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Familial Hypercholesterolaemia (FH) Calculator
Lipid Disorders

Familial Hypercholesterolemia (FH) Calculator

Estimate the likelihood that a patient has familial hypercholesterolaemia using the Dutch Lipid Clinic Network (DLCN) criteria — the most widely used FH probability score internationally, first published in 1999.

Answer the items below to calculate the DLCN score. Within each category, only the single highest-scoring item is counted, in line with the published criteria. For a detailed explanation of FH diagnosis, genetics, and treatment, read our guide on Familial Hypercholesterolaemia.

0 of 5 sections
Family History
First-degree relative with premature cardiovascular disease or known high cholesterol? 1 pt
First-degree includes parents, siblings, or children. Premature means men <55, women <65.
First-degree relative with tendon xanthomata or arcus cornealis, or child <18 with high cholesterol? 2 pts
Clinical History
Does the patient have premature coronary artery disease? 2 pts
Men <55, women <65. Includes heart attack, coronary stent, bypass surgery, or severe blockages on CT scan.
Premature cerebral or peripheral vascular disease? 1 pt
Includes stroke, TIA, or peripheral artery disease diagnosed before age 55 (men) or 65 (women).
Physical Examination
Arcus cornealis at age <45? 4 pts
A white or grey ring around the edge of the cornea, seen in younger patients.
Cholesterol deposits in tendons, most commonly the Achilles tendon or hand tendons.
LDL Cholesterol
Highest LDL-C level (convert mg/dL → mmol/L)
mmol/L
Was the patient on lipid-lowering therapy at time of LDL-C test?
Which medication and dose?
Genetic Testing
Functional mutation in LDLR, APOB, or PCSK9? 8 pts
If genetic testing has been performed and a causative mutation was identified.
Dutch Lipid Clinic Network Score
Answer the questions above to calculate the DLCN score.
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Understanding the DLCN Score

Familial hypercholesterolaemia (FH) is one of the most common inherited lipid disorders, affecting roughly 1 in 250 people. It causes markedly elevated LDL cholesterol from birth and, left untreated, substantially raises the risk of premature coronary artery disease.

The Dutch Lipid Clinic Network (DLCN) score estimates the probability that a patient's elevated cholesterol is due to FH rather than polygenic or lifestyle-related causes. First published in 1999, it remains the most widely used FH scoring system internationally.

The score draws on five domains: LDL cholesterol level, personal history of premature coronary artery disease, family history of early cardiovascular disease or hypercholesterolaemia, physical signs such as tendon xanthomata or corneal arcus, and genetic testing where available. Within each domain, only the single highest-scoring item is counted. For patients on lipid-lowering therapy, the calculator back-calculates an estimated untreated LDL-C before scoring.

DLCN Score Interpretation

DLCN ScoreInterpretationClinical Implication
< 3Unlikely FHFH unlikely. Standard risk-factor management applies.
3 – 5Possible FHFurther evaluation warranted. Consider family screening and repeat lipid testing.
6 – 8Probable FHConsider genetic testing and referral to a lipid specialist.
> 8Definite FHGenetic testing and specialist referral strongly recommended. Cascade screening of first-degree relatives indicated.
Important: the DLCN score estimates probability — it does not replace clinical judgement. Genetic testing or lipid-clinic referral may be appropriate regardless of the score. For help distinguishing FH from common hyperlipidaemia, see our guide on familial versus simple hypercholesterolaemia.

When Should FH Be Suspected?

Consider familial hypercholesterolaemia in any patient with:

  • LDL-C ≥ 5.0 mmol/L (190 mg/dL) in adults, or ≥ 4.1 mmol/L (160 mg/dL) in children — particularly if persistent despite lifestyle measures.
  • Premature coronary artery disease — myocardial infarction, coronary stenting, or bypass before age 55 (men) or 65 (women).
  • A family history of severe hypercholesterolaemia or early cardiovascular events across multiple generations.
  • Physical signs: tendon xanthomata (especially Achilles or hand extensor tendons), xanthelasma, or corneal arcus before age 45.

Early detection allows treatment with high-intensity statins, ezetimibe, and — where indicated — PCSK9 inhibitors or inclisiran, which can substantially reduce lifetime cardiovascular risk when started early. For more on FH genetics, diagnosis, and treatment, read our guide on Familial Hypercholesterolaemia.

