Triglycerides

Clinical utility

Triglycerides (TG) are measured mainly for two purposes: as a marker of triglyceride-rich lipoproteins (chylomicrons, VLDL, and their remnants) that are causally related to atherosclerotic cardiovascular disease, and to assess risk of acute pancreatitis, which rises sharply at very high concentrations (roughly above 500 mg/dL). TG is a core component of the minimal and standard lipid profile alongside total cholesterol, since measuring cholesterol or LDL-C alone can miss severe hypertriglyceridemia. Nonfasting TG is now considered acceptable, and in fact nonfasting samples better capture postprandial remnant lipoproteins linked to cardiovascular events.

Dyslipidemia

How it's measured

Reference methods

Original CDC chemical (chromotropic acid) reference method

The historical CDC reference method for TG is a manual chemical procedure based on extraction and alkaline hydrolysis of the sample to liberate glycerol, which is then oxidized with periodate and reacted with chromotropic acid to form a colored chromogen that is measured photometrically:

TG --KOH (alkaline hydrolysis)--> Fatty acids + Glycerol
Glycerol --Periodate--> Formaldehyde + Formic acid
Formaldehyde + Chromotropic acid --> Chromogen

A designated comparison method later refined this by following the same extraction/hydrolysis steps with more robust enzymatic quantitation of the released glycerol.

Isotope dilution mass spectrometry (GC-IDMS)

A newer reference method chemically reduces all glycerides (TG, diglycerides, monoglycerides) to glycerol, which is then measured by gas chromatography-isotope dilution mass spectrometry. The source does not describe this reaction in enough detail to write a balanced equation.

Routine enzymatic methods

Modern clinical laboratories measure TG enzymatically. All commercial enzymatic methods share the same first two steps, converting TG to glycerophosphate:

TG + 3 H2O --Lipase--> Glycerol + 3 Fatty acids
Glycerol + ATP --Glycerokinase--> Glycerophosphate + ADP

The glycerophosphate (or a downstream product) is then quantified by one of several coupled-enzyme detection schemes:

Glycerophosphate oxidase/peroxidase detection (most common)

Glycerophosphate + O2 --Glycerophosphate oxidase--> Dihydroxyacetone phosphate + H2O2
H2O2 + Phenol + 4-Aminoantipyrine --Peroxidase--> Quinoneimine dye + 2 H2O

Glycerophosphate dehydrogenase/diaphorase detection

Glycerophosphate + NAD+ --Glycerophosphate dehydrogenase--> Dihydroxyacetone phosphate + NADH + H+
NADH + Tetrazolium dye --Diaphorase--> NAD+ + Formazan (the NADH can alternatively be measured directly by absorbance at 340 nm)

Pyruvate kinase/lactate dehydrogenase (ADP-coupled) detection

ADP + Phosphoenolpyruvate --Pyruvate kinase--> ATP + Pyruvate
Pyruvate + NADH + H+ --Lactate dehydrogenase--> Lactate + NAD+

Enzymatic assays are typically linear to about 1000 mg/dL (11.3 mmol/L) and are calibrated with pure glycerol or serum-based secondary calibrators; because all of them measure the glycerol moiety, any free (non-TG-derived) glycerol in the sample is co-measured. This free glycerol is usually clinically insignificant and ignored, but can be markedly elevated in glycerol kinase deficiency, causing spurious "hypertriglyceridemia" (pseudohypertriglyceridemia) unless a glycerol blank is subtracted.

Typical reference interval

The source presents triglyceride values as clinical decision cut points (desirable/borderline/high/very high) rather than a single reference range, with different cut points for adults versus children/adolescents:

Group	Reference interval / decision limits
Adults	Desirable <150 mg/dL (<1.7 mmol/L); Borderline-high 150–199 mg/dL (1.7–2.3 mmol/L); High 200–499 mg/dL (2.3–5.7 mmol/L); Very high ≥500 mg/dL (≥5.7 mmol/L)
Children/adolescents, 0–9 y	Acceptable <75 mg/dL (<0.8 mmol/L); Borderline 75–99 mg/dL (0.8–1.1 mmol/L); Abnormal ≥100 mg/dL (≥1.1 mmol/L)
Children/adolescents, 10–19 y	Acceptable <90 mg/dL (<1.0 mmol/L); Borderline 90–129 mg/dL (1.0–1.5 mmol/L); Abnormal ≥130 mg/dL (≥1.4 mmol/L)

The source also reports NHANES 2015–2016 population percentile distributions of serum TG by age and sex (5th–95th percentile), which vary widely by age/sex group (e.g., 5th–95th percentile roughly 30–347 mg/dL in adults 18–29 years), but does not present these as a single "normal" cutoff.

Sources: Ch36 Lipids and lipoprotein.pdf · Extracted 2026-08-17 · Approved 2026-08-19

Method comparison

Beckman Coulter AU5800

kinetics endpoint λ 660 / 800 nm AMR 10-1,000 mg/dL LoD 0.81 mg/dL LoQ 5 mg/dL

Triglycerides + 3 H2O --lipase--> Glycerol + 3 Fatty acids
Glycerol + ATP --glycerol kinase,Mg2+--> Glycerol-3-phosphate + ADP
Glycerol-3-phosphate + O2 --glycerol phosphate oxidase--> Dihydroxyacetone phosphate + H2O2
2 H2O2 + 4-aminoantipyrine + MADB --peroxidase--> Blue dye + OH- + H2O

Coupled enzymatic endpoint assay (lipase/GK/GPO/POD, GPO-PAP/Trinder-type chromogenic indicator reaction), bichromatic read at 660/800 nm.

