Author(s): Karlsson M, Blennow M, Nemeth A, Winbladh B
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Abstract AIM: To investigate: 1) the occurrence of hypoxic hepatitis in full-term infants after birth asphyxia, 2) the temporal enzyme pattern in asphyxiated newborn infants, and 3) whether the degree of hypoxic hepatitis, as reflected by the rise in aminotransferase, correlates with the severity of the asphyxia and CNS symptomatology. METHODS: Serum aminotransferases, lactate dehydrogenase, gamma-glutamyl transferase, total and conjugated bilirubin, cholinesterase activity, albumin, international normalized ratio (INR), and nucleated red blood cell count were prospectively measured in full-term asphyxiated newborn infants (n=26). Samples were collected three times during the first 72 h and once between days 6 and 12 after birth. Samples from healthy newborns (n=56), collected 24-172 h after birth, served as controls. RESULTS: In 12 of the 26 asphyxiated infants, a serum alanine aminotransferase (S-ALAT) pattern compatible with hypoxic hepatitis was found. Five infants showed increased S-ALAT activity but with a different pattern. Similar patterns were seen in serum aspartate aminotransferase (S-ASAT). S-ALAT and -ASAT concentrations 0-72 h after birth correlated significantly with severity of hypoxic-ischaemic encephalopathy. CONCLUSION: Birth asphyxia can induce an enzyme pattern in serum compatible to hypoxic hepatitis. There seems to be a correlation between aminotransferases in serum and the extent of CNS injury.
This article was published in Acta Paediatr
and referenced in Journal of Neonatal Biology