Alpha-1-Acid Glycoprotein Unit Converter
Alpha-1-Acid Glycoprotein Unit Converter
Convert alpha-1-acid glycoprotein (orosomucoid) between g/L and mg/dL — and use it for what it is actually good for: a correction factor, because it binds basic drugs and a raised level cuts the free fraction at an unchanged total concentration.
Alpha-1-Acid Glycoprotein converter
g/L ⇄ mg/dLAlpha-1-acid glycoprotein 0.75 g/L in a well outpatient, then 2.25 g/L after cardiac surgery
The conversion, and why the protein is worth measuring at all
mg/dL = g/L × 100
and there is no molar unit: orosomucoid is variably glycosylated, with carbohydrate making up around 45% of its mass
- g/L ⇄ mg/dL
- a factor of 100, and the only arithmetic here. An orosomucoid of 0.75 g/L is 75 mg/dL
- no molar unit
- alpha-1-acid glycoprotein is roughly 41–43 kDa depending on glycosylation, which varies both between people and with inflammation. A mass concentration against a reference preparation is the only meaningful report
- orosomucoid = AAG = AGP
- three names for the same protein. "Orosomucoid" is the older name, AGP is the abbreviation used in the nutrition literature, and the gene products are ORM1 and ORM2
- the free fraction relationship
- AAG is the principal plasma carrier of <b>basic</b> (cationic) drugs, as albumin is for acidic ones. Free fraction falls as carrier concentration rises, so doubling the AAG roughly halves the free fraction of a drug that is extensively bound to it — at an unchanged total measured concentration
- which drugs
- lidocaine, disopyramide, quinidine, propranolol, methadone, tricyclic antidepressants, imatinib and several others. The clinically important cases are the ones with a narrow therapeutic index where only the total is measured
Worked example
Alpha-1-acid glycoprotein 0.75 g/L in a well outpatient, then 2.25 g/L after cardiac surgery
0.75 g/L = 75 mg/dL — mid-interval against 39–115 mg/dL, and the whole of the arithmetic
Now the same patient a few days after cardiac surgery, with an orosomucoid of 2.25 g/L (225 mg/dL) — a threefold acute-phase rise, which on its own tells you nothing a CRP would not have told you sooner
What it does tell you concerns the lidocaine infusion running alongside it. Lidocaine is extensively bound to alpha-1-acid glycoprotein, so tripling the carrier substantially lowers the free fraction — the pharmacologically active part — at an unchanged total concentration
So a total lidocaine level reported as "high therapeutic" in this patient overstates the free drug available, and a level that looks reassuringly mid-range after the orosomucoid falls again may correspond to more free drug than it did a week earlier
The same logic runs in reverse in nephrotic syndrome or severe liver disease: a low orosomucoid raises the free fraction, and toxicity can appear at an apparently therapeutic total level
What alpha-1-acid glycoprotein is actually used for
| Use | Standing |
|---|---|
| Interpreting total concentrations of basic drugs | The main clinical use. AAG is the principal carrier of cationic drugs — lidocaine, disopyramide, quinidine, propranolol, methadone, tricyclic antidepressants, imatinib. A raised AAG binds more drug, so the free active fraction falls while the measured total does not, and the reverse holds when AAG is low. Where only a total concentration is available in an acutely ill patient, the AAG is what explains a discrepancy between the level and the effect |
| Detecting inflammation in nutritional and iron-status surveys | An established use. Ferritin, retinol-binding protein and retinol are all distorted by inflammation. The BRINDA approach uses CRP and AGP together to adjust them, AGP contributing the later, more prolonged phase of the response that CRP has already left behind |
| As a general inflammatory marker | Adds little to CRP. It rises more slowly — over a day or two rather than hours — and falls more slowly, which is exactly why it complements CRP in survey work, but it is not a better acute-phase test and is not worth ordering as one |
| Glycosylation analysis in chronic disease | A research and specialist tool. The glycoforms of AAG change with the nature and duration of inflammation, which is of interest in liver disease and malignancy but has no routine role |
| Diagnosing any particular disease | No role. A raised AAG is an acute-phase response and is not specific to anything |
Free fraction, and the direction of the error
| Situation | AAG | Free fraction of a basic drug | Practical consequence |
|---|---|---|---|
| Acute illness, trauma, surgery, malignancy, active rheumatoid arthritis, pregnancy | Raised, often two- to threefold | Falls | A total concentration overstates the active drug. A level near the top of the therapeutic range may be pharmacologically modest — and as the AAG falls during recovery, the same total corresponds to more free drug |
| Nephrotic syndrome, protein-losing enteropathy, severe liver disease, severe malnutrition | Low | Rises | A total concentration understates the active drug, and toxicity can appear at an apparently therapeutic level |
| Neonates | Low relative to adults | Raised | One of the reasons adult total-concentration targets do not transfer to neonates for highly bound basic drugs |
| Acidic drugs — phenytoin, warfarin, salicylate, valproate | Irrelevant | Governed by albumin, not AAG | For these the correction that matters is for albumin — which is why a low-albumin patient on phenytoin needs the Sheiner–Tozer adjustment rather than an AAG |
An acute-phase protein whose real use is as a correction factor
The conversion is a factor of one hundred: an alpha-1-acid glycoprotein of 0.75 g/L is 75 mg/dL. There is no molar unit, because the protein is variably glycosylated — carbohydrate accounts for around 45% of its mass, and the glycoforms shift with inflammation — so no single molecular weight applies and a mass concentration against a reference preparation is the only meaningful report. The names are worth knowing too: orosomucoid, alpha-1-acid glycoprotein, AAG and AGP are all the same protein, and the nutrition literature almost always calls it AGP.
