Triglycerides

Serum (preferred) or plasma

1 mL

0.7 mL (Note: This volume does not allow for repeat testing.)

Red-top tube, gel-barrier tube, or green-top (lithium heparin) tube. Do not use oxalate, EDTA, or citrate plasma.

Patient should fast overnight (12 hours preferred; eight hours acceptable) preceding collection of specimen.

Evaluate turbid samples of blood, plasma, and serum; work up of chylomicronemia; evaluate hyperlipidemia; occasional cases of diabetes mellitus and/or pancreatitis are detected by hypertriglyceridemia. High levels may occur with hypothyroidism, nephrotic syndromes, carbohydrate-sensitive hypertriglyceridemia, glycogen storage disease, and in hyperlipoproteinemias type I, IIb, III, IV, and V. Some alcoholics have hypertriglyceridemia which disappears with abstinence. Extremely high triglyceride levels may occur with alcohol abuse. Triglyceride is needed for calculation of LDL-C (low-density lipoprotein cholesterol) concentration. Disturbances in triglyceride metabolism relate to diabetes and are a risk factor for atherosclerotic disease, but not an independent one.¹

Although the role of hypertriglyceridemia as a risk factor for coronary arterial disease has been controversial, a more consistent association for women exists and analysis of preliminary data supports triglyceride levels as a predictor in men with lower LDL cholesterol levels² and with cholesterol values <220 mg/dL.³

In familial combined hyperlipidemia, hypertriglyceridemia may be found before hypercholesterolemia. Nevertheless, a strong case is not available for primary triglyceride evaluation of healthy persons without positive family history of coronary disease or other risk factors. Some knowledgeable authorities favor testing with lipid panels, including triglycerides, for reasons discussed elsewhere in this listing.

In exogenous hypertriglyceridemia, chylomicrons float as a layer in the tube of refrigerated, stored serum.

If triglyceride is >800 mg/dL, LDL cannot be calculated accurately by the NIH formula. Some women on estrogens and high estrogen oral contraceptives have an increase of triglyceride. Increases occur with pregnancy, similar to those with oral contraceptives. The most common cause of triglyceride increase is inadequate patient fasting. Hypertriglyceridemia is associated with use of thiazide diuretics and β-adrenergic blocking agents.

Enzymatic

• Normal: <150 mg/dL

• Borderline-high: 150−199 mg/dL

• High: 200−499 mg/dL

• Very high: >500 mg/dL

Triglycerides commonly increase with obesity and may increase with chronic renal or liver disease. A positive association exists between diabetes mellitus and hypertriglyceridemia. Extremely high triglyceride levels suggest the possibility of pancreatitis. Chylomicronemia, although associated with pancreatitis, is not accompanied by increased atherogenesis. Chylomicrons are not seen in normal fasting serum, but are found in the sera of normal subjects following a fatty meal as exogenous triglycerides. Left refrigerated, chylomicrons float to the surface of a sample overnight; VLDL remain in suspension. Triglyceride physiologically is carried mostly as very low-density lipoproteins (VLDL). The triglyceride in VLDL is endogenous from hepatic synthesis.

When turbidity of blood, serum, or plasma is seen, triglyceride is often >350 mg/dL. Fasting chylomicronemia occurs with but is not limited to deficiency of apo-CII (apolipoprotein work-up). It occurs also with deficiency of lipoprotein lipase, an enzyme.

A positive association exists between gout and hypertriglyceridemia.

Drug effects have been summarized.⁴