Phenylalanine Unit Converter
Phenylalanine Unit Converter
Convert phenylalanine between mg/dL and µmol/L, and read the answer against the right figure — because the PKU treatment target sits above the untreated reference interval, and Europe and the ACMG no longer agree on where it ends.
Phenylalanine converter
mg/dL ⇄ µmol/LPhenylalanine 1.2 mg/dL, read against the adult reference interval
Formula and conversion factor
mg/dL = µmol/L ÷ 60.5364
- 60.5364
- derived from the molecular weight of L-phenylalanine, 165.19 Da. 1 mg/dL is 0.01 g/L, and 0.01 ÷ 165.19 mol/L is 60.54 µmol/L
- the two anchors
- 2 mg/dL is 121 µmol/L, the bottom of every PKU treatment target and roughly the upper limit of normal. 20 mg/dL is 1,211 µmol/L, the order of level an untreated classical PKU carries
- dried blood spot
- newborn screening measures phenylalanine on a heel-prick spot, not on plasma. Spot and plasma results are not interchangeable analyte for analyte, and a screening result is always confirmed on a quantitative plasma sample
- target is above interval
- the untreated adult reference interval tops out around 85–106 µmol/L; the treatment target starts at 120. A treated person at target is, by design, above the reference interval printed on the same report
Worked example
Phenylalanine 1.2 mg/dL, read against the adult reference interval
1.2 × 60.5364 = 72.64 µmol/L, reported as 73 µmol/L
Within the 35–85 µmol/L adult interval used here — though Mayo's adult interval is 45–106 and Labcorp's 33.6–101.9, so the verdict on a borderline value depends on whose interval is printed beside it
The two figures either side are worth knowing: 2 mg/dL is 121 µmol/L, the floor of every PKU treatment target, and 20 mg/dL is 1,211 µmol/L
A phenylalanine on its own never separates PKU from a transient rise — the phenylalanine to tyrosine ratio does, because true phenylalanine hydroxylase deficiency raises one while lowering the other
Treatment targets — two current guidelines, two answers
| µmol/L | mg/dL | |
|---|---|---|
| European guidelines 2017 — target to age 12, and in pregnancy | 120 – 360 | 2.0 – 6.0 |
| European guidelines 2017 — target from age 12 | 120 – 600 | 2.0 – 9.9 |
| ACMG 2023 — target, lifelong, not age-stratified | ≤ 360 | ≤ 6.0 |
| Untreated level below which no treatment is advised (European) | < 360 | < 6.0 |
| Untreated level prompting treatment to age 12 (European) | 360 – 600 | 6.0 – 9.9 |
| Untreated level prompting lifelong treatment (European) | > 600 | > 9.9 |
| Upper limit of normal — hyperphenylalaninaemia above this | ≈ 120 | ≈ 2.0 |
Reference intervals are age-dependent and laboratory-specific
| Source | Adult reference interval (µmol/L) | Youngest band published (µmol/L) |
|---|---|---|
| Labcorp | 33.6 – 101.9 (over 15 years) | 28.5 – 108.2 (0–30 days) |
| Mayo Clinic Laboratories | 45 – 106 (18 years and over) | 36 – 105 (under 24 months) |
| The Hospital for Sick Children, Toronto | 40 – 85 (over 19 years) | 49 – 107 (0–6 days) |
| Figure used on this page | 35 – 85 | 29 – 108 (under 2 years) |
The number, and the number it is read against
Phenylalanine is an essential amino acid that the liver enzyme phenylalanine hydroxylase converts to tyrosine, using tetrahydrobiopterin as a cofactor. When that enzyme is deficient, phenylalanine accumulates and is neurotoxic to the developing brain; untreated classical phenylketonuria causes irreversible intellectual disability, and treatment started in the first weeks of life prevents it almost entirely. That is why phenylalanine is measured on a dried blood spot in every newborn screening programme, and why the arithmetic on this page matters: 1 mg/dL is 60.54 µmol/L, so 2 mg/dL is 121 µmol/L and 20 mg/dL is 1,211 µmol/L.
