What is a dangerous bilirubin level?

In adults, total bilirubin above 2.5–3 mg/dL causes visible jaundice. Levels above 10 mg/dL indicate severe hyperbilirubinemia and require urgent evaluation. In newborns, dangerous levels depend on age in hours and gestational age — total serum bilirubin above 20–25 mg/dL in a full-term neonate may cause kernicterus (bilirubin encephalopathy) and requires immediate phototherapy or exchange transfusion. Use age-specific nomograms (Bhutani nomogram) to assess neonatal risk.

What is the difference between direct and indirect bilirubin?

Indirect (unconjugated) bilirubin is fat-soluble, bound to albumin in the blood, and has not yet been processed by the liver. It is elevated in hemolysis, Gilbert syndrome, and ineffective erythropoiesis. Direct (conjugated) bilirubin has been conjugated with glucuronic acid in the liver, making it water-soluble. It is elevated in biliary obstruction, hepatitis, and cholestasis. The distinction helps clinicians determine whether the problem is pre-hepatic, hepatic, or post-hepatic.

What does high bilirubin mean?

High bilirubin (hyperbilirubinemia) indicates either increased bilirubin production (hemolysis, ineffective erythropoiesis), decreased hepatic uptake/conjugation (Gilbert syndrome, liver disease), or impaired excretion (biliary obstruction, cholestasis). The pattern of elevation — predominantly direct vs. indirect — guides the differential diagnosis. Mild unconjugated hyperbilirubinemia (1.2–3 mg/dL) with otherwise normal labs is most commonly Gilbert syndrome, affecting 5–10% of the population.

Is Gilbert syndrome serious?

No. Gilbert syndrome is a benign hereditary condition affecting 5–10% of the population, caused by reduced UGT1A1 enzyme activity. It produces mild, fluctuating unconjugated hyperbilirubinemia (typically 1–4 mg/dL) that worsens with fasting, stress, illness, or dehydration. Liver function is otherwise normal, and the condition requires no treatment. It is important mainly because it can cause mild jaundice that may be confused with more serious liver disease.

What bilirubin level causes jaundice?

Jaundice (icterus) becomes clinically visible when total serum bilirubin exceeds approximately 2.5–3.0 mg/dL (43–51 µmol/L) in adults. Scleral icterus (yellowing of the whites of the eyes) is often the earliest sign, detectable at bilirubin levels around 2–2.5 mg/dL, because the sclera has high elastin content with affinity for bilirubin. In dark-skinned individuals, jaundice is best assessed in the sclera, under the tongue, and on the palms.

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Bilirubin Levels — Normal Range & Meaning

Complete reference on total, direct, and indirect bilirubin normal ranges, causes of high bilirubin including Gilbert syndrome, and neonatal jaundice thresholds.

⚡ Quick Answer — Normal Bilirubin Range

Total: 0.1–1.2 mg/dL (1.7–20.5 µmol/L)

Direct: 0.0–0.3 mg/dL (0–5.1 µmol/L)

Indirect: 0.2–0.8 mg/dL (3.4–13.7 µmol/L)

Neonates have higher levels — up to 12–15 mg/dL is common in the first week of life. Visible jaundice appears at ≥2.5 mg/dL in adults.

What Is Bilirubin?

Bilirubin is the orange-yellow pigment produced from the breakdown of heme, primarily from senescent red blood cells. Approximately 250–350 mg of bilirubin is produced daily in a healthy adult. The reticuloendothelial system (mainly the spleen) converts heme → biliverdin → unconjugated bilirubin, which circulates bound to albumin.

In the liver, unconjugated bilirubin is conjugated with glucuronic acid by the enzyme UDP-glucuronosyltransferase (UGT1A1), producing water-soluble conjugated (direct) bilirubin. This is excreted into bile, passes through the intestines, and is ultimately eliminated in stool (as stercobilin, giving stool its brown color) and urine (as urobilinogen).

Clinically, bilirubin measurement helps diagnose and differentiate hemolytic anemias, liver diseases, and biliary obstruction. The pattern of direct vs. indirect elevation points to the underlying mechanism — pre-hepatic (increased production), hepatic (impaired conjugation/uptake), or post-hepatic (impaired excretion).

Normal Bilirubin Range

Bilirubin Type / Age	Conventional (mg/dL)	SI (µmol/L)
Total bilirubin (adults)	0.1–1.2	1.7–20.5
Direct (conjugated) bilirubin	0.0–0.3	0–5.1
Indirect (unconjugated) bilirubin	0.2–0.8	3.4–13.7
Neonatal Bilirubin (Full-term)
Cord blood	<2.0	<34
Day 1 (0–24 hours)	<6.0	<103
Day 2 (24–48 hours)	<10.0	<171
Day 3–5 (peak)	<12.0 (up to 15 in breastfed)	<205 (up to 257)
By day 7–10	<1.5 (approaching adult levels)	<26

Reference ranges from Tietz Clinical Guide to Laboratory Tests, 4th edition, and AAP 2004 guidelines for neonatal jaundice. Conversion: 1 mg/dL = 17.1 µmol/L.

What Does a High Bilirubin Mean?

