Copper (serum)
Serum copper rises markedly in pregnancy due to estrogen-stimulated ceruloplasmin synthesis. Levels peak in mid-pregnancy and remain elevated until delivery.
| Units | Nonpregnant Adult | 1st Trimester | 2nd Trimester | 3rd Trimester |
|---|---|---|---|---|
| µg/dL | 70 – 140 | 112 – 199 | 165 – 221 | 130 – 240 |
| µmol/L | 11 – 22 | 18 – 31 | 26 – 35 | 21 – 38 |
Pregnancy physiology
- Estrogen increases hepatic ceruloplasmin synthesis → higher serum copper.
- Values rise 2–3× above baseline by mid-pregnancy.
- Essential for fetal neurodevelopment, collagen formation, bone growth, and angiogenesis.
- Ceruloplasmin-bound copper increases most; free copper remains low.
Causes of elevated copper
- Normal pregnancy (physiologic)
- Oral contraceptives / estrogen therapy
- Inflammation (ceruloplasmin is an acute-phase reactant)
- Cholestatic liver disease
- High environmental or dietary copper exposure
- Menkes carriers (mild increase)
- Post–iron chelation therapy (ceruloplasmin rebound)
Marked copper elevation suggests inflammation, hepatobiliary disease, or excessive copper exposure rather than pregnancy alone.
Causes of decreased copper
- Wilson disease (low ceruloplasmin + low copper)
- Menkes disease (severe congenital deficiency)
- Malnutrition or malabsorption (celiac disease, Crohn disease, bariatric surgery)
- Nephrotic syndrome
- Protein-losing enteropathy
- Severe liver failure
- Excess zinc intake (competitive inhibition)
True copper deficiency in pregnancy is uncommon and usually reflects malnutrition or impaired absorption.
References
- Abbassi-Ghanavati M, Greer LG, Cunningham FG. Pregnancy and laboratory studies: a reference table for clinicians. Obstet Gynecol. 2009;114:1326–31.