Hemolytic disease of the fetus and newborn (HDFN) can lead to iron accumulation, which in turn causes liver damage and coagulation problems. Researchers determined that chelation therapy may be a viable treatment option for HDFN, as illustrated by a recently published case report in the Journal of Clinical Medicine.
The two main clinical manifestations that characterize HDFN are derived from the destruction of fetal red blood cells (hemolysis), which causes anemia and accumulation of bilirubin (hyperbilirubinemia). However, other complications are also possible, as the severity of the disease can vary significantly among individuals.
Hemolysis and the subsequent administration of blood transfusion can lead to excessive iron accumulation in the liver, which eventually results in liver damage.
Learn more about HDFN causes and risk factors
“Excess iron accumulation can lead to hepatic dysfunction, coagulation disorders, and cholestasis,” the authors wrote. “These complications are more common in neonates who have undergone intrauterine blood transfusions due to anemia, most often in the course of Rhesus immunization with the anti-D antibodies present in the maternal serum .”
The authors described a case involving a girl born through C-section after 33 weeks of gestation; she was the product of a third pregnancy, with the first one occurring without complications and the second one resulting in fetal death due to HDFN.
Several intrauterine transfusions were performed during the pregnancy due to fetal anemia; further complications during the pregnancy included diet-controlled diabetes mellitus and hypothyroidism in the mother.
The infant was born in poor condition due to bleeding during the pregnancy and required cardiac resuscitation and ventilatory support after the C-section. The patient required seven transfusions during the first 30 days of life. Furthermore, the patient developed a condition known as disseminated intravascular coagulation (CID) during the first days of life: a condition in which the blood produces excessive clots, leading to platelet spending and bleeding. The patient also developed liver failure during that first month.
The patient received chelation therapy, a treatment focusing on removing excessive iron through urine. This treatment, combined with platelet and red blood cell transfusions, appropriate nutritional support and phototherapy led to the discharge of the patient, who is currently two years old.
“Severe symptomatic liver dysfunction due to iron overload requiring chelation therapy. In patients with life-threatening complications, appropriate medical care may result in normal development with no long-term consequences. In light of this case report, chelating agents may be considered as a treatment option in HDFN-associated liver failure,” the authors concluded.