References
  1. Nordestgaard BG, Chapman MJ, Humphries SE, et al. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population. Eur Heart J. 2013;34(45):3478–3490. doi:10.1093/eurheartj/eht273
  2. Defesche JC, Gidding SS, Harada-Shiba M, et al. Familial hypercholesterolaemia. Nat Rev Dis Primers. 2017;3:17093. doi:10.1038/nrdp.2017.93
  3. Mach F, Baigent C, Catapano AL, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J. 2020;41(1):111–188. doi:10.1093/eurheartj/ehz455
  4. World Health Organization. Familial hypercholesterolaemia (FH): report of a second WHO consultation. Geneva: WHO; 1999.

Frequently Asked Questions

What is the Dutch Lipid Clinic Network (DLCN) score?

The DLCN score is a clinical scoring system developed in the Netherlands to estimate the probability of familial hypercholesterolaemia. It combines LDL cholesterol level, personal and family history, physical signs, and genetic test results to classify FH as unlikely, possible, probable, or definite. It is the most widely used FH scoring tool internationally and is recommended by both European and international lipid guidelines.

What is the difference between familial hypercholesterolaemia and common high cholesterol?

Familial hypercholesterolaemia is a single-gene (monogenic) disorder present from birth, caused by a mutation in the LDLR, APOB, or PCSK9 gene. It produces very high LDL cholesterol lifelong and clusters strongly within families. Common — or polygenic — high cholesterol results from many small genetic variants together with diet, weight, and other lifestyle factors, and usually produces more modest LDL elevations. The distinction matters because FH carries a higher lifetime cardiovascular risk and warrants earlier, more intensive treatment and family screening. For a stepwise approach, see our guide on familial versus simple hypercholesterolaemia.

Can this calculator diagnose familial hypercholesterolaemia?

No. The calculator provides an estimate of probability, not a definitive diagnosis. A DLCN score of 6 or above suggests probable or definite FH and warrants genetic testing for confirmation. Genetic testing can identify mutations in the LDLR, APOB, or PCSK9 genes that cause FH. Clinical evaluation by a lipid specialist is recommended for all patients with suspected FH.

Is familial hypercholesterolaemia inherited?

Yes. FH is usually inherited in an autosomal dominant pattern, meaning each first-degree relative — parents, siblings, and children — of an affected person has about a 50% chance of also carrying the condition. This is why cascade screening of close relatives is recommended once FH is identified. Rarely, a person inherits two FH genes (homozygous FH), which causes a far more severe form requiring specialist management.

Who should be screened for familial hypercholesterolaemia?

Screening should be considered in adults with LDL cholesterol ≥5.0 mmol/L (190 mg/dL), children with LDL ≥4.1 mmol/L (160 mg/dL), individuals with premature coronary artery disease, and anyone with a first-degree relative diagnosed with FH. Cascade screening — testing family members of a confirmed FH patient — is the most cost-effective strategy and is recommended by Australian, European, and international guidelines.

Why is early detection of FH important?

Individuals with untreated heterozygous FH have approximately a 50% risk of coronary heart disease by age 50 in men and age 60 in women. Early treatment with high-intensity statins and, where needed, additional lipid-lowering therapies can reduce this risk substantially. The earlier treatment begins, the greater the cumulative benefit — which is why identifying FH in childhood or early adulthood is so important.

How is familial hypercholesterolaemia treated?

Treatment centres on lowering LDL cholesterol as early and as much as possible. High-intensity statins are first-line; ezetimibe is commonly added, and PCSK9 inhibitors or inclisiran are used when LDL targets are not reached or statins are not tolerated. Most patients with FH are treated to an LDL-C target below 1.8 mmol/L, or below 1.4 mmol/L where there is established cardiovascular disease. Lifestyle measures support but do not replace medication in FH. See our guide on Familial Hypercholesterolaemia for more detail.

What does it mean if the patient is on statin therapy?

If the LDL cholesterol was measured while the patient was taking lipid-lowering medication, the calculator applies a correction factor to estimate the untreated LDL level. This matters because the DLCN score was designed using untreated cholesterol values. The correction factor depends on the specific medication and dose — for example, Atorvastatin 40 mg typically reduces LDL by about 50%, so the measured LDL is multiplied by 2 to estimate the pre-treatment level.

Dr Reza Moazzeni, Cardiologist
Reviewed by
Dr Reza Moazzeni MD FRACP
Consultant Cardiologist · Heartcare Sydney

Dr Moazzeni is a consultant cardiologist practising in Westmead, Sydney with expertise in preventive cardiology, echocardiography, and cardiovascular risk assessment. He is a Fellow of the Royal Australasian College of Physicians.