Test performed at Canterbury Health Laboratories
Fasting does not significantly affect result and is not necessary.
Units: g/L
Population ranges:
Male: 0.52-1.09 g/L
Female: 0.49-1.03 g/L
Recommended level (moderate risk): <1.0 g/L
(target levels may be lower in high risk patients on aggressive lipid lowering treatment)
Uncertainty of Measurement
: 6%
Apolipoprotein B (commonly abbreviated 'apoB') is the main structural protein of atherogenic lipid particles: very low density lipoproteins (VLDL), intermediate density particles (IDL/remnant particles), low density lipoprotein (LDL), and lipoprotein (a).
Regardless of size, each apoB-containing particle has strictly only one apoB molecule. Hence measuring apoB gives a direct measure of the number of circulating atherogenic particles (not their cholesterol content).
The assay measures both apoB100 particles (originating from the liver) and the shorter form of apoB (apoB48) from the intestine. However, the number of apoB48 particles is usually <1% of the total. In most settings about 90% of all measured apoB is present in LDL particles. However, the proportion of other particles (VLDL, IDL/remnants, Lp(a)) increases in some acquired and genetic disorders.
With the exception of Lipoprotein (a), which can be separately measured, upstream VLDL and IDL particles are larger, do not penetrate the vessel wall as readily, and are therefore less atherogenic than LDL, however chronically increased amounts can contribute to atherosclerosis.
The total amount of cholesterol contained in the atherogenic particle cascade (VLDL, IDL, LDL) can be measured as non-HDL cholesterol:
Non-HDL cholesterol = Total cholesterol - HDL cholesterol
The upstream, pre-LDL component can be expressed as:
Residual particle cholesterol (mostly VLDL, IDL) = Total cholesterol ? HDL cholesterol ? LDL cholesterol
Generally the amount of cholesterol in VLDL and IDL particles in plasma is low, and not more than 0.8mmol/L. However, this difference can increase in conditions such as diabetes, obesity and metabolic syndrome, and in some genetic disorders with poor lipid particle clearance. In such patients non-HDL is usually adequate to convey the total risk, but apoB may also sometimes be helpful.
When should apoB be measured?
Population evidence indicates that apoB and non-HDL cholesterol perform as well, and in some equivocal risk groups, better, than LDL in predicting future vascular events, however the largest trial evidence and focus is on LDL reduction as the primary treatment marker.
The lipid profile (esp. the total cholesterol/HDL ratio) is currently recommended for assessing cardiovascular risk in locally validated algorithms (Predict) and in the US, European and Australian guidelines. For most patients the value of measuring apoB is limited and does not justify the significant added expense.
ApoB and non-HDL cholesterol are recognised as secondary risk factors or risk enhancers in major guidelines. The percent reduction between of LDL and apoB is similar in most large randomised trials. ApoB assays are also not fully standardised and treatment thresholds and targets are not agreed, and they differ between expert groups (De Oliveira-Gomez 2024).
Monogenic disorders such as familial hypercholesterolaemia (FH) can be recognised from the standard lipid panel and other clues such as family history and clinical features, without need to measure apoB. In patients with an unexplained early personal or family history of CVD lipoprotein (a) should also be measured once to exclude a genetically high level.
Measuring apoB is occasionally helpful, but is only recommended in specific settings and by secondary care specialists who are aware of it's advantages and limitations:
- as an additional risk marker when discordance between cholesterol content and particle number is suspected, e.g. identifying residual risk in high risk patients on intensive statin therapy and others with persisting increases in triglycerides (2-10mmol/L). Note, however, that the calculated LDL result provided by Auckland laboratories (using Sampson NIH formula) is accurate and can be reliably used as a treatment and risk marker in most patients with triglycerides up to 8.9 mmol/L.
- apoB may help identify occasional patients with familial dysbetalipoproteinaemia (type III) from other forms of mixed dyslipidaemia
- to identify genetic overproduction of apoB containing particles not fully reflected in raised LDL. This is sometimes termed familial combined hyperlipidaemia (FCH), however unlike familial hypercholesterolaemia (FH), the condition is not well defined either clinically or genetically. It has no diagnostic gold standard and has variable presentation in different family members, with raised cholesterol, triglycerides, or both. It is likely due to a combination of polygenic risk factors and acquired factors such as obesity and insulin resistance.
- rarely an extremely low apoB level can confirm genetically low cholesterol levels (hypo- or abetalipoproteinaemia). All such patients should have specialist review.
References:
Langlois MR, Nordestgaard BG, Langsted A, et al. Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM. Clin Chem Lab Med 2020; 58(4): 496-517
De Oliveira-Gomes D, Joshi PH, Peterson ED, et al. Apolipoprotein B: Bridging the gap between evidence and clinical practice. Circulation 2024; 150:62-79.
The chemical pathology team can be reached via email: chemicalpathologist@adhb.govt.nz or via Lablink (09) 307 4949 ext 22000 or 09-3078995
Emails will receive priority attention from the on-call chemical pathologist. Include the patients NHI.
After-hours: contact Lablink (Auckland City Hospital ext. 22000 or 09-3078995) or hospital operator for on duty staff after hours .
- Dr Samarina Musaad (Clinical Lead) : SamarinaM@adhb.govt.nz ext. 22402
- Dr Cam Kyle : CampbellK@adhb.govt.nz ext 22052
- Dr Weldon Chiu : WeldonC@adhb.govt.nz ext. 23427
- Dr Campbell Heron : CHeron@adhb.govt.nz ext. 23427
- Dr Sakunthala Jayasinghe Saku.Jayasinghe@adhb.govt.nz
- Dr Owen Yi WenyiYi@adhb.govt.nz