Tyrosine Unit Converter
Tyrosine Unit Converter
Convert tyrosine between mg/dL and µmol/L, with the age-dependent reference intervals — and why tyrosine is the wrong analyte to screen for tyrosinaemia type I with.
Tyrosine converter
mg/dL ⇄ µmol/LTyrosine 1.0 mg/dL, read against the adult reference interval
Formula and conversion factor
mg/dL = µmol/L ÷ 55.1907
- 55.1907
- derived from the molecular weight of L-tyrosine, 181.19 Da. Tyrosine is phenylalanine plus one hydroxyl group, which is why its factor is the smaller of the two
- read with phenylalanine
- the two move in opposite directions in phenylalanine hydroxylase deficiency, which is what makes the Phe:Tyr ratio more specific than either alone
- succinylacetone, not tyrosine
- newborn screening for tyrosinaemia type I is done on succinylacetone. Screening on tyrosine alone both misses affected infants and flags large numbers of unaffected ones
- age matters
- the neonatal interval reaches about 187 µmol/L against an adult upper limit near 90. A value that is unremarkable at three days old is clearly raised at thirty years
Worked example
Tyrosine 1.0 mg/dL, read against the adult reference interval
1.0 × 55.1907 = 55.19 µmol/L, reported as 55 µmol/L
Within the 30–90 µmol/L adult interval used here
The same 55 µmol/L in a three-day-old sits in the middle of a neonatal interval that runs from about 21 to 187 µmol/L — the number has not changed, the interval has
Alongside a phenylalanine of 620 µmol/L this would give a Phe:Tyr ratio of 11.2, well above 3 and consistent with PKU
Alongside a normal phenylalanine it says almost nothing on its own, which is why tyrosine is rarely reported in isolation
Adult reference intervals published for tyrosine
| Source | Adult reference interval (µmol/L) | Neonatal band |
|---|---|---|
| Labcorp | 31.1 – 118.1 (over 15 years) | 21.4 – 186.9 (0–30 days) |
| Mayo Clinic Laboratories | 36 – 113 (18 years and over) | 27 – 188 (under 24 months) |
| The Hospital for Sick Children, Toronto | 28 – 87 (over 19 years) | 27 – 187 (0–30 days) |
| Figure used on this page | 30 – 90 | 21 – 187 (0–30 days) |
What raises and lowers tyrosine
| Direction | Cause | What separates it |
|---|---|---|
| Raised, newborn | Transient tyrosinaemia of the newborn — immaturity of 4-hydroxyphenylpyruvate dioxygenase, prematurity, high protein intake, low ascorbate | Much the commonest cause. Resolves spontaneously; succinylacetone is absent |
| Raised | Tyrosinaemia type I (fumarylacetoacetate hydrolase deficiency) | Succinylacetone present. Tyrosine may be only modestly raised, or normal early on |
| Raised | Tyrosinaemia type II — oculocutaneous, with corneal erosions and palmoplantar keratosis | Usually a markedly raised tyrosine, often above 1,000 µmol/L, without succinylacetone |
| Raised | Liver disease and acute liver failure | Raised alongside methionine and the other aromatic amino acids; the Fischer ratio falls |
| Low | Phenylketonuria, treated or untreated | Read with the phenylalanine — the Phe:Tyr ratio is the comparison that matters |
| Low | Over-restriction on a phenylalanine-free protein substitute | A management question for the metabolic service, not a new diagnosis |
Rarely read alone
Tyrosine is a non-essential amino acid, made from phenylalanine by phenylalanine hydroxylase and used to build catecholamines, thyroid hormone and melanin. The conversion is straightforward — 1 mg/dL is 55.19 µmol/L, from a molecular weight of 181.19 Da — but tyrosine is one of the analytes whose number means almost nothing without the company it keeps. It is reported as part of a plasma amino acid profile, and it is read against the phenylalanine measured on the same sample.
That pairing is the whole point in newborn screening. Phenylalanine hydroxylase deficiency raises phenylalanine and lowers tyrosine, because the tyrosine is no longer being made from it. A raised phenylalanine from any other cause — prematurity, parenteral nutrition, liver disease, a sample taken before feeding is established — leaves tyrosine normal or high. The ratio of the two therefore moves further from normal in true PKU than either value does alone, and stays low when the phenylalanine rise is something else. A low tyrosine also has a management meaning of its own in treated PKU, where the protein substitute has to supply it.
The other direction has a different lesson. In a newborn, much the commonest cause of a raised tyrosine is transient tyrosinaemia of the newborn: immaturity of 4-hydroxyphenylpyruvate dioxygenase, compounded by prematurity, a high protein intake and relatively low ascorbate. It resolves without treatment. The inherited tyrosinaemias are rare by comparison, and tyrosinaemia type I — the dangerous one, causing liver failure, renal tubular disease and hepatocellular carcinoma — is not reliably detected by tyrosine at all. Screening programmes moved to succinylacetone because tyrosine both misses affected infants, whose tyrosine can be unremarkable early on, and flags large numbers of unaffected ones.
Age is the last thing to hold in mind. Neonatal reference intervals for tyrosine run to roughly 187 µmol/L against an adult upper limit near 90, so the same measured value can be entirely ordinary at three days old and clearly raised at thirty years. Published adult intervals themselves disagree by more than 30 µmol/L at the upper end. Convert the number, check it against the interval your own laboratory prints for that age, and read it beside the phenylalanine rather than on its own.
Frequently asked questions
How do I convert tyrosine from mg/dL to µmol/L?
Multiply by 55.1907, derived from the molecular weight of tyrosine, 181.19 Da. A tyrosine of 1.0 mg/dL is 55 µmol/L. To go the other way, divide the µmol/L figure by 55.1907.
What is a normal tyrosine level?
Roughly 30–90 µmol/L in an adult on this page, though published adult intervals run from about 28–87 to 36–113 µmol/L. Intervals are strongly age-dependent: the neonatal range reaches about 187 µmol/L, so a newborn value has to be read against a newborn interval.
What does a low tyrosine mean?
Most often phenylketonuria, treated or untreated, because tyrosine is made from phenylalanine and a block in phenylalanine hydroxylase leaves it low. In treated PKU it can also reflect a protein substitute that is not supplying enough. It should be read alongside the phenylalanine, not alone.
Does a raised tyrosine mean tyrosinaemia?
Usually not, especially in a newborn, where transient tyrosinaemia of the newborn is much the commonest cause and resolves on its own. Liver disease raises it too. Tyrosinaemia type I is diagnosed on succinylacetone, which is why newborn screening programmes use that rather than tyrosine.
Why do screening programmes measure succinylacetone instead of tyrosine?
Because tyrosine is neither sensitive nor specific for tyrosinaemia type I. Affected infants can have an unremarkable tyrosine early on, and large numbers of unaffected newborns have a raised one. Succinylacetone is produced only when fumarylacetoacetate hydrolase is deficient, so it identifies the condition directly.
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References
- Chinsky JM, Singh R, Ficicioglu C, et al. Diagnosis and treatment of tyrosinemia type I: a US and Canadian consensus group review and recommendations. Genet Med. 2017;19(12):1380–1395.
- Lepage N, McDonald N, Dallaire L, Lambert M. Age-specific distribution of plasma amino acid concentrations in a healthy pediatric population. Clin Chem. 1997;43(12):2397–2402.
- 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.
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.