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Impaired Activity of Blood Coagulant Factor XIII in Patients with Necrotizing Enterocolitis

  • Guo Zhong Tao
  • , Bo Liu
  • , Rong Zhang
  • , Gigi Liu
  • , Fizan Abdullah
  • , Mary Cay Harris
  • , Mary L. Brandt
  • , Richard A. Ehrenkranz
  • , Corinna Bowers
  • , Camilia R. Martin
  • , R. Lawrence Moss
  • , Karl G. Sylvester
  • Stanford University
  • Johns Hopkins University
  • Ann & Robert H. Lurie Children's Hospital
  • The Children's Hospital of Philadelphia
  • Baylor College of Medicine
  • Yale University
  • Nationwide Children’s Hospital
  • Ohio State University
  • Beth Israel Deaconess Medical Center
  • Lucile Packard Children’s Hospital/Stanford University School of Medicine

Producción científicarevisión exhaustiva

12 Citas (Scopus)

Resumen

Necrotizing enterocolitis (NEC) is the most common gastrointestinal (GI) medical/surgical emergency of the newborn and a leading cause of preterm neonate morbidity and mortality. NEC is a challenge to diagnose since it often shares similar clinical features with neonatal sepsis. In the present study, plasma protein profiling was compared among NEC, sepsis and control cohorts using gel electrophoresis, immunoblot and mass spectrometry. We observed significant impairment in the formation of fibrinogen-3 dimers (FGG-dimer) in the plasma of newborns with NEC that could efficiently differentiate NEC and sepsis with a high level of sensitivity and specificity. Interestingly, the impaired FGG-dimer formation could be restored in NEC plasma by the addition of exogenous active factor XIII (FXIII). Enzymatic activity of FXIII was determined to be significantly lower in NEC subject plasma for crosslinking FGG when compared to sepsis. These findings demonstrate a potential novel biomarker and related biologic mechanism for diagnosing NEC, as well as suggest a possible therapeutic strategy.

Idioma originalEnglish
Número de artículo13119
PublicaciónScientific Reports
Volumen5
DOI
EstadoPublished - 17 ago 2015
Publicado de forma externa

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