Reaction notes:
The signal actually monitored is the blue quinoneimine dye (proportional to H2O2 generated at the GPO step), not glycerol or triglyceride directly. Ascorbate oxidase is also present in the reagent to destroy interfering ascorbate before it can quench the chromogen-forming peroxidase step -- it is not part of the main triglyceride-quantitation pathway. The insert does not state the sample:reagent dilution ratio used in the final reaction mixture, so which of ATP, 4-aminoantipyrine, or MADB is truly limiting vs. in excess relative to analyte cannot be determined from the stated final concentrations alone.
Kinetics: Read as an endpoint colorimetric reaction (not explicitly described as a monitored rate) rather than assigned zero/first-order kinetics. Linear/reportable range is 10-1,000 mg/dL; results above this require dilution and repeat. GPO-based methods including this one show a strong negative interference in grossly lipemic samples (typically >1,700 mg/dL) that can slip past the automated Data Check flags -- the insert recommends routinely diluting such samples 1:4 with saline and multiplying the result by 5.
Readout: Bichromatic absorbance is measured at 660 nm (primary) and 800 nm (secondary); the increase in absorbance from the blue quinoneimine chromophore is proportional to triglyceride concentration.
What's measured: Measures total triglycerides via enzymatic hydrolysis to glycerol; the method is not blanked for endogenous free glycerol, so free glycerol in the sample (or glycerol contamination from collection/storage equipment) will be measured as triglyceride -- the insert specifically warns to keep collection equipment glycerol-free.
Interference implications: Ascorbate (up to 20 mg/dL), bilirubin (up to 40 mg/dL), and hemolysis (up to 500 mg/dL hemolysate) were tested per CLSI EP07-based studies and show no significant interference (recovery within 10% of initial value). Metamizole (dipyrone) given at or near the time of venipuncture may cause falsely low triglyceride results -- draw before dosing when possible. Separately, grossly lipemic samples with extremely elevated triglyceride (>1,700 mg/dL) can show a strong negative bias characteristic of GPO methods and should be diluted if suspected, even if not flagged.
Known bias: Method comparison of DxC 500 AU (Y) vs. DxC 700 AU (X), patient serum samples: Deming regression slope 0.987, intercept 2.563, r=0.9999, n=115, range 27.20-937.84 mg/dL -- indicates close agreement between these two analyzer platforms.

Interferences & pre-/post-analytical notes

Interferences

Known interferences

Metamizole (Dipyrone): May cause falsely low triglyceride results (Venipuncture performed during or immediately after Metamizole administration)

Validated -- no significant interference

Ascorbate: No significant interference (recovery within 10% of initial value) (up to 20 mg/dL ascorbate) — Ref. 10: CLSI. Interference Testing in Clinical Chemistry, 3rd ed., CLSI guideline EP07; Wayne, PA: CLSI; 2018.
Bilirubin: No significant interference (recovery within 10% of initial value) (up to 40 mg/dL bilirubin) — Ref. 10: CLSI. Interference Testing in Clinical Chemistry, 3rd ed., CLSI guideline EP07; Wayne, PA: CLSI; 2018.
Hemolysis: No significant interference (recovery within 10% of initial value) (up to 500 mg/dL hemolysate) — Ref. 10: CLSI. Interference Testing in Clinical Chemistry, 3rd ed., CLSI guideline EP07; Wayne, PA: CLSI; 2018.

Pre-analytical

Fasting (≥12 hours) serum, free from hemolysis and removed from the clot, is the recommended specimen; K2/K3 EDTA and Li/Na heparin plasma are the suggested alternatives if plasma must be used.
Serum triglyceride is stable 7 days at 2-8°C and 3 months frozen at ≤-20°C.
All equipment used in collection and storage of samples must be free from glycerol contamination, since the assay is not blanked for free glycerol.
Venipuncture should be performed prior to Metamizole (Dipyrone) administration; drawing during or immediately after dosing may cause falsely low triglyceride results.

Post-analytical

Samples exceeding the upper limit of linearity (1,000 mg/dL) should be diluted and repeated; the AUTO REPEAT RUN function can perform this automatically.
Grossly lipemic samples (typically triglyceride >1,700 mg/dL) can show a strong negative bias characteristic of GPO-based methods and may evade the analyzer's Data Check flags (F, Z, @, &); such samples should routinely be diluted 1 part sample to 4 parts saline and the result multiplied by 5.
Default reported unit is mg/dL; multiply by 0.0113 to convert to SI units (mmol/L).

Source: package insert (PDF, Cat #OSR60118) · Extracted 2026-08-17 · Approved 2026-08-19

Ortho VITROS 4600

kinetics endpoint λ 540 nm AMR 10.0–525.0 mg/dL (0.11–5.93 mmol/L; 0.10–5.25 g/L) LoQ 10.0 mg/dL (0.11 mmol/L); total allowable error goal used to accept the LoQ was ≤5 mg/dL (0.06 mmol/L)

Triglyceride-lipoprotein complex --Triton X-100--> Triglycerides + Proteins
Triglycerides + H2O --lipase--> Glycerol + Fatty acids
Glycerol + ATP --glycerol kinase/MgCl2--> L-α-glycerophosphate + ADP
L-α-glycerophosphate + O2 --L-α-glycerophosphate oxidase--> Dihydroxyacetone phosphate + H2O2
H2O2 + Leuco dye --peroxidase--> Dye + 2H2O

Enzymatic endpoint method (Spayd et al.) on a multilayered dry-slide element; final dye density is measured by reflectance spectrophotometry and is proportional to triglyceride concentration.

