Glycine Unit Converter

Q: How do I convert glycine from mg/dL to µmol/L?

Multiply by 133.209, derived from the molecular weight of glycine, 75.07 Da. A glycine of 2.5 mg/dL is 333 µmol/L. Glycine is the smallest amino acid, so this is the largest conversion factor of the twenty. To go the other way, divide by 133.209.

Q: What is a normal glycine level?

There is no agreed single figure, and this is the amino acid where that matters most. Mayo publishes 80–500 µmol/L for every age from birth; Labcorp publishes 132–467 µmol/L for adults and three narrower bands for children. GeneReviews gives normal plasma glycine as 125–450 µmol/L. Use the interval your own laboratory prints.

Q: How is non-ketotic hyperglycinaemia diagnosed?

On the ratio of CSF glycine to plasma glycine, measured on samples taken at the same time, not on the plasma level. The ratio is normally 0.02 or less, with published medians of 0.13 in attenuated and 0.22 in severe disease. The CSF must be free of blood contamination, and molecular testing follows.

Q: Does a normal plasma glycine exclude non-ketotic hyperglycinaemia?

No. Plasma glycine in attenuated disease has been reported from 342 µmol/L, which overlaps the upper part of the normal range, so a plasma level inside the reference interval does not exclude it. That overlap is precisely why the CSF to plasma ratio is the diagnostic measure.

Q: Can valproate raise glycine?

Yes. Valproate suppresses the glycine cleavage system and can reversibly raise CSF glycine above 60 µmol/L, mimicking the biochemistry of non-ketotic hyperglycinaemia. It has to be excluded before an inherited cause is considered — and any change to the drug is a decision for the prescriber, not something to act on from a converted number.

Convert glycine between mg/dL and µmol/L — and see why the plasma level is not the diagnostic measure in non-ketotic hyperglycinaemia, where the CSF to plasma glycine ratio is, and why valproate has to be excluded first.

Last updated 12 Sep 2026

Glycine converter

mg/dL ⇄ µmol/L

Glycine

Multiply mg/dL by 133.21 to get µmol/L. This converts plasma and CSF glycine alike — the molecule is the same — but the two are measured on simultaneous samples and read as a ratio, not compared against one another's intervals.

Reference groupPublished intervals assume a fasting sample separated promptly — Mayo states its values are for fasting patients, and amino acids shift with feeding and again in the tube if the blood is left to stand. In an infant, the sample is taken immediately before a feed or at the interval the metabolic service specifies. Glycine is the amino acid where a single adult figure is least meaningful: Mayo publishes one interval, 80–500 µmol/L, for every age from birth onwards, while Labcorp publishes four narrower bands. The groups below are the Labcorp bands; a glycine of 100 µmol/L is low against them and normal against Mayo's.

333µmol/LExample

Plasma glycine 2.5 mg/dL, read against the adult reference interval

Formula and conversion factor

µmol/L = mg/dL × 133.209
mg/dL = µmol/L ÷ 133.209

133.209: derived from the molecular weight of glycine, 75.07 Da. Glycine is the smallest amino acid, C₂H₅NO₂, so this is the largest mg/dL to µmol/L factor of the twenty
CSF : plasma ratio: the diagnostic measure in non-ketotic hyperglycinaemia, on samples taken at the same time. Normally 0.02 or less; around 0.13 in attenuated and 0.22 in severe disease
blood in the CSF: invalidates the ratio entirely. Plasma glycine is roughly fifty times the CSF concentration, so even slight contamination of the CSF sample raises the numerator and the ratio with it
valproate first: valproate suppresses the glycine cleavage system and reversibly raises CSF glycine above 60 µmol/L. It has to be excluded before an inherited cause is entertained

Worked example

Plasma glycine 2.5 mg/dL, read against the adult reference interval
2.5 × 133.209 = 333.02 µmol/L, reported as 333 µmol/L
Within the Labcorp adult band of 132–467 µmol/L used here, and within Mayo's 80–500 µmol/L
Also within the 125–450 µmol/L GeneReviews gives as the normal plasma glycine, and well below the 822 µmol/L median of attenuated non-ketotic hyperglycinaemia
None of which excludes attenuated disease, because reported plasma values in attenuated NKH start at 342 µmol/L — lower than this result. The ratio is what separates them: paired with a CSF glycine of 6 µmol/L this gives 0.018, at or under the normal 0.02
Paired instead with a CSF glycine of 40 µmol/L it gives 0.12, which is attenuated-NKH territory and a reason to go on

Why the ratio, and not the plasma level, is the diagnostic measure

Median with range, from GeneReviews. Read the two bold figures together: plasma glycine in both severe and attenuated disease starts at the same 342 µmol/L, and the ranges overlap the top of normal. The plasma level cannot separate severe from attenuated disease, and a plasma level inside the reference interval does not exclude the attenuated form. The ratio, measured on simultaneous samples with CSF free of blood, does most of the work — and none of these figures is a diagnosis by itself.
	CSF glycine (µmol/L)	Plasma glycine (µmol/L)	CSF : plasma ratio
Normal	< 20 (over 1 year; higher in neonates)	125 – 450	≤ 0.02
Attenuated non-ketotic hyperglycinaemia	99 (41 – 230)	822 (342 – 1,590)	0.13 (0.04 – 0.22)
Severe non-ketotic hyperglycinaemia	228 (40 – 510)	1,133 (342 – 2,363)	0.22 (0.09 – 0.45)
Valproate treatment	can exceed 60	may be raised	raised, and reversible on stopping

