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Anemia of prematurity (AOP) refers to a form of anemia affecting preterm infants [1] with decreased hematocrit. [2] AOP is a normochromic, normocytic hypoproliferative anemia. The primary mechanism of AOP is a decrease in erythropoietin (EPO), a red blood cell growth factor.
Neonatal alloimmune thrombocytopenia (NAITP, NAIT, NATP or NAT) is a disease that affects babies in which the platelet count is decreased because the mother's immune system attacks her fetus' or newborn's platelets. A low platelet count increases the risk of bleeding in the fetus and newborn.
Hemolytic disease of the fetus and newborn (HDN) is a condition where the passage of maternal antibodies results in the hemolysis of fetal/neonatal red cells. The antibodies can be naturally occurring such as anti-A, and anti-B, or immune antibodies developed following a sensitizing event. [ 11 ]
If the anemia is severe, it can be treated with a blood transfusion, however this is rarely needed. On the other hand, neonates have underdeveloped livers that are unable to process large amounts of bilirubin and a poorly developed blood–brain barrier that is unable to block bilirubin from entering the brain.
Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis, [1] [2] is an alloimmune condition that develops in a fetus at or around birth, when the IgG molecules (one of the five main types of antibodies) produced by the mother pass through the placenta.
Drug-induced folate deficiency anemia: D52.1: Protein-deficiency anemia: Protein deficiency anemia is an anemia that results from an inadequate intake of dietary protein. [14] Scurvy: E54: 13930: Scurvy is a disease resulting from a deficiency of vitamin C, [15] which is required for the synthesis of collagen in humans.
Treatment of acute episodes may include medications for infection, stopping the offending medication, or blood transfusions. [3] Jaundice in newborns may be treated with bili lights. [2] It is recommended that people be tested for G6PDD before certain medications, such as primaquine, are taken. [2] About 400 million people have the condition ...
Family history of jaundice and anemia, family history of neonatal or early infant death due to liver disease, maternal illness suggestive of viral infection (fever, rash or lymphadenopathy), maternal drugs (e.g. sulphonamides, anti-malarials causing red blood cell destruction in G6PD deficiency) are suggestive of pathological jaundice in neonates.