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Characteristic feature of jaundice, yellowing of skin and eyes, is caused by excess bilirubin in the blood. Bilirubin is a natural byproduct of the destruction of "used" or death red blood cells, infants tend to produce large amounts of bilirubin, as the have, in the first weeks of life, one too many red blood cells (a child needs many more red blood cells during intrauterine until after delivery). Normally, bilirubin is metabolized in the liver and, further, by bacterial enzymes in the intestine, where it is destroyed so they could be eliminated in the faeces. But often the child's liver is too immature and intestinal enzymes are still inactive for him to process the bilirubin quickly enough, so that between the second and fifth days of life the child, bilirubin remains in the blood, producing what is called "physiological" jaundice.
Neonatal jaundice is one of the most common signs seen in the at term newborn baby 45-60%, and up to 80% at premature newborns, important by neurotoxic type side effects of indirect bilirubin and elucidation of pathogenetic mechanisms for several types of jaundice.
It is the most frequent cause of prolonged neonatal hospitalization and re-admission within two weeks. Related to risk factors for neonatal jaundice it was found that hyperbilirubin is more common in boys.
Among the environmental factors, altitude increases the risk of hyperbilirubin , at 3100m incidence of hyperbilirubin in newborn babies is increased of 2 times than at the altitude of 1600m.
Jaundice is more common in white people than black. The type of birth influences bilirubin in the newborn. Spontaneous birth (especially pelvic) is more jaundice producing than caesarean. Caesarean section performed in the absence of fetal suffering is more jaundice producing than by emergency Caesarean section.
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