Reaction notes:
The assay does not monitor glycerol or triglyceride directly; it monitors the colored dye formed in the final peroxidase step. The insert states reactive-ingredient loadings per cm² (lipase 0.08 U, glycerol kinase 0.35 U, L-α-glycerophosphate oxidase 0.19 U, peroxidase 0.52 U, ATP 0.14 mg), and lipase carries the lowest activity loading of the four enzymes, consistent with the initial hydrolysis step being the pacing step for the cascade; the insert does not give sample-side reagent ratios, so a numeric excess fold cannot be derived from the stated concentrations alone.
Kinetics: This is a fixed-time endpoint assay: reflectance is read once, after a fixed ~5 minute incubation at 37°C, and converted to concentration using a software-resident endpoint colorimetric math model calibrated per slide lot. Linearity/reportable range is bounded by the stated measuring range (10.0–525.0 mg/dL); samples above this range must be diluted rather than relying on extended reaction time.
Readout: Reflectance spectrophotometry at 540 nm measures the density of the dye produced when peroxidase oxidizes the leuco dye using the H2O2 generated upstream; dye density is proportional to triglyceride concentration.
What's measured: The method measures total triglycerides via lipase-released glycerol, but free (endogenous) glycerol already present in the sample enters the same glycerol kinase/GPO/peroxidase cascade and is indistinguishable from triglyceride-derived glycerol. Patients or drugs associated with elevated free glycerol will therefore show TRIG results that do not reflect true serum triglyceride content.
Interference implications: Of the substances the insert tested (CLSI EP7-A2 protocol), the great majority — roughly 58 endogenous compounds and drugs including acetaminophen, salicylates, bilirubin (conjugated and unconjugated), hemoglobin, cholesterol, phospholipids, and a wide range of medications — showed no significant interference (bias <12 mg/dL at ~150 mg/dL TRIG or <8% at ~500 mg/dL TRIG) at the concentrations tested. Four substances were confirmed interferents with a negative (falsely low) bias: ethamsylate, hydroxyurea, and L-dopa show increasing negative bias at their upper therapeutic concentrations, while N-acetylcysteine's bias at its upper therapeutic concentration falls back below the specificity requirement. Separately, free glycerol is a structural confounder (co-measured with triglyceride-derived glycerol), and grossly lipemic samples slow color development, producing a negative bias and often requiring dilution.
Known bias: Method comparison (CLSI EP9-A2) of VITROS 5,1 FS vs. an Enzymatic Total Glycerol comparative method (n=119) gave slope 0.99, correlation 0.999, intercept -1.36 mg/dL, Sy.x 5.13 mg/dL (SI: slope 0.99, intercept -0.02 mmol/L, Sy.x 0.06 mmol/L). Cross-system comparisons against VITROS 5,1 FS (applicable to VITROS 450/4600) showed slopes of 0.99–1.00 and correlation coefficients of 1.000 for VITROS 950, VITROS 350, and VITROS 5600 (applicable to XT 3400/XT 7600), indicating close agreement across platforms.

Interferences & pre-/post-analytical notes

Interferences

Known interferences

Ethamsylate: Negative bias on TRIG result (Lowest interfering concentration 6.8 mg/dL (0.26 mmol/L) at TRIG ~149 mg/dL (bias -12.0 mg/dL/-0.14 mmol/L); 9.8 mg/dL (0.37 mmol/L) at TRIG ~443 mg/dL (bias -35.4 mg/dL/-0.40 mmol/L). At upper therapeutic concentration 25 mg/dL (0.95 mmol/L): bias -32 mg/dL (-0.36 mmol/L) at TRIG ~141 mg/dL; -98 mg/dL (-1.11 mmol/L) at TRIG ~465 mg/dL.) — CLSI EP7-A2, Interference Testing in Clinical Chemistry
Hydroxyurea: Negative bias on TRIG result (Lowest interfering concentration 27.2 mg/dL (3.56 mmol/L) at TRIG ~154 mg/dL (bias -12.3 mg/dL/-0.14 mmol/L); 16.2 mg/dL (2.12 mmol/L) at TRIG ~477 mg/dL (bias -38.2 mg/dL/-0.43 mmol/L). At upper therapeutic concentration 65 mg/dL (8.51 mmol/L): bias -26 mg/dL (-0.29 mmol/L) at TRIG ~152 mg/dL; -116 mg/dL (-1.31 mmol/L) at TRIG ~485 mg/dL.) — CLSI EP7-A2, Interference Testing in Clinical Chemistry
L-Dopa: Negative bias on TRIG result (Lowest interfering concentration 2.0 mg/dL (0.10 mmol/L) at TRIG ~142 mg/dL (bias -12.0 mg/dL/-0.14 mmol/L); 3.7 mg/dL (0.19 mmol/L) at TRIG ~456 mg/dL (bias -36.5 mg/dL/-0.41 mmol/L). At upper therapeutic concentration 12 mg/dL (0.60 mmol/L): bias -30 mg/dL (-0.34 mmol/L) at TRIG ~140 mg/dL; -92 mg/dL (-1.04 mmol/L) at TRIG ~452 mg/dL.) — CLSI EP7-A2, Interference Testing in Clinical Chemistry
N-Acetylcysteine: Negative bias on TRIG result at the lowest interfering concentration; note the bias at its upper therapeutic concentration does not meet or exceed the specificity requirement. (Lowest interfering concentration 109.9 mg/dL (6.7 mmol/L) at TRIG ~150 mg/dL (bias -12.0 mg/dL/-0.14 mmol/L); 185.5 mg/dL (11.4 mmol/L) at TRIG ~500 mg/dL (bias -40.0 mg/dL/-0.45 mmol/L).) — CLSI EP7-A2, Interference Testing in Clinical Chemistry
Free glycerol: Free glycerol in serum is measured along with the glycerol released from hydrolysis of triglycerides and diglycerides; samples with high endogenous free glycerol (certain clinical conditions, some drugs) give TRIG results that do not reflect actual serum triglyceride content.
Grossly lipemic samples: Slower rate of color development than clear serum, producing a negative bias; these samples often exceed the measuring range and should be diluted prior to testing.

