Bile acids are end products of cholesterol metabolism. They belong to the group of steroids (substance class of lipids). Bile acids are formed in the liver from cholesterol by hydroxylation reactions (reaction to introduce one or more hydroxyl groups) and oxidative shortening of the side chain located on ring D. Bile acids include:
- Chenodeoxycholic acid
- Cholic acid
- Dehydrocholic acid
- Deoxycholic acid
- Glycocholic acid
- Lithocholic acid
- Taurocholic acid
Bile acids, which are part of bile, are essential for fat digestion. They allow the emulsification and absorption of fats and fat-soluble vitamins. Bile acids undergo an enterohepatic cycle, i.e. circulation from the liver via the gallbladder to the intestine and back to the liver. At the end of the process, conjugation and deconjugation produce secondary bile acids that are excreted in the stool. In the case of occlusive icterus (jaundice caused by bile stasis due to an obstruction of outflow), bile acids enter the blood along with bilirubin (a breakdown product of hemoglobin).
The procedure
Material needed
- 0.5 ml serum
Preparation of the patient
- Blood collection fasting (approximately 12 hours of food abstinence; otherwise strong postprandial rise (rise after a meal)).
Confounding factors
- Under therapy with UDCA (ursodeoxychloric acid) falsely high values are measured. Such samples are therefore not suitable for analysis.
Standard values
| Age | Normal values in µmol/l |
| <1 year | < 25 µmol/l |
| 1- < 2 years | < 9 µmol/l |
| ≥ 2 years | < 8 (10) µmol/l |
Indications
- Assessment of hepatobiliary function (function of the liver and gallbladder).
- Diagnosis of intrahepatic cholestasis of pregnancy (IPC; biliary congestion within the liver).
Interpretation
Interpretation of increased values
- All forms of intrahepatic and extrahepatic cholestasis (bile stasis inside and outside the liver).
- Intrahepatic cholestasis of pregnancy (ICP) → risk of intrauterine fetal death ↑
- Liver disease
- Acute and chronic hepatitis (inflammation of the liver).
- Chronic liver disease (e.g., alcohol abuse, liver cirrhosis/ irreversible (non-reversible) damage to the liver and marked remodeling of liver tissue)
- Hepatocellular carcinoma
- Toxic liver injury (liver damage caused by toxins).
- Liver damage caused by drugs
- Reye syndrome (acute encephalopathy (pathological change of the brain) with concomitant fatty liver hepatitis (inflammation of the fatty liver) following a passed viral infection in young children; occurs on average one week after the previous illness has subsided)
Further notes
- Values > 40 µmol/l (fasting serum) during pregnancy are suspected of intrahepatic pregnancy cholestasis. This is accompanied by pruritus (itching) and jaundice (jaundice). Diagnosis is based on elevation of serum bile acids and alanine aminotransferase (ALT; GPT). Gamma-GT is usually within the normal range. ‘Differential diagnoses: gestational fatty liver and HELLP syndrome (H = hemolysis/dissolution of erythrocytes (red blood cells) in the blood), EL = elevated liver enzymes, LP = low platelets; ICD-10-GM O14. 2: HELLP syndrome); often associated with preeclampsia/any (even preexisting) elevated blood pressure ≥ 140-90 mmHg in pregnancy with at least one new-onset organ manifestation that cannot be attributed to any other cause).
- Risk of intrauterine fetal death (IUFT) increases 30-fold above 100 μmol/l, especially after 35 weeks’ gestation (SSW).