A raised phenylalanine on screening is not a diagnosis. Prematurity, parenteral nutrition, liver disease and a sample taken before milk feeding is established all raise it, and in those situations tyrosine is normal or high. The phenylalanine to tyrosine ratio separates them, because true hydroxylase deficiency raises phenylalanine while tyrosine — no longer being made from it — falls or stays low. Defects of tetrahydrobiopterin synthesis or recycling produce the same amino acid pattern as classical PKU and need entirely different treatment, so pterin studies and dihydropteridine reductase activity belong in every confirmatory work-up rather than being added when the diet fails.
For someone already diagnosed, the useful comparison is not the reference interval at all but the treatment target, and the target sits above the interval. The 2017 European guideline recommends 120 to 360 µmol/L up to the age of 12 and in pregnancy, and relaxes to 120 to 600 µmol/L from 12 onwards. The 2023 ACMG guideline declines to stratify by age and recommends 360 µmol/L or less for life, on the grounds of intellectual outcome and of teratogenicity in anyone who might become pregnant. Both are current, both are evidence-graded, and they disagree by 240 µmol/L for an adult. There is no honest way to present one as the answer.
What follows from that is practical rather than dramatic. A single phenylalanine is one point on a curve that moves with intake, illness, growth and catabolism, and metabolic services read the trend and the variability rather than any individual value. A result below target matters too: phenylalanine is essential, and over-restriction causes poor growth, skin and hair changes and a catabolic state that releases still more phenylalanine from muscle. Convert the number, note which target your service uses, and take the result to the team who know the person it belongs to.
Frequently asked questions
How do I convert phenylalanine from mg/dL to µmol/L?
Multiply by 60.5364, derived from the molecular weight of phenylalanine, 165.19 Da. So 1.2 mg/dL is 73 µmol/L, 2 mg/dL is 121 µmol/L, and 20 mg/dL is 1,211 µmol/L. To go the other way, divide the µmol/L figure by 60.5364.
What is the target phenylalanine range in PKU?
Two current guidelines differ. The 2017 European guideline recommends 120–360 µmol/L up to age 12 and in pregnancy, and 120–600 µmol/L from age 12. The 2023 ACMG guideline recommends 360 µmol/L or less lifelong, without age stratification. Which applies is a decision for the metabolic service looking after the person.
What is a normal phenylalanine level?
Roughly 35–85 µmol/L in an adult on this page, though published adult intervals run from about 34–102 to 45–106 µmol/L depending on the laboratory, and intervals are age-dependent. A phenylalanine above about 120 µmol/L on a normal diet is hyperphenylalaninaemia and needs investigation.
Why is the phenylalanine to tyrosine ratio needed as well?
Because a raised phenylalanine has causes other than PKU — prematurity, parenteral nutrition, liver disease, a sample taken too early. In those the tyrosine is normal or high and the ratio stays low. In phenylalanine hydroxylase deficiency the tyrosine falls as the phenylalanine rises, so the ratio moves twice as far as either value alone.
What is a BH4 defect and why does it have to be excluded?
Tetrahydrobiopterin is the cofactor phenylalanine hydroxylase needs, and defects in making or recycling it raise phenylalanine in exactly the same pattern as classical PKU. They account for a small minority of raised results but need different treatment, including neurotransmitter replacement, so pterin studies and dihydropteridine reductase activity are part of the standard confirmatory work-up.
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References
- van Spronsen FJ, van Wegberg AMJ, Ahring K, et al. Key European guidelines for the diagnosis and management of patients with phenylketonuria. Lancet Diabetes Endocrinol. 2017;5(9):743–756.
- Smith WE, Berry SA, Bloom K, et al. Phenylalanine hydroxylase deficiency diagnosis and management: a 2023 evidence-based clinical guideline of the American College of Medical Genetics and Genomics (ACMG). Genet Med. 2024:101289.
- Regier DS, Greene CL. Phenylalanine Hydroxylase Deficiency. In: GeneReviews. Seattle: University of Washington; 2000, updated 2017.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.