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Coumarin embryopathy in an extremely low birth weight infant associated with neonatal hepatitis and ocular
Patrick G Hetzel1, René Glanzmann, Pascal W Hasler
1Department of Neonatology, University Children's Hospital, Basel, Switzerland. patrick.hetzel@ukbb.ch
Insights
Prenatal exposure to vitamin K antagonists can cause Coumarin embryopathy (CE). This case highlights neonatal hepatopathy as a rare but serious CE manifestation, emphasizing cautious use during pregnancy.
Area of Science:
- Medical Science
- Neonatology
- Toxicology
Background:
- Coumarin embryopathy (CE) is a known condition resulting from prenatal exposure to vitamin K antagonists.
- Vitamin K antagonists are often prescribed for pregnant women with mechanical heart valves.
Observation:
- A premature infant (25 weeks' gestation) exposed to phenprocoumon in utero presented with typical CE features.
- The infant exhibited impaired coagulation, cerebral hemorrhages, and midface hypoplasia.
- Additionally, the infant developed prolonged neonatal hepatopathy, including conjugated hyperbilirubinemia, elevated liver enzymes, and hypoglycemia.
Findings:
- This case is the first to describe neonatal hepatopathy as a component of Coumarin embryopathy.
- Ocular abnormalities included corneal opacity, anterior segment dysgenesis, cataract, and persistent pupillary membrane.
Implications:
- Neonatal hepatopathy is a significant, albeit uncommon, side effect of in utero vitamin K antagonist exposure.
- Anticoagulation with vitamin K antagonists in pregnant women with mechanical heart valves requires extreme caution.
Abstract:
Coumarin embryopathy (CE) is a well-documented sequelae of prenatal exposure to vitamin K antagonists. We report on a female premature infant (25 weeks' gestation) born to a mother who had received phenprocoumon during pregnancy following mechanical heart valve replacement. The infant presented with impaired coagulation, intraventricular and minor parenchymal cerebral haemorrhages and midface hypoplasia typical of CE. In addition, there was hepatopathy with conjugated hyperbilirubinemia, elevated liver enzymes and repeated episodes of hypoglycemia upon attempts to discontinue glucose supplementation, all lasting for 4 months. There was corneal opacity with anterior segment dygenesis in the left eye, and persistent pupillary membrane, cataract and persistent hyperplastic primary vitreous in the right eye. While liver disease is an uncommon but serious side effect of vitamin K antagonists, this is the first report describing neonatal hepatopathy as part of CE. In anticoagulation of pregnant women with mechanical heart valves, vitamin K antagonists should be used with utmost restraint.
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