Validated -- no significant interference

Acetaminophen: No significant interference (20.01 mg/dL (1324 μmol/L)) — CLSI EP7-A2
Acetylsalicylic acid: No significant interference (65.2 mg/dL (3.62 mmol/L)) — CLSI EP7-A2
Alprazolam: No significant interference (0.2 mg/dL (6.48 μmol/L)) — CLSI EP7-A2
Para-Aminosalicylic acid: No significant interference (79.4 mg/dL (5.22 mmol/L)) — CLSI EP7-A2
Amitriptyline: No significant interference (1.001 μg/mL (3.61 μmol/L)) — CLSI EP7-A2
Amlodipine: No significant interference (0.01 mg/dL (245 nmol/L)) — CLSI EP7-A2
Amoxicillin: No significant interference (7.53 mg/dL (206 μmol/L)) — CLSI EP7-A2
Ascorbic acid: No significant interference (6.02 mg/dL (342 μmol/L)) — CLSI EP7-A2
Atorvastatin: No significant interference (600 μg/L (519 nmol/L)) — CLSI EP7-A2
Azithromycin: No significant interference (1.15 mg/dL (15.3 μmol/L)) — CLSI EP7-A2
Bilirubin, conjugated: No significant interference (38.9 mg/dL (462 μmol/L)) — CLSI EP7-A2
Bilirubin, unconjugated: No significant interference (27 mg/dL (462 μmol/L)) — CLSI EP7-A2
Carbenicillin: No significant interference (200 mg/dL (5.31 mmol/L)) — CLSI EP7-A2
Cephalexin: No significant interference (11.7 mg/dL (337 μmol/L)) — CLSI EP7-A2
Cholesterol: No significant interference (evaluated using patient samples with TRIG concentrations of 57–446 mg/dL, 0.64–5.04 mmol/L) (503 mg/dL (13 mmol/L)) — CLSI EP7-A2
Ciprofloxacin: No significant interference (1 mg/dL (30.2 μmol/L)) — CLSI EP7-A2
Clonidine: No significant interference (0.01 μg/mL (43.5 nmol/L)) — CLSI EP7-A2
Clopidogrel: No significant interference (18 mg/dL (560 μmol/L)) — CLSI EP7-A2
Cystine: No significant interference (7 mg/dL (291 μmol/L)) — CLSI EP7-A2
Diatrizoate, sodium (Hypaque): No significant interference (521 mg/dL (8.2 mmol/L)) — CLSI EP7-A2
Dipyrone: No significant interference (120 mg/dL (3.6 mmol/L)) — CLSI EP7-A2
Dopamine: No significant interference (0.899 μg/mL (5.87 μmol/L)) — CLSI EP7-A2
Estradiol: No significant interference (1.2 ng/mL (4.41 nmol/L)) — CLSI EP7-A2
Ethanol: No significant interference (400 mg/dL (86.8 mmol/L)) — CLSI EP7-A2
Fenofibrate: No significant interference (4.5 mg/dL (125 μmol/L)) — CLSI EP7-A2
Furosemide: No significant interference (6 mg/dL (181 μmol/L)) — CLSI EP7-A2
Gentisic acid: No significant interference (1.79 mg/dL (117 μmol/L)) — CLSI EP7-A2
Glutathione: No significant interference (92 mg/dL (3 mmol/L)) — CLSI EP7-A2
Glyburide: No significant interference (1.92 μg/mL (3.89 μmol/L)) — CLSI EP7-A2
Hemoglobin: No significant interference (600 mg/dL (6 g/L)) — CLSI EP7-A2
Hydrochlorothiazide: No significant interference (0.6 mg/dL (20.2 μmol/L)) — CLSI EP7-A2
Hydrocodone: No significant interference (0.02 mg/dL (0.67 μmol/L)) — CLSI EP7-A2
Ibuprofen: No significant interference (50.02 mg/dL (2425 μmol/L)) — CLSI EP7-A2
Insulin: No significant interference (300 μIU/mL (1986.8 pmol/L)) — CLSI EP7-A2
Isoniazid: No significant interference (4 mg/dL (292 μmol/L)) — CLSI EP7-A2
Levothyroxine: No significant interference (0.1 mg/dL (1.29 μmol/L)) — CLSI EP7-A2
Lisinopril: No significant interference (0.03 mg/dL (0.74 μmol/L)) — CLSI EP7-A2
Metformin: No significant interference (4 mg/dL (310 μmol/L)) — CLSI EP7-A2
Methicillin sodium: No significant interference (24.02 mg/dL (597 μmol/L)) — CLSI EP7-A2
Methimazole: No significant interference (1.2 mg/dL (105 μmol/L)) — CLSI EP7-A2
Methotrexate: No significant interference (91 mg/dL (2 mmol/L)) — CLSI EP7-A2
Methyldopa: No significant interference (1.5 mg/dL (71 μmol/L)) — CLSI EP7-A2
Metoprolol: No significant interference (0.5 mg/dL (18.7 μmol/L)) — CLSI EP7-A2
Naproxen: No significant interference (49.75 mg/dL (2170 μmol/L)) — CLSI EP7-A2
Niacin: No significant interference (40 mg/dL (3.25 mmol/L)) — CLSI EP7-A2
Omega-3 Fatty Acid, DHA (docosahexaenoic acid): No significant interference (90 mg/dL (2.74 mmol/L)) — CLSI EP7-A2
Omega-3 Fatty Acid, EPA (eicosapentaenoic acid): No significant interference (111.6 mg/dL (3.69 mmol/L)) — CLSI EP7-A2
Omeprazole: No significant interference (0.6 mg/dL (17.4 μmol/L)) — CLSI EP7-A2
Phospholipids: No significant interference (852 mg/dL (11.1 mmol/L)) — CLSI EP7-A2
Pioglitazone: No significant interference (2.7 mg/dL (76 μmol/L)) — CLSI EP7-A2
Prednisone: No significant interference (0.03 mg/dL (0.84 μmol/L)) — CLSI EP7-A2
Rifampin: No significant interference (6.43 mg/dL (78.1 μmol/L)) — CLSI EP7-A2
Sertraline: No significant interference (0.06 mg/dL (1.96 μmol/L)) — CLSI EP7-A2
Sitagliptin: No significant interference (5.22 mg/dL (128.2 μmol/L)) — CLSI EP7-A2
Terazosin: No significant interference (3.02 μg/mL (7.8 μmol/L)) — CLSI EP7-A2
Total protein: No significant interference (10 g/dL (100 g/L)) — CLSI EP7-A2
Triamterene: No significant interference (0.89 mg/dL (35 μmol/L)) — CLSI EP7-A2
L-Tyrosine: No significant interference (72.48 mg/dL (4000 μmol/L)) — CLSI EP7-A2
Warfarin: No significant interference (10.02 μg/mL (32.5 μmol/L)) — CLSI EP7-A2