Elevated bilirubin (hyperbilirubinemia) can be classified by the predominant fraction:

Predominantly Unconjugated (Indirect) Hyperbilirubinemia

Gilbert syndrome — the most common cause in adults (5–10% prevalence). Mild, fluctuating indirect bilirubin (typically 1–4 mg/dL). Worsened by fasting, stress, illness. Benign, requires no treatment.
Hemolytic anemias — sickle cell disease, hereditary spherocytosis, G6PD deficiency, autoimmune hemolysis, transfusion reactions. Increased RBC destruction produces excess unconjugated bilirubin.
Ineffective erythropoiesis — thalassemia major, megaloblastic anemia (B12/folate deficiency).
Crigler-Najjar syndrome — rare, severe genetic deficiency of UGT1A1 (Type I: absent activity, life-threatening; Type II: reduced activity, milder).
Neonatal physiological jaundice — immature UGT1A1 activity in newborns, peaking on days 3–5 of life.
Breast milk jaundice — prolonged unconjugated hyperbilirubinemia in breastfed infants, lasting up to 12 weeks; benign.

Predominantly Conjugated (Direct) Hyperbilirubinemia

Biliary obstruction — gallstones (choledocholithiasis), pancreatic head cancer, cholangiocarcinoma. Bilirubin may exceed 10–30 mg/dL.
Hepatitis — viral (hepatitis A, B, C, E), alcoholic, autoimmune, drug-induced.
Cholestasis — primary biliary cholangitis, primary sclerosing cholangitis, drug-induced cholestasis, intrahepatic cholestasis of pregnancy.
Dubin-Johnson syndrome — benign hereditary conjugated hyperbilirubinemia due to impaired canalicular excretion.
Rotor syndrome — another benign hereditary conjugated hyperbilirubinemia; impaired hepatic storage.
Biliary atresia — in neonates; direct bilirubin >1 mg/dL or >20% of total in newborns is always pathological and requires urgent evaluation.

Symptoms of High Bilirubin

Jaundice (yellow discoloration of skin and sclera) appears when total bilirubin exceeds ~2.5–3.0 mg/dL. Dark urine (tea-colored) occurs with conjugated hyperbilirubinemia (water-soluble bilirubin excreted by kidneys). Pale/clay-colored stools (acholic) occur in biliary obstruction. Pruritus is a hallmark of cholestatic disease (due to bile salt deposition). In newborns, severe hyperbilirubinemia can cause kernicterus — bilirubin encephalopathy with lethargy, hypotonia, seizures, and permanent neurological damage.

What Does a Low Bilirubin Mean?

Low bilirubin levels are generally not clinically significant and require no further workup. Some population studies have associated very low bilirubin with increased cardiovascular risk, as bilirubin has antioxidant properties, but this is not established enough to guide clinical management.

Mildly elevated bilirubin (as in Gilbert syndrome) may actually be modestly cardioprotective due to bilirubin's antioxidant effects.

Related Tests & Calculators

Bilirubin fractionation (direct and indirect) — essential for determining the mechanism of hyperbilirubinemia.
AST, ALT, ALP, GGT — liver enzymes to differentiate hepatocellular injury from cholestasis. See ALP Levels Reference.
LDH, haptoglobin, reticulocyte count, peripheral smear — hemolysis workup for indirect hyperbilirubinemia.
Prothrombin time (INR), albumin — markers of hepatic synthetic function.
Abdominal ultrasound — first-line imaging for conjugated hyperbilirubinemia to evaluate for ductal dilation and gallstones.
MELD Score — MELD Calculator — uses bilirubin as a key component for liver disease severity scoring.
Child-Pugh Score — Child-Pugh Calculator — incorporates bilirubin for cirrhosis classification.

About This Test

Clinical Pearls

🔑 Key Points for Clinicians

Gilbert syndrome tip: If indirect bilirubin is 1–4 mg/dL with otherwise normal LFTs, CBC, and reticulocyte count, the diagnosis is almost certainly Gilbert syndrome. Genetic testing is rarely needed. Confirming with a 48-hour fast (bilirubin rises 2–3×) was historically used but is unnecessary in practice.
Direct bilirubin in newborns is always pathological. Direct bilirubin >1.0 mg/dL or >20% of total bilirubin in a neonate should prompt urgent evaluation for biliary atresia, which requires a Kasai procedure within the first 60 days of life for optimal outcomes.
Bilirubin can cause interference with certain lab assays (e.g., creatinine measured by Jaffé method may be falsely low in jaundiced patients).
Delta bilirubin (biliprotein) is bilirubin covalently bound to albumin. It has a half-life of ~17 days (same as albumin), which explains why jaundice resolves slowly even after the underlying cause is corrected.
The MELD score uses total bilirubin, and the Child-Pugh score stratifies bilirubin into three categories — both are essential prognostic tools in liver disease.

Specimen Notes

Bilirubin is measured from serum or plasma. The sample should be protected from light, as bilirubin is photosensitive and light exposure can cause falsely low results. Hemolysis causes minimal interference with most modern diazo-based assays but may affect direct spectrophotometric methods used in neonates.

References

Burtis CA, Ashwood ER, Bruns DE. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier; 2018:680-690.
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004;114(1):297-316.
Bosma PJ, Chowdhury JR, Bakker C, et al. The genetic basis of the reduced expression of bilirubin UDP-glucuronosyltransferase 1 in Gilbert's syndrome. N Engl J Med. 1995;333(18):1171-1175.
Friedman LS. Approach to the patient with abnormal liver biochemical and function tests. UpToDate. Accessed January 2025.
Maisels MJ, McDonagh AF. Phototherapy for neonatal jaundice. N Engl J Med. 2008;358(9):920-928.
Vítek L, Tiribelli C. Bilirubin: the yellow hormone? J Hepatol. 2021;75(6):1485-1490.

References last verified: February 2026