Abstract
Intestinal fatty acid binding protein (I-FABP) is released from mature enterocytes when cell membrane integrity is disrupted. This study aimed to prospectively investigate the physiologic significance of early urinary I-FABP and whether it might reflect intestinal compromise in preterm infants. We conducted a prospective cohort study of 100 preterm infants weighing <1250 g and collected serial urine samples at 12, 24, and 48 h after birth. The correlations between initial urinary I-FABP/urinary creatinine (creatinineu) levels and associated factors were analyzed. Among 100 patients, 15 were diagnosed with meconium obstruction of prematurity, and five were diagnosed with necrotizing enterocolitis during the hospital stay. Early urinary I-FABP/creatinineu levels were inversely correlated with both gestational age (Spearman’s rank correlation coefficient (Rs) −0.381, p < 0.01) and birth weight ((Rs) −0.424, p < 0.01). Early urinary I-FABP/creatinineu levels were associated with cord pH ((Rs) −0.436, p < 0.01) and base excess ((Rs) −0.258, p = 0.021). There were significantly positive correlations between early urinary I-FABP/creatinineu levels and the time to full enteral feeding in preterm infants without specific intestinal morbidities. Therefore, a more premature gut with acute perinatal ischemia is expected to exhibit increased I-FABP levels shortly after birth. Because of small sample size, further large-scale studies are needed.
Highlights
Intestinal fatty acid binding protein (I-FABP) comprises a 15-kDa cytosolic watersoluble protein located in the small and large intestines and is released when the intestinal mucosa is disrupted [1]
We evaluated the correlations between early urinary I-FABP/creatinineu levels and the time required to achieve full enteral feeding in the normal group, which included preterm infants without any intestinal morbidities such as meconium obstruction of prematurity (MOP) or necrotizing enterocolitis (NEC)
We investigated the physiological significance of early urinary I-FABP levels for the h after birth in the NEC group were not significantly different from those in the normal first 48 h after birth in preterm infants
Summary
Intestinal fatty acid binding protein (I-FABP) comprises a 15-kDa cytosolic watersoluble protein located in the small and large intestines and is released when the intestinal mucosa is disrupted [1]. I-FABP, which reflects mucosal compromise, can be used as a promising biomarker of acute intestinal mucosa damage, including necrotizing enterocolitis (NEC) in preterm infants, and assesses the extent and severity of intestinal involvement even before the development of disease [2,3,4,5,6]. The intestine is susceptible to blood flow redistribution, especially that associated with fetal intestinal hypoperfusion caused by placental insufficiency [7,8]. Few studies have demonstrated that a decreased intrauterine vascular supply to the gastrointestinal tract predisposes patients with fetal growth retardation to NEC development [9,10]. Chorioamnionitis may contribute to fetal gut immune alterations through activation of the maternal innate immune system, which activates a strong fetal inflammatory response [11,12]
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