Article Text

SERUM PROCALCITONIN AND C-REACTIVE PROTEIN IN NEONATES WITH HYPOXIC-ISHEMIC ENCEPHALOPATHY AND INTRACRANIAL HEMORRHAGE
  1. M Pavcnik-Arnol1,
  2. B Bonac-Tuma1,
  3. M Derganc1
  1. 1Department of Paediatric Surgery and Intensive Care, University Medical Centre, Ljubljana, Slovenia

Abstract

Objective To evaluate the serum concentration of procalcitonin (PCT) and C-reactive protein (CRP) in neonates with hypoxic-ishemic encephalopathy and intracranial hemorrhage.

Methods This prospective, observational study was conducted in a multidisciplinary, tertiary-care neonatal and pediatric intensive care unit. We enrolled twenty-four neonates with hypoxic-ischemic encephalopathy and intracranial hemorrhage (median gestational age 38.9 weeks, median 1- and 5- minute Apgar scores 3 and 6). Sixteen neonates with respiratory distress served as controls. Serum PCT and C-reactive protein (CRP) were measured on three consecutive days.

Results Median PCT concentration was significantly higher in neonates with hypoxic-ishemic encephalopathy and intracranial hemorrhage than in neonates with respiratory distress on all 3 determinations (day 0: 19.7 μg/L vs. 1.1 μg/L, p = 0.001; day 1: 16.6 μg/L vs. 1.2 μg/L, p = 0.001; day 2: 5.8 μg/L vs. 1.2 μg/L, p = 0.011). Neonates with hypoxic-ishemic encephalopathy and intracranial hemorrhage had significantly lower median CRP concentration than neonates with respiratory distress on first two days (day 0: 5 mg/L vs. 14 mg/L, p < 0.0001; day 1: 6 mg/L vs. 18.5 mg/L, p = 0.021), but not on the third day (9 mg/L vs. 7 mg/L, p = 0.5).

Conclusions Serum PCT concentration is increased in neonates with hypoxic brain damage and intracranial hemorrhage. This suggests that PCT could be released directly from the damaged neurons. On the other hand, CRP concentration remains low in neonates with hypoxic brain damage and intracranial hemorrhage.

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