Pre-analytical

Specimen of choice is serum; lithium or sodium heparin plasma is also acceptable (heparin plasma results reported within 1% of serum). EDTA plasma is not recommended.
Centrifuge specimens and remove serum/plasma from cellular material within 4 hours of collection.
Equipment must be soap-free and glycerol-free; do not use collection tubes with glycerol-lubricated stoppers.
Handle and store specimens in stoppered containers to avoid contamination/evaporation; mix by gentle inversion and bring to room temperature (18–28°C) before analysis.
Specimen stability: Room temperature (18–28°C) ≤3 days; refrigerated (2–8°C) ≤7 days; frozen (≤-18°C) ≤6 months. Avoid repeated freeze-thaw cycles.
Grossly lipemic samples or samples exceeding the measuring range should be diluted with VITROS 7% BSA (manual) or the system's on-analyzer dilution procedure before testing.
Reaction uses 5.5 μL sample volume, ~5 minute incubation at 37°C (98.6°F).

Post-analytical

Results can be reported in conventional (mg/dL), SI (mmol/L, mg/dL × 0.01129), or alternate (g/L, mg/dL × 0.01) units.
If a result exceeds the analytical measuring range (10.0–525.0 mg/dL), dilute the sample and multiply the result by the dilution factor to estimate the original triglyceride concentration.
Triglyceride classification (Normal <150, Borderline High 150–199, High 200–499, Very High ≥500 mg/dL) per NCEP ATP III guidelines applies to samples collected from fasting patients.

Source: package insert (PDF, rev 8.0) · Extracted 2026-08-17 · Approved 2026-08-19

Roche Cobas c503

kinetics endpoint λ 505 / 700 nm AMR 0.1-10.0 mmol/L (8.85-885 mg/dL) LoD 0.1 mmol/L (8.85 mg/dL) LoQ 0.1 mmol/L (8.85 mg/dL)

Triglycerides + 3 H2O --lipoprotein lipase--> Glycerol + 3 RCOOH
Glycerol + ATP --glycerol kinase--> Glycerol-3-phosphate + ADP
Glycerol-3-phosphate + O2 --glycerol phosphate oxidase--> Dihydroxyacetone phosphate + H2O2
H2O2 + 4-Aminophenazone + 4-Chlorophenol --peroxidase--> 4-(p-benzoquinone-monoimino)-phenazone + 2 H2O + HCl

Enzymatic colorimetric test (GPO-PAP method), Trinder endpoint reaction.