As an acute-phase protein it is unremarkable. It is made in the liver, it rises two- to threefold in infection, trauma, surgery, malignancy, active rheumatoid arthritis and pregnancy, and it falls in hepatic failure, nephrotic syndrome, protein-losing enteropathy and severe malnutrition. Ordered as an inflammatory marker it adds very little to a CRP: it responds more slowly, over a day or two rather than hours, and it subsides more slowly as well. There is rarely a good reason to measure it to answer the question of whether a patient is inflamed.
Its real use is as a correction factor, and that turns on a single pharmacological fact. Alpha-1-acid glycoprotein is the principal plasma carrier of basic, cationic drugs, as albumin is for acidic ones. Only the unbound drug is pharmacologically active, and the free fraction falls as the carrier concentration rises — so a patient whose orosomucoid has trebled after surgery has substantially less free drug at the same measured total concentration. Lidocaine and disopyramide are the textbook examples, and quinidine, propranolol, methadone, the tricyclic antidepressants and imatinib behave the same way. The consequence is a discrepancy that looks inexplicable if the carrier is not considered: a total level near the top of the therapeutic range with no evident effect in an acutely ill patient, or, in nephrotic syndrome or advanced liver disease where the orosomucoid is low, toxicity at an apparently therapeutic total. The mirror-image mistake is to correct the wrong way — phenytoin, warfarin, valproate and salicylate are acidic and are carried by albumin, which is why a hypoalbuminaemic patient on phenytoin needs an albumin-based adjustment rather than an orosomucoid.
The second genuine use is in nutritional and iron-status assessment. Ferritin, retinol and retinol-binding protein are all distorted by inflammation, and the BRINDA approach corrects them using CRP and AGP together — AGP contributing the later and more prolonged part of the acute-phase response, which CRP has often already left behind. In that setting the slow kinetics that make orosomucoid a poor acute-phase test are precisely what make it useful.
Frequently asked questions
How do you convert alpha-1-acid glycoprotein between g/L and mg/dL?
Multiply g/L by 100 to get mg/dL, or divide mg/dL by 100 to get g/L. An orosomucoid of 0.75 g/L is 75 mg/dL. There is no molar unit: the protein is variably glycosylated, with carbohydrate making up about 45% of its mass, so no single molecular weight applies.
Is orosomucoid the same as alpha-1-acid glycoprotein?
Yes — orosomucoid, alpha-1-acid glycoprotein, AAG and AGP are four names for the same liver-derived acute-phase protein, encoded by the ORM1 and ORM2 genes. “Orosomucoid” is the older clinical name and AGP is the abbreviation used in the nutrition and micronutrient literature.
Why does a raised alpha-1-acid glycoprotein matter for drug levels?
Because it is the main plasma carrier of basic drugs, and only unbound drug is active. When AAG rises — typically two- to threefold in infection, trauma, surgery or active inflammation — more of the drug is bound, so the free, active fraction falls even though the measured total concentration has not changed. Lidocaine and disopyramide are the classic examples; quinidine, propranolol, methadone, tricyclic antidepressants and imatinib behave similarly. A low AAG does the reverse and can produce toxicity at an apparently therapeutic total level.
Should alpha-1-acid glycoprotein be used instead of CRP?
No. It adds little as a general inflammatory marker: it rises over a day or two rather than hours and falls more slowly, so CRP is both faster and more useful for detecting and following acute inflammation. The slower kinetics are an advantage in only one setting — correcting micronutrient biomarkers in surveys, where the BRINDA approach uses CRP and AGP together because AGP covers the later part of the response that CRP has already left.
Why is it used to adjust ferritin and retinol?
Because inflammation raises ferritin and lowers retinol and retinol-binding protein independently of iron and vitamin A status, so uncorrected values misclassify deficiency. The BRINDA method uses CRP and alpha-1-acid glycoprotein as the two inflammation markers for that adjustment, with AGP capturing the more prolonged phase of the acute-phase response. It is a population and survey technique rather than something applied to an individual patient’s result at the bench.
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References
- Mayo Clinic Laboratories. Test ID: FA1GP — Alpha-1-Acid Glycoprotein. Performed at Quest Diagnostics Nichols Institute by fixed-rate time nephelometry. Reference values: ≥18 years 39–115 mg/dL; under 18 years not established.
- Israili ZH, Dayton PG. Human alpha-1-glycoprotein and its interactions with drugs. Drug Metab Rev. 2001;33(2):161–235.
- Namaste SM, Rohner F, Huang J, et al. Adjusting ferritin concentrations for inflammation: Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia (BRINDA) project. Am J Clin Nutr. 2017;106(Suppl 1):359S–371S. doi:10.3945/ajcn.116.141762
- Fournier T, Medjoubi-N N, Porquet D. Alpha-1-acid glycoprotein. Biochim Biophys Acta. 2000;1482(1-2):157–171.
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.