal weight.
  • Levels in African Americans are approximately 10 to 20 mg/dL lower than in people of European descent.


• Evaluate known or suspected disorders associated with altered TG levels.

• Identify hyperlipoproteinemia (hyperlipidemia) in patients with a family history of the disorder.

• Monitor the response to drugs known to alter TG levels.

• Screen adults who are either over 40 yr or obese to estimate the risk for atherosclerotic cardiovascular disease.


Factors that may alter the results of the study

• Drugs and other substances that may increase TG levels include acetylsalicylic acid, atenolol, bisoprolol, beta-blockers, bendroflumethiazide, cholestyramine, conjugated estrogens, cyclosporine, estrogen/progestin therapy, estropipate, ethynodiol, etretinate, furosemide, glucocorticoids, hydrochlorothiazide, isotretinoin, labetalol, levonorgestrel, medroxyprogesterone, mepindolol, methyclothiazide, metoprolol, miconazole, mirtazapine, nadolol, nafarelin, oral contraceptives, oxprenolol, pindolol, prazosin, propranolol, tamoxifen, thiazides, ticlopidine, timolol, and tretinoin. 

• Drugs and other substances that may decrease TG levels include anabolic steroids, ascorbic acid, beclobrate, bezafibrate, captopril, carvedilol, celiprolol, chenodiol, cholestyramine, cilazapril, ciprofibrate, clofibrate, colestipol, danazol, doxazosin, enalapril, eptastatin (type IIb only), fenofibrate, flaxseed oil, fluvastatin, gemfibrozil, halofenate, insulin, levonorgestrel, levothyroxine, lifibrol, lovastatin, medroxyprogesterone, metformin, niacin, niceritrol, Norplant, pentoxifylline, pindolol, pravastatin, prazosin, probucol, simvastatin, and verapamil.


Increased in

• Acute myocardial infarction (AMI) (elevated TG is identified as an independent risk factor in the development of coronary artery disease [CAD])

• Alcohol misuse (related to decreased breakdown of fats in the liver and increased blood levels)

• Anorexia nervosa (compensatory increase secondary to starvation)

• Chronic ischemic heart disease (elevated TG is identified as an independent risk factor in the development of CAD)

• Cirrhosis (increased TG blood levels related to decreased breakdown of fats in the liver)

• Glycogen storage disease (G6PD deficiency, e.g., von Gierke disease, results in hepatic overproduction of very-low-density lipoprotein [VLDL] cholesterol, the TG-rich lipoprotein)

• Gout (TG is frequently elevated in patients with gout, possibly related to alterations in apolipoprotein E genotypes)

• Hyperlipoproteinemia (related to increase in transport proteins)

• Hypertension (associated with elevated TG, which is identified as an independent risk factor in the development of CAD)

• Hypothyroidism (significant relationship between elevated TG and decreased metabolism)

• Impaired glucose tolerance (increase in insulin stimulates production of TG by liver)

• Metabolic syndrome (syndrome consisting of obesity, high blood pressure, and insulin resistance)

• Nephrotic syndrome (related to absence or insufficient levels of lipoprotein lipase to remove circulating TG and to decreased catabolism of TG-rich VLDL lipoproteins)

• Obesity (significant and complex relationship between obesity and elevated TG)

• Pancreatitis (acute and chronic; related to effects on insulin production)

• Pregnancy (increased demand for production of hormones related to pregnancy)

• Chronic kidney disease (related to diabetes; elevated insulin levels stimulate production of TG by liver)

• Respiratory distress syndrome (related to artificial lung surfactant used for therapy)

• Stress (related to poor diet; effect of hormones secreted under stressful situations that affect glucose levels)

• Werner’s syndrome (clinical features resemble metabolic syndrome)

Decreased in

• End-stage liver disease (related to cessation of liver function that results in decreased production of TG and TG transport proteins)

• Hyperthyroidism (related to increased catabolism of VLDL transport proteins and general increase in metabolism)

• Hypolipoproteinemia and abetalipoproteinemia (related to decrease in transport proteins)

• Intestinal lymphangiectasia

• Malabsorption disorders (inadequate supply from dietary sources)

• Malnutrition (inadequate supply from dietary sources)


Nutrition (related to excess caloric intake with large amounts of dietary sodium and fat; cultural lifestyle; overeating associated with anxiety, depression, compulsive disorder; genetics; inadequate or unhealthy food resources)

Observable obesity, high fat or sodium food selections, high BMI, high consumption of ethnic foods, sedentary lifestyle, dietary religious beliefs and food selections, binge eating, diet high in refined sugar, repetitive dieting and failure

Tissue perfusion (related to hypovolemia, decreased haemoglobin, interrupted arterial flow, interrupted venous flow)

Hypotension, dizziness, cool extremities, pallor, capillary refill greater than 3 sec in fingers and toes, weak pedal pulses, altered level of consciousness, altered sensation


Teaching the Patient What to Expect

➧ Inform the patient this test can assist in monitoring and evaluating lipid levels.

➧ Explain that a blood sample is needed for the test.

Potential Nursing Actions

➧ Evaluate for the presence of other risk factors, such as family history of heart disease, smoking, obesity, diet, lack of physical activity, hypertension, diabetes, previous myocardial infarction, and previous 


Treatment Considerations

➧ Tissue Perfusion: Monitor blood pressure; assess for dizziness, capillary refill, pedal pulses, numbness, tingling, hyperesthesia, hypoesthesia, and extremities for deep venous thrombosis. Monitor skin temperature, color, and warmth. Instruct in careful use of heat and cold on affected areas and the use of a foot cradle to keep pressure off of affected body parts.

Nutritional Considerations

➧ Discuss ideal body weight and the purpose of and relationship between ideal weight and caloric intake to support cardiac health. Review ways to decrease intake of saturated fats and increase intake of polyunsaturated fats. Discuss limiting intake of refined processed sugar and sodium; discuss limiting cholesterol intake to less than 300 mg per day. Encourage the intake of fresh fruits and vegetables, unprocessed carbohydrates, poultry, and grains.

➧ Sensitivity to Social and Cultural Issues: Numerous studies point to the prevalence of excess body weight in American children and adolescents. Findings from the 2015-2016 National Health and Nutrition Examination Survey (NHANES), regarding the prevalence of obesity in younger members of the population, estimate that obesity is present in 13.9% of the population ages 2-5 yr, 18.4% ages 6 to 11 yr, and 20.6% ages 12-19 yr. The medical, social, and emotional consequences of excess body weight are significant. Special attention should be given to instructing the pediatric patient and caregiver regarding health risks and weight management education. 

➧ Nutritional therapy is recommended for those with identified CAD risk, especially for those with elevated LDL cholesterol levels, other lipid disorders, diabetes, insulin resistance, or metabolic syndrome. Always consider cultural influences with dietary choices to ensure better adherence to a change in lifestyle. A variety of dietary patterns are beneficial for people with ASCVD. For additional information regarding nutritional guidelines, refer to the study titled “Cholesterol, Total and Fractions.”

➧ Other changeable risk factors warranting education include strategies to encourage regular participation in moderate aerobic physical activity three to four times per week, eliminating tobacco use, and adhering to a heart healthy diet.

➧ Those with elevated triglycerides should be advised to eliminate or reduce alcohol.


Please enter your comment!
Please enter your name here