Share this article on:

Fecal S100A12: Identifying Intestinal Distress in Very-Low-Birth-Weight Infants

Däbritz, Jan*; Foell, Dirk; Wirth, Stefan; Jenke, Andreas

Journal of Pediatric Gastroenterology and Nutrition: August 2013 - Volume 57 - Issue 2 - p 204–210
doi: 10.1097/MPG.0b013e3182946eb2
Original Articles: Gastroenterology

Objectives: The aim of the study was to determine whether longitudinal measurements of fecal S100A12, a damage-associated molecular pattern protein, which is released from neutrophils or monocytes under stress, can detect very-low-birth-weight (VLBW) infants at risk for intestinal distress apart from necrotizing enterocolitis.

Methods: This prospective study included 46 VLBW infants with intestinal distress and 49 reference patients. Meconium and stool samples were collected prospectively on alternate days for 4 weeks, and fecal S100A12 was measured by enzyme-linked immunosorbent assay.

Results: Gestational age and weight at birth were significantly lower in patients with intestinal distress when compared to unaffected reference infants. Median levels of fecal S100A12 were significantly higher in patients with intestinal distress at onset of disease and before compared with unaffected reference infants. Median levels of fecal S100A12 declined steadily to baseline levels within 2 weeks after disease onset. The ideal cutoff value for identifying patients with intestinal distress within 7 days before disease onset was 60 μg/kg (sensitivity 0.73; specificity 0.55).

Conclusions: Fecal S100A12 levels are increased in VLBW infants with intestinal distress; however, the potential for S100A12 as an early biomarker is largely limited by overlaps between values of infants with intestinal distress and the reference population.

*Royal Children's Hospital Melbourne, Murdoch Children's Research Institute, Parkville, Australia

Department of Pediatric Rheumatology and Immunology, University Children's Hospital Münster, Münster, Germany

Department of Pediatrics, Helios Klinikum Wuppertal, Wuppertal, Germany.

Address correspondence and reprint requests to Jan Däbritz, MD, Department of Pediatric Rheumatology and Immunology, University Children's Hospital Münster, Röntgenstrasse 21, D-48149 Münster, Germany (e-mail: Jan.Daebritz@uni-muenster.de).

Received 20 February, 2013

Accepted 27 March, 2013

This study was funded by the HELIOS Research Center (Germany), which had no involvement in the study design; the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the manuscript for publication.

The authors report no conflicts of interest.

© 2013 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,