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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.
Physiologic jaundice can be a benign condition that presents in newborns until two weeks of life. [2] However, jaundice that continues after two weeks requires follow up with measurement of total and conjugated bilirubin. [3] Elevated levels of conjugated bilirubin are never benign and require further evaluation for neonatal cholestasis. [3]
Neonatal Hemochromatosis is a rare and severe liver disease of unknown origin, though research suggests that it may be alloimmune condition. Its characteristics are similar to hereditary hemochromatosis , where iron deposition causes damage to the liver and other organs and tissues.
CHA is distinguished by variable anemia, chronic extravascular hemolysis, decreased erythrocyte life span, splenomegaly, jaundice, biliary lithiasis, and iron overload. Immune-mediated mechanisms may play a role in the pathogenesis of these uncommon diseases, despite the paucity of data regarding the immune system's involvement in CHAs.
Early symptoms include anemia, jaundice, splenomegaly, and fatigue. [2] Acute cases can threaten to cause hypoxia secondary to anemia and acute kernicterus through high blood levels of bilirubin, particularly in newborns. Most cases can be detected soon after birth. Testing for HS is available for the children of affected adults.
Mild jaundice may appear under conditions of exertion, stress, fasting, and infections, but the condition is otherwise usually asymptomatic. [7] [8] Severe cases are seen by yellowing of the skin tone and yellowing of the conjunctiva in the eye. [9] Gilbert syndrome has been reported to contribute to an accelerated onset of neonatal jaundice.
Jaundice in infants, as in adults, is characterized by increased bilirubin levels (infants: total serum bilirubin greater than 5 mg/dL). Normal physiological neonatal jaundice is due to immaturity of liver enzymes involved in bilirubin metabolism, immature gut microbiota, and increased breakdown of fetal hemoglobin (HbF). [ 54 ]
When an infant is suspected to have hemolytic jaundice, abnormal morphologies of erythrocytes can be analyzed to find out the causes of hemolysis. [34] A Coomb's test should be performed, and end-tidal carbon monoxide concentration should be monitored to understand the rate of hemolysis in the infant's body. [35]