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alpha-1-Acid Glycoprotein
Synonyms
- Alpha-1-Acid Glycoprotein
- AAG
- AGP
- Orosomucoid
- ORM (gene symbol: ORM1/ORM2)
- α1-glycoprotein
Units of Measurement
mmol/L, µmol/L, g/L, mg/dL, mg/100mL, mg%, mg/mL
Description
Alpha-1-Acid Glycoprotein (AAG) is a major acute-phase reactant synthesized in the liver.
It is a highly glycosylated plasma protein (~45% carbohydrate) and plays a critical role in:
- Inflammation & immune modulation
- Drug binding (pharmacokinetics)
- Transport of endogenous compounds
- Protective anti-inflammatory roles
AAG is classified as a positive acute-phase protein, increasing significantly in infection, inflammation, and malignancy.
Physiological Role
1. Binding & Transport Protein
AAG binds many basic (cationic) drugs, affecting:
- Distribution
- Free (active) fraction
- Drug clearance
Key drugs bound by AAG:
- Lidocaine
- Propranolol
- Imipramine
- Amitriptyline
- Fentanyl
- Methadone
- Diazepam (partially)
2. Acute-Phase Response
During inflammation:
- IL-6, IL-1β, TNF-α → stimulate hepatic synthesis
- AAG increases 2–5× normal levels
- Important in sepsis and systemic inflammation
3. Anti-Inflammatory Functions
- Neutralizes endotoxins
- Modulates neutrophil activation
- Protects tissues from inflammatory damage
Clinical Significance
Increased AAG
Seen in:
1. Acute & Chronic Inflammation
- Sepsis
- Pneumonia
- TB
- Severe bacterial/viral infections
2. Chronic Diseases
- Cancer
- Autoimmune disorders
- IBD
- Rheumatoid arthritis
3. Physiological/Other Causes
- Pregnancy
- Stress
- Burns
- Post-surgical states
Clinical Effect
↑ AAG → ↓ free active drug levels
(important in drug dosing of basic drugs)
Decreased AAG
Seen in:
- Liver cirrhosis (↓ synthesis)
- Nephrotic syndrome (protein loss)
- Malnutrition
- Estrogen therapy
- Advanced cancer
Clinical Effect
↓ AAG → ↑ free drug levels → toxicity risk
Especially for:
- Lidocaine
- Propranolol
- Tricyclic antidepressants
- Fentanyl
Reference Intervals
(Tietz 8E + Mayo + IFCC + ARUP)
Adults
- 0.55 – 1.4 g/L
- 55 – 140 mg/dL
- ≈ 8.3 – 21 µmol/L
(based on MW ≈ 41,000–44,000 g/mol depending on glycosylation)
Children
- Slightly lower: 0.4 – 1.0 g/L
Pregnancy
- Levels increase up to 1.8 g/L
Interpretation
- Increased AAG = inflammation, cancer, trauma
- Decreased AAG = liver disease, nephrotic syndrome, malnutrition
- Always consider AAG when adjusting drug dosing
Unit Meanings
| Unit | Meaning |
| mmol/L | millimole per liter |
| µmol/L | micromole per liter |
| g/L | grams per liter |
| mg/dL | milligrams per deciliter |
| mg/100mL | same as mg% |
| mg% | milligram per 100 mL |
| mg/mL | milligram per milliliter |
Analytical Notes
- Measured using:
- Immunoturbidimetry
- Nephelometry
- LC-MS/MS (research)
- Immunoturbidimetry
- Avoid hemolysis (minimal effect but dilutes sample).
- AAG varies greatly in inflammation → always interpret with CRP.
Clinical Pearls
- AAG is the main binder of basic drugs → influences drug dosing more than albumin for many medications.
- In acute inflammation, a 2–3× rise in AAG can significantly reduce free lidocaine/fentanyl.
- Low AAG in cirrhosis → high free fractions of basic drugs → major toxicity risk.
- AAG rises later than CRP but stays elevated longer in chronic disease.
Interesting Fact
AAG was first identified in 1950 as a glycoprotein with unusually high carbohydrate content. Its extreme glycosylation enables rapid changes in concentration in response to inflammation.
References
- Tietz Clinical Chemistry and Molecular Diagnostics, 8th Edition - Plasma Proteins.
- Mayo Clinic Laboratories - Alpha-1-Acid Glycoprotein (AGP) Test.
- ARUP Consult - Acute Phase Proteins.
- IFCC Guidelines - Protein Measurement Standards.
- NIH / MedlinePlus - AGP Overview.
- Pharmacokinetics Texts - Drug Binding to AAG.