What else raises glycine, and what has to be excluded first

The first and last rows are the two that most often produce a spurious diagnosis: a drug nobody thought to ask about, and a traumatic tap. Both are checked before an inherited disorder is considered, and the work-up is directed by a metabolic service rather than by any single result.
Cause	Pattern	How it is separated
Valproate	Glycine raised, CSF glycine can exceed 60 µmol/L	Reversible. Stopping or changing the drug, under the prescriber’s direction, and repeating
Organic acidurias — propionic, methylmalonic, isovaleric	Ketotic hyperglycinaemia: glycine raised with ketosis and acidosis	Urine organic acids and an acylcarnitine profile. The name is the distinction — non-ketotic means the ketosis is absent
Liver failure	Glycine raised alongside a disturbed whole amino acid profile	The clinical picture and liver function; the aromatic amino acids rise too
Hypoxic-ischaemic injury, intracerebral haemorrhage	CSF glycine raised, ratio can be raised transiently	History, imaging, and repeating once the acute event has passed
Blood-stained CSF	CSF glycine falsely raised, ratio falsely raised	Plasma glycine is about fifty times the CSF level, so the sample is repeated rather than interpreted

A ratio, not a level

Glycine is the smallest amino acid, C₂H₅NO₂, with a molecular weight of 75.07 Da — which gives it the largest mg/dL to µmol/L factor of the twenty, 133.21. It is non-essential, made largely from serine, and broken down by the glycine cleavage system, a four-protein mitochondrial complex. When that system fails, glycine accumulates in plasma and, far more importantly, in cerebrospinal fluid, where it acts on NMDA and inhibitory glycine receptors. The resulting disorder is non-ketotic hyperglycinaemia, also called glycine encephalopathy.

The single most important thing about glycine as a test is that the plasma level is not what makes that diagnosis. The measure is the ratio of CSF glycine to plasma glycine on samples taken at the same time. Normally the ratio is 0.02 or less; published medians are 0.13 in attenuated disease and 0.22 in severe disease. Plasma glycine in both severe and attenuated non-ketotic hyperglycinaemia has been reported from the same lower figure of 342 µmol/L, overlapping the upper end of normal, so the plasma value can neither grade the disorder nor exclude the attenuated form. The CSF sample must be free of blood, because plasma glycine is roughly fifty times the CSF concentration and a traumatic tap raises the numerator and the ratio with it.

Reversible causes come first. Valproate suppresses the glycine cleavage system and can reversibly raise CSF glycine above 60 µmol/L, which is why the drug history is taken before anything inherited is entertained. Liver failure, hypoxic-ischaemic injury and intracerebral haemorrhage all raise glycine, and the organic acidurias — propionic, methylmalonic, isovaleric — produce a ketotic hyperglycinaemia that the word non-ketotic exists to distinguish, identified on urine organic acids and an acylcarnitine profile.

Reference intervals for glycine deserve more scepticism than most. Mayo publishes a single interval, 80–500 µmol/L, for every age from birth to adulthood; Labcorp publishes four age bands, none of them that wide, with an adult range of 132–467 µmol/L. A glycine of 100 µmol/L is normal against the first and low against the second. Both assume a fasting sample separated promptly, since amino acids shift with feeding and drift again in blood left standing. Convert the number, note which interval is printed beside it, and take an abnormal result to the metabolic service rather than to a conclusion.

Frequently asked questions

How do I convert glycine from mg/dL to µmol/L?

Multiply by 133.209, derived from the molecular weight of glycine, 75.07 Da. A glycine of 2.5 mg/dL is 333 µmol/L. Glycine is the smallest amino acid, so this is the largest conversion factor of the twenty. To go the other way, divide by 133.209.

What is a normal glycine level?

There is no agreed single figure, and this is the amino acid where that matters most. Mayo publishes 80–500 µmol/L for every age from birth; Labcorp publishes 132–467 µmol/L for adults and three narrower bands for children. GeneReviews gives normal plasma glycine as 125–450 µmol/L. Use the interval your own laboratory prints.

How is non-ketotic hyperglycinaemia diagnosed?

On the ratio of CSF glycine to plasma glycine, measured on samples taken at the same time, not on the plasma level. The ratio is normally 0.02 or less, with published medians of 0.13 in attenuated and 0.22 in severe disease. The CSF must be free of blood contamination, and molecular testing follows.

Does a normal plasma glycine exclude non-ketotic hyperglycinaemia?

No. Plasma glycine in attenuated disease has been reported from 342 µmol/L, which overlaps the upper part of the normal range, so a plasma level inside the reference interval does not exclude it. That overlap is precisely why the CSF to plasma ratio is the diagnostic measure.

Can valproate raise glycine?

Yes. Valproate suppresses the glycine cleavage system and can reversibly raise CSF glycine above 60 µmol/L, mimicking the biochemistry of non-ketotic hyperglycinaemia. It has to be excluded before an inherited cause is considered — and any change to the drug is a decision for the prescriber, not something to act on from a converted number.

Related calculators

References

Van Hove JLK, Coughlin C II, Swanson M, Hennermann JB. Nonketotic Hyperglycinemia. In: GeneReviews. Seattle: University of Washington; 2002, updated 2019.
Coughlin CR II, Swanson MA, Kronquist K, et al. The genetic basis of classic nonketotic hyperglycinemia due to mutations in GLDC and AMT. Genet Med. 2017;19(1):104–111.
Davis JS, Darcy CJ, Piera K, et al. Ex-vivo changes in amino acid concentrations from blood stored at room temperature or on ice. BMC Clin Pathol. 2009;9:10.

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.