Reaction notes:
The signal actually monitored is the red quinoneimine (Trinder) dye formed in the final peroxidase step, not glycerol or triglyceride directly. The insert gives reagent cosubstrate concentrations (ATP ≥1.4 mmol/L, 4-aminophenazone ≥0.13 mmol/L, 4-chlorophenol 4.7 mmol/L) and enzyme activities (lipoprotein lipase ≥83 μkat/L, glycerol kinase ≥3 μkat/L, glycerol phosphate oxidase ≥41 μkat/L, peroxidase ≥1.6 μkat/L) but not the final in-cuvette concentrations after sample/diluent mixing, so no reliable fold-excess or rate-limiting step can be derived from what's stated.
Kinetics: This is a fixed-time (10 minute) endpoint colorimetric read, not a continuous-rate reaction, consistent with the defined analytical measuring range of 0.1-10.0 mmol/L; at very high triglyceride concentrations the reaction can outrun available dissolved oxygen, producing a prozone effect (falsely low result) that the analyzer flags as >Kin rather than reading as simply out-of-range high.
Readout: Bichromatic absorbance is read at 505 nm (primary) against 700 nm (secondary), with the end-of-reaction (10 min) absorbance of the red quinoneimine dye directly proportional to triglyceride concentration.
What's measured: The assay measures total triglycerides via the glycerol liberated by lipase/esterase hydrolysis; it does not distinguish this from pre-existing endogenous free (unesterified) glycerol, which will falsely elevate results unless corrected by subtracting 0.11 mmol/L (10 mg/dL) as the insert instructs. Intralipid (an IV lipid emulsion) is measured directly as if it were analyte, producing falsely high results.
Interference implications: Icterus (conjugated and unconjugated bilirubin up to I index 10) and hemolysis (up to H index 700) are validated as non-interfering, as are common drugs at therapeutic concentrations. Lipemia does not track reliably with the L index and can paradoxically normalize very high triglyceride results. Several substances/conditions are documented to cause falsely low results with quantified thresholds where given: ascorbic acid, calcium dobesilate, N-acetylcysteine (>166 mg/L), and Metamizole (>0.05 mg/mL plasma, timing-dependent). Dicynone/etamsylate, NAPQI, and gammopathy are flagged with hedged/theoretical language ("may cause", "very rare cases") and no insert-specific quantification, so are treated as suspected rather than confirmed.
Known bias: Passing/Bablok method comparisons (same reagent, different cobas c-series analyzers) showed close agreement: c503 vs c501 y=1.015x+0.0125 mmol/L, r=0.999 (n=74); c303 vs c501 y=1.019x-0.00772 mmol/L, r=1.000 (n=74); c703 vs c503 y=1.018x-0.0236 mmol/L, r=1.000 (n=75) — no clinically meaningful bias between analyzer models using this reagent.

Interferences & pre-/post-analytical notes

Interferences

Known interferences

Lipemia (turbidity, L index): L index correlates with sample turbidity but not with triglyceride level; extremely lipemic samples (triglycerides > 3000 mg/dL) can produce falsely normal (low) results — Shephard MDS, Whiting MJ. Falsely low estimation of triglycerides in lipemic plasma by the enzymatic triglyceride method with modified Trinder's chromogen. Clin Chem 1990;36(2):325-329.
Very high triglyceride concentration (prozone effect, flagged by >Kin): False low results due to oxygen depletion during the assay reaction
Endogenous free (unesterified) glycerol: Falsely elevates serum triglyceride results
Ascorbic acid: Causes artificially low triglyceride results
Calcium dobesilate: Causes artificially low triglyceride results
Intralipid: Directly measured as analyte, leading to falsely high triglyceride results
N-Acetylcysteine: Causes falsely low results (plasma concentration above 166 mg/L)
Metamizole: Falsely low results if venipuncture occurs during/immediately after administration (significant interference may occur at plasma Metamizole concentrations above 0.05 mg/mL)

Suspected / theoretical

Dicynone (Etamsylate): May lead to false-low results at therapeutic concentrations (therapeutic concentrations) — Dastych M, Wiewiorka O, Benovska M. Ethamsylate (Dicynone) Interference... Clin Lab 2014;60:1373-1376.
N-acetyl-p-benzoquinone imine (NAPQI, acetaminophen metabolite): May independently cause falsely low results
Gammopathy (in particular IgM type, Waldenström's macroglobulinemia): May cause unreliable results in very rare cases — Bakker AJ, Mücke M. Gammopathy interference in clinical chemistry assays. Clin Chem Lab Med 2007;45(9):1240-1243.

Validated -- no significant interference

Conjugated bilirubin (icterus): No significant interference (up to I index of 10 (approx. 171 μmol/L or 10 mg/dL conjugated bilirubin)) — Glick MR, Ryder KW, Jackson SA. Graphical Comparisons of Interferences in Clinical Chemistry Instrumentation. Clin Chem 1986;32:470-475.
Unconjugated bilirubin (icterus): No significant interference (up to I index of 10 (approx. 171 μmol/L or 10 mg/dL unconjugated bilirubin)) — Glick MR, Ryder KW, Jackson SA. Graphical Comparisons of Interferences in Clinical Chemistry Instrumentation. Clin Chem 1986;32:470-475.
Hemolysis (hemoglobin): No significant interference (up to H index of 700 (approx. 434 μmol/L or 700 mg/dL hemoglobin)) — Glick MR, Ryder KW, Jackson SA. Graphical Comparisons of Interferences in Clinical Chemistry Instrumentation. Clin Chem 1986;32:470-475.
Common drugs at therapeutic concentrations (standard drug panels): No interference found (therapeutic concentrations) — Breuer J. Eur J Clin Chem Clin Biochem 1996;34:385-386; Sonntag O, Scholer A. Ann Clin Biochem 2001;38:376-385.

Pre-analytical

Acceptable sample types tested: serum, Li-heparin plasma, and K2-EDTA plasma only; centrifuge samples containing precipitates before performing the assay.
Serum stability: 2 days at 20-25°C, 10 days at 4°C, 3 months at -20°C, several years at -70°C (freeze only once).
Plasma stability: 2 days at 20-25°C, 15 days at 4°C, 3 months at -20°C, several years at -70°C (freeze only once).
Venipuncture should be performed prior to Metamizole administration; drawing immediately after or during administration may cause falsely low results if plasma Metamizole exceeds 0.05 mg/mL.

Post-analytical

Samples above the 10.0 mmol/L measuring range should be reanalyzed via the rerun function (1:5 dilution); results are automatically multiplied by 5.
If free glycerol is to be accounted for, subtract 0.11 mmol/L (10 mg/dL) from the reported triglycerides value.
A >Kin flag indicates a possible prozone effect from extremely high triglyceride concentration causing false low results; such results warrant dilution/rerun.

