BACKGROUND: Intrauterine growth retardation is one of the major causes of perinatal mortality and morbidity. To date, there are no reliable methods to detect brain damage in these patients. METHODS: We conducted a case-control study in tertiary NICUs from December 2001 to December 2003 with 42 intrauterine growth retardation infants and 84 controls. Routine laboratory variables, neurologic outcome at 7-day follow-up, ultrasound imaging, and urine concentrations of S100B protein were determined at 5 time points. Urine S100B levels were measured by an immunoluminometric assay at first urination, 24, 48, and 72 hours, and 7 days after birth. Routine laboratory parameters and neurologic patterns were assessed at the same time as urine sampling. RESULTS: S100B protein was significantly higher at all of the monitoring time points in urine taken from intrauterine growth retardation newborns than in control infants. When intrauterine growth retardation infants were corrected for the presence of abnormal (group A) or normal (group B) neurologic examination 7 days after birth, S100B was significantly higher at all of the predetermined monitoring time points in group A infants than in group B or controls. At a cutoff of 7.37 multiples of median at first urination, S100B achieved a sensitivity of 95% and a specificity of 99.1% as a single marker for predicting an adverse neurologic outcome. Twenty of 126 patients had neurologic abnormalities, making an overall prevalence of the disease in our population of 15.9% (pretest probability). With respect to the performance of S100B in predicting brain damage, its positive and negative predictive values were 91.0% and 99.0%, respectively. CONCLUSIONS: Increased urine S100B protein levels in intrauterine growth retardation newborns in the first week after birth suggest the presence of brain damage reasonably because of intrauterine hypoxia. Longitudinal S100B protein measurements soon after birth are a useful tool to identify which intrauterine growth retardation infants are at risk of possible neurologic sequelae.
BACKGROUND:Intrauterine growth retardation is one of the major causes of perinatal mortality and morbidity. To date, there are no reliable methods to detect brain damage in these patients. METHODS: We conducted a case-control study in tertiary NICUs from December 2001 to December 2003 with 42 intrauterine growth retardationinfants and 84 controls. Routine laboratory variables, neurologic outcome at 7-day follow-up, ultrasound imaging, and urine concentrations of S100B protein were determined at 5 time points. Urine S100B levels were measured by an immunoluminometric assay at first urination, 24, 48, and 72 hours, and 7 days after birth. Routine laboratory parameters and neurologic patterns were assessed at the same time as urine sampling. RESULTS:S100B protein was significantly higher at all of the monitoring time points in urine taken from intrauterine growth retardation newborns than in control infants. When intrauterine growth retardationinfants were corrected for the presence of abnormal (group A) or normal (group B) neurologic examination 7 days after birth, S100B was significantly higher at all of the predetermined monitoring time points in group A infants than in group B or controls. At a cutoff of 7.37 multiples of median at first urination, S100B achieved a sensitivity of 95% and a specificity of 99.1% as a single marker for predicting an adverse neurologic outcome. Twenty of 126 patients had neurologic abnormalities, making an overall prevalence of the disease in our population of 15.9% (pretest probability). With respect to the performance of S100B in predicting brain damage, its positive and negative predictive values were 91.0% and 99.0%, respectively. CONCLUSIONS: Increased urine S100B protein levels in intrauterine growth retardation newborns in the first week after birth suggest the presence of brain damage reasonably because of intrauterine hypoxia. Longitudinal S100B protein measurements soon after birth are a useful tool to identify which intrauterine growth retardationinfants are at risk of possible neurologic sequelae.
Authors: An N Massaro; Taeun Chang; Nadja Kadom; Tammy Tsuchida; Joseph Scafidi; Penny Glass; Robert McCarter; Stephen Baumgart; Gilbert Vezina; Karin B Nelson Journal: J Pediatr Date: 2012-04-10 Impact factor: 4.406
Authors: E Mazarico; E Llurba; R Cumplido; A Valls; J C Melchor; M Iglesias; L Cabero; E Gratacós; M D Gómez-Roig Journal: Pediatr Res Date: 2017-05-31 Impact factor: 3.756
Authors: Lara A Friel; Roberto Romero; Sam Edwin; Jyh Kae Nien; Ricardo Gomez; Tinnakorn Chaiworapongsa; Juan Pedro Kusanovic; Jorge E Tolosa; Sonia S Hassan; Jimmy Espinoza Journal: J Perinat Med Date: 2007 Impact factor: 1.901
Authors: Jan Florian Heuer; Paolo Pelosi; Peter Hermann; Christina Perske; Thomas A Crozier; Wolfgang Brück; Michael Quintel Journal: Intensive Care Med Date: 2011-05-05 Impact factor: 17.440
Authors: Alessandro Varrica; Angela Satriano; Alessandro Frigiola; Alessandro Giamberti; Guido Tettamanti; Luigi Anastasia; Erika Conforti; Antonio D W Gavilanes; Luc J Zimmermann; Hans J S Vles; Giovanni Li Volti; Diego Gazzolo Journal: Biomed Res Int Date: 2015-08-31 Impact factor: 3.411