Source: package insert (PDF, Cat #08058687190, rev V 6.0) · Extracted 2026-08-17 · Approved 2026-08-19

Siemens Atellica CH

kinetics endpoint λ 505 / 694 nm AMR 15–1000 mg/dL (0.17–11.30 mmol/L) LoD 6 mg/dL (0.07 mmol/L) LoQ 15 mg/dL (0.17 mmol/L)

Triglycerides --LPL--> Glycerol + Fatty Acids
Glycerol + ATP --GK--> Glycerol-3-Phosphate + ADP
Glycerol-3-Phosphate + O2 --GPO--> Dihydroxyacetone phosphate + H2O2
2H2O2 + Aminoantipyrine + 4-Chlorophenol --POD--> Quinoneimine + HCl + 4H2O

Enzymatic (LPL/GK/GPO), Trinder-type peroxidase-coupled endpoint assay; bichromatic (505/694 nm) read.

Limiting reagent: None of the auxiliary reagents are limiting across the AMR — ATP, chromogens, and enzymes are all in molar excess relative to substrate (ATP ≈27-fold excess over triglyceride at the top of the 1000 mg/dL AMR, derived from insert-stated reagent concentrations [ATP 9 mmol/L in R1] and dispense volumes [35.5 µL R1 + 59.2 µL water + 5.3 µL of a 1:5-prediluted sample into a 100 µL reaction]); the analyte (via released glycerol) is effectively what determines the endpoint signal.
Reaction notes:
LPL hydrolysis of triglycerides is the analyte-defining step; GK/ATP, GPO, and the POD/Trinder chromogens are all present in substantial molar excess relative to substrate across the reportable range (ATP alone is roughly 27-fold in excess of triglyceride at the top of the 1000 mg/dL AMR, computed from the insert's stated ATP concentration and the dispense/dilution volumes), so the reaction goes to completion and the analyte is what's rate/amount-limiting, not the reagents. The signal actually monitored is quinoneimine absorbance, which per the insert is 'directly proportional to the total amount of glycerol and its precursors in the sample' — i.e., total glycerol (from LPL-released triglyceride glycerol plus any endogenous free glycerol), not triglyceride mass directly.
Kinetics: Read as a bichromatic (505/694 nm) fixed-time endpoint after 37°C incubation, not a rate — appropriate because reagents are in excess and the reaction is driven to completion. Linear reportable range is 15–1000 mg/dL (0.17–11.30 mmol/L); the lower bound is set by the LoQ, and values above 1000 mg/dL can trigger an automatic dilution/repeat extending measurement to 10,000 mg/dL (113.00 mmol/L) if configured.
Readout: Bichromatic endpoint absorbance (505 nm primary / 694 nm secondary) of the red quinoneimine dye formed in the peroxidase/Trinder step; per the insert, this signal is 'directly proportional to the total amount of glycerol and its precursors in the sample,' so it reflects total glycerol yield from the coupled reaction cascade rather than triglyceride concentration measured directly.
What's measured: Measures triglycerides indirectly via enzymatically liberated glycerol; the insert's own wording ('total amount of glycerol and its precursors') means any endogenous free glycerol present in the sample would also contribute to the signal, though the insert does not separately quantify or correct for this. Assay is validated only for serum, potassium EDTA plasma, lithium heparin plasma, and sodium heparin plasma — the insert explicitly states the assay 'is limited to the detection of triglyceride' in these specimen types.
Interference implications: Hemoglobin, conjugated bilirubin, unconjugated bilirubin, ascorbic acid, and etamsylate were each tested at the concentrations shown and all produced ≤10% bias, the insert's own cutoff for interference — so none of these are considered clinically significant by the manufacturer's criterion. Notably, the Limitations section separately and more emphatically warns against hemolyzed samples in general ('may cause significant interference'), which sits somewhat at odds with the quantified Hemoglobin interference data (only 1–3% bias at 300 mg/dL Hb) — bench staff should still reject grossly hemolyzed specimens per that caution. N-Acetyl Cysteine and Metamizole (Sulpyrine) are flagged as having potential to falsely depress results if given before specimen collection.
Known bias: Method comparison vs. Dimension TGL (Deming regression, CLSI EP09-A3): y = 0.99x + 2 mg/dL (y = 0.99x + 0.02 mmol/L), r = 0.997, N = 102, over 36–822 mg/dL (0.41–9.29 mmol/L) — essentially no proportional bias (slope ≈1.00) and a small constant offset (+2 mg/dL).

Interferences & pre-/post-analytical notes

Interferences

Suspected / theoretical

Hemolyzed samples (general caution): Insert states (Limitations) that hemolyzed samples 'may cause significant interference' — a hedged, unquantified caution that is not fully reconciled with the quantified Hemoglobin interference data above (only 1–3% bias at 300 mg/dL Hb)
N-Acetyl Cysteine / Metamizole (Sulpyrine): Potential for falsely depressed triglyceride results if specimen collection occurs after administration of these drugs

Validated -- no significant interference

Hemoglobin: Bias +3% at 199 mg/dL analyte level and +1% at 414 mg/dL analyte level (both ≤10%, the insert's own interference threshold) (Tested at 300 mg/dL (3.0 g/L) hemoglobin; assay designed for ≤10% interference (bias >10% is considered interference))
Bilirubin, conjugated: Bias -6% at 196 mg/dL analyte level and -5% at 404 mg/dL analyte level (≤10%) (Tested at 15 mg/dL (256.5 μmol/L) conjugated bilirubin)
Bilirubin, unconjugated: Bias +3% at 200 mg/dL analyte level and 0% at 416 mg/dL analyte level (≤10%) (Tested at 5 mg/dL (85.5 μmol/L) unconjugated bilirubin)
Ascorbic acid: Bias -7% at 200 mg/dL analyte level and -2% at 417 mg/dL analyte level (≤10%; listed as non-interfering) (Tested at 3 mg/dL (170.3 μmol/L) ascorbic acid)
Etamsylate: Bias -6% at 188 mg/dL analyte level and -5% at 414 mg/dL analyte level (≤10%; listed as non-interfering) (Tested at 2 mg/dL (76.0 μmol/L) etamsylate)

Pre-analytical

Accepted specimen types: serum, potassium EDTA plasma, lithium heparin plasma, sodium heparin plasma.
Sample volume required: 5.3 μL (system dispenses 50 μL sample + 200 μL Atellica CH Diluent into a dilution cuvette, then draws 5.3 μL of the prediluted sample into the reaction).
Specimens with high turbidity or particulates should be centrifuged before analysis.
Allow blood specimens to clot completely before centrifugation; keep tubes capped at all times.
Do not use hemolyzed samples, as they may cause significant interference with this assay.
Ensure samples are free of bubbles/foam and fibrin/other particulate matter before placing on the system; do not use samples with apparent contamination.
Separated venous specimens are stable up to 7 days at 2–8°C; separated capillary serum up to 7 days at 2–8°C or 24 hours at 20–25°C; venous specimens may be frozen up to 30 days at ≤ -20°C (do not use a frost-free freezer; mix and centrifuge thawed specimens before use).
Specimen collection should occur prior to N-Acetyl Cysteine or Metamizole (Sulpyrine) administration due to the potential for falsely depressed results.

Post-analytical

Report results below the measuring interval as < 15 mg/dL (0.17 mmol/L).
An automatic repeat condition extends the measuring interval to 10,000 mg/dL (113.00 mmol/L) for all validated specimen types; autorepeat results are flagged 'Autorepeat'.
Conversion formula: mg/dL x 0.0113 = mmol/L.
If QC results fall outside the expected control interval, do not report patient results; perform corrective action per laboratory protocol.
Analyte results should not be corrected based on HIL bias.
Results should always be interpreted in conjunction with the patient's medical history, clinical presentation, and other findings.

Source: package insert (PDF, Cat #11537222, rev Rev. 06, 2026-06) · Extracted 2026-08-17 · Approved 2026-08-19

Comparison highlights

All four use the shared lipase→glycerol kinase→GPO cascade, matching the overview's "most common" glycerophosphate oxidase/peroxidase detection scheme rather than the diaphorase or PK/LDH alternatives — but VITROS swaps the Trinder-type aminoantipyrine chromogen used by Beckman, Roche, and Siemens for a leuco dye read by reflectance on a dry-slide element, shifting its wavelength to 540 nm versus 660/800 (Beckman), 505/700 (Roche), and 505/694 (Siemens).
Only Roche gives a numeric free-glycerol correction: all four flag that endogenous free glycerol co-measures as triglyceride, but Roche's insert specifies subtracting 0.11 mmol/L (10 mg/dL), while Beckman, VITROS, and Siemens only warn qualitatively without a correction factor — meaning samples with elevated free glycerol (e.g., glycerol kinase deficiency) may be handled inconsistently depending on platform.
Ascorbic acid interference is discordant across platforms: Roche lists it as a known cause of falsely low results, whereas Beckman (validated to 20 mg/dL), VITROS (validated to 6.02 mg/dL), and Siemens (validated at 3 mg/dL, -7%/-2% bias) all report no significant interference — a specimen with high ascorbate could plausibly shift low on Roche but not on the others.
Metamizole/dipyrone is actively disputed between methods: Beckman and Roche both document falsely low TG tied to draw timing around administration, VITROS specifically tested dipyrone and found no significant interference at 120 mg/dL, and Siemens only flags it as a hedged "potential" effect — chemists drawing after metamizole dosing should not assume the same bias applies on every platform.
Ethamsylate/etamsylate shows the same negative-bias direction but different certainty: VITROS provides quantified dose-response data (bias up to -98 mg/dL at high drug/TG levels), Siemens validates no significant interference at the concentration it tested (2 mg/dL), and Roche lists it only as "suspected" with hedged language — so confidence in this interferent's impact varies more than the underlying chemistry would suggest.
Very high triglyceride can bias low by more than one mechanism: Roche describes a prozone-like effect from oxygen depletion at very high TG plus an L-index that can paradoxically normalize grossly lipemic (>3000 mg/dL) samples, Beckman notes a GPO-characteristic negative bias above 1700 mg/dL requiring dilution, and VITROS notes slowed color development in lipemic samples — all three GPO-based methods share this oxygen-limited failure mode near the top of their ranges, worth remembering before extending linearity claims.
Reported method comparisons are within-vendor, not cross-vendor: Beckman compares its own DxC 500 vs 700, Roche compares its own c503/c501/c303/c703, and VITROS compares its own instrument family — all showing slopes near 1.0, but none of the four datasets directly cross-validates one manufacturer's result against another's, so close agreement within a vendor's line shouldn't be extrapolated to cross-platform interchangeability.
Siemens' insert has an internal inconsistency worth flagging to bench staff: its quantified hemoglobin interference data shows only 1-3% bias at 300 mg/dL Hb (well under its own 10% cutoff), yet a separate Limitations statement warns hemolyzed samples "may cause significant interference" without reconciling the two — none of the other three platforms carry this kind of contradictory hemolysis guidance.

Generated 2026-08-19 · Approved 2026-08-19

Lab comparison

No lab offerings recorded for